Dr.wali Khan Thesis on RA2

RHEUMATOID ARTHRITIS AND ITS MANAGEMENT

A Thesis Submitted to Open International University for Complementary Medicines

(Pakistan Campus) affiliated to Open International University for Complementary Medicines

(OIUCM) Colombo in Fulfillment of the Requirements for the Degree of

Doctor of Alternative Medicines, MD (Alt.Med)

BY

HOMOEOPATHIC DR.WALI KHAN

DHMS, RHMP, M.Sc (Biochemistry)

[email protected]

Rheumatoid Arthritis and Its Management


APPROVAL

Name: Dr.Wali Khan

Degree: Doctor of Alternative Medicine, MD (Alt.Med)

Title of Thesis: Rheumatoid Arthritis and its Management

Examining Committee:

Chairman: Prof.Dr.Mendis

Signature and Seal: _____________________________________________

Supervisor: Prof.Dr.Indrapala

Signature and Seal: _______________________________________________

Date of Approval: _____________________________________________

I

I dedicate this humble effort, the fruit of my

thoughts and study to

my affectionate father and mother who groomed

and inspired me to

higher ideas of life.

Acknowledgement

It is the day of great pleasure for me that with the blessing of Almighty Allah and my

continuous hard work I have achieved my target to complete this thesis.

I am very thankful to Homoeopathic Professor Dr Inamullah Mirza Ex-President

National Council for Homoeopathy (Govt: Pakistan) for providing me this opportunity

to complete this thesis. He always responded quickly whenever, I called him for

guidance.

I am also thankful to Assistant Professor Dr.Roshan Ali PhD (Biotechnology)

Department of Biochemistry Khyber Medical University Peshawar Khyber

Pakhtunkhwa for his generous guidance.

I am also thankful to my mother and grand mother who always prayed for my success

in all fields of life and after death.

I am very thankful to Mr.Fazal Rahim junior clerk NTFP Department Bajaur Agency

who worked day and night on computer for typing this thesis.

Homoeopathic Doctor Wali Khan

M.Sc (Biochemistry) DHMS

[email protected]


Preface

There are over 400,000 people with rheumatoid arthritis (RA) in the UK.Although this

makes it a common disorder, there are numerous other conditions ahead of it in terms

of numbers, and indeed as causes of excess mortility.What this does not capture

however, is the dreadful morbidity associated with the disease. The synovitis.Four of

RA affects multiple sites causing widespread pain, and the subsequent destruction of

the joints can lead to severe disability affecting all aspects of motor function from

walking to fine movements of hand.Further-more,RA is not simply a disease of the

joints but can affect many other organs causing, for example, widespread vasculitis or

severe lung fibrosis. More recently it has become apparent that RA is associated with

an increased prevalence of coronary artery disease and significant increased risk of

premature mortality.

Fortunately there are a considerable number of disease-modifying and anti-

inflammatory agents which can significantly reduce the impact of RA.Some of these,

for example corticosteroids,sulphasalazine or methotrexate,have been available for

many years, and rheumatologists are well used to balancing the benefits and side-

effects of these drugs. More recently, targeted disease-modifying and anti-

inflammatory therapies, particularly the anti-TNF agents, have emerged, and have

proved effective in many patients. While it is encouraging that there is such a wide

range of treatment available, the choice brings with it difficult questions concerning the

best sequencing of therapy. Moreover, the newer drugs are expensive. The high

impact of the disease and the need to make best use of the available treatment RA a

highly suitable subject for the rheumatologists and other professionals.

This venture is a modest attempt to present to the reader a Synopses of a veritable

disease which is generally not taken as a serious cause for concern.

Most often it is reckoned as an ailment of trivial significance, despite, its wide and wild

effects upon general health and well being of the peoples. Statistics with respect to the

magnitude, extent and prevalence of the disease in Pakistan are too inadequate. And

III

practically speaking there is no reliable data base is available on the topic Rheumatoid

Arthritis.

The salient features highlighted in this article show the way for forward planning and

study in greater depth.

A comparative study of the various therapies, briefly discussing their merits and

demerits has also been sufficiently incorporated the value and worth of any type of

medical treatment must necessary rest upon:

Simplicity

Efficacy and adequacy

Economy in cost

Harmlessness

Availability of expertise

Popularity

Duration of treatment till cure

Commitment and dedication of the professionals

No opinion has been expressed about the preference of one thereby over the

other, this being a matter for the experts from every discipline to decide in

particular and individual cases.

The opening chapters of this article present over all view and explain what

Rheumatoid Arthritis is? The scope of this dissert under the guide lines provided by

the Open International University for Complementary Medicines Colombo (OIUCM),

has been kept in view and dealt with accordingly.

Appropriate and effective management of Rheumatoid Arthritis is based upon:

Etiology

Epidemiology

Immunopathogenesis

Diagnosis

Prognosis

Treatment under various therapies

Prevention and Cure

IV


The desertion has been prepared in fulfillment of pre-requisite and as a part of

curriculum exercise toward the accomplishment of the MD degree programme the

OIUCM.

Homoeopathic Doctor Wali Khan

M.Sc (Biochemistry), DHMS

V

Table of Contents: Page #Dedication iAcknowledgment iiPreface iii List of Abbreviations ixCHAPTER -1 11.1 Complementary and alternative medicines: 11.2 Alternative Medicine 3CHAPTER - 2 72.1 Introduction to rheumatoid arthritis 7CHAPTER - 3 9 3.1Signs and Symptoms of Rheumatoid arthritis 93.2 Joints 103.3 Deformities 11

3.3.1 Hands and wrists 11

3.3.2 Feet and ankles 11

3.3.3 Knee 12

3.3.4 Cervical Spine 12

3.4 Skin 133.5 Lungs 143.6 Kidneys 143.7 Heart and blood vessels. 15

3.8 Other 15

3.8.1 Musculoskeletal 15

3.8.2 Ocular 15

3.8.3 Hepatic 16

3.8.4 Hematological. 16

3.8.5 Neurological 16

3.8.6 Constitutional symptoms 17

3.8.7Osteoporosis 17

3.8.8 Lymphoma 17

CHAPTER - 4 18

4.1 Diagnosis 18

4.1.1 Physical Examination 184.1.2 Imaging 23

VI


4.1.3 Blood tests 24

CHAPTER - 5 27

5.1 Rheumatoid arthritis classification criteria 27

5.2 Types of Rheumatoid Arthritis 29

5.3 Juvenile Rheumatoid Arthritis 31

5.4 Palindromic Rheumatoid Arthritis 32

5.5 Pannus Rheumatoid Arthritis 33

5.6 Seronegative Rheumatoid Arthritis 35

5.7 Seropositive Rheumatoid Arthritis 36

CHAPTER- 6 37

6.1 Differential diagnoses 376.2 Diseases with Symptoms Similar to Rheumatoid Arthritis 40

6.3 Monitoring progression 40

CHAPTER- 7 42

7.1 Pathophysiology and causes 42

7.2 Possible infectious triggers 437.3 Psychological factors 447.4 Continued abnormal immune response 447.5 Role of vitamin D 45

CHAPTER - 8 48

8.1 Complications 48CHAPTER- 9 499.1 Rheumatoid arthritis and pregnancy 499.2 Rheumatoid arthritis makes it difficult to conceive 49CHAPTER-10 5110.1 Management of Rheumatoid Arthritis under various therapies 52

10.2 Disease modifying anti-rheumatic drugs (DMARDs) 53

10.3 Traditional small molecular mass drugs 53

10.4 Agents biological 56

VII

10.5 DMARDs for Treatment of Rheumatoid Arthritis 5710.6 Anti-inflammatory agents and analgesics 6210.7 Surgery. 64

10.8 Non-Pharmacological Treatment. 64

10.9 Other therapies 6510.9.1 Homeopathic Treatment of Rheumatoid Arthritis 66

71

10.9.2 Acupuncture for Rheumatoid Arthritis 7210.9.3 Ayurveda for Rheumatoid Arthritis. 75

10.9.4 Reflexology. 7610.9.5 Yoga Treatment of Rheumatoid Arthritis. 79CHAPTER- 11 7911.1 Prognosis: 8111.2 Prognostic factors 8111.3 Mortality 81

CHAPTER-12 82

12. Epidemiology 82

CHAPTER -13 83

13. History 83CHAPTER- 14 8414. Photographs 84 15. References 115

VIII


List of Abbreviations

ANA Antinuclear AntibodyACR American College of RheumatologyALT Alanine TransaminaseAST Aspartate TransaminaseACPAs Anticitrullinated Protein AntibodiesCAM Complementary Alternative MedicineCBC Complete Blood CountCCP Cyclic Citrullinated PeptideCRP C-Reactive ProteinCNHC Complementary and Natural Healthcare CouncilDNA Deoxy Ribonucleic AcidDAS Disease Activity ScoreDIP Distal InterphalangealDMARs Disease Modifying Anti Rheumatic DrugsESR Erythrocyte Sedimentation RateEULAR European League Against RheumatismEBV Epstein-Barv VirusFDA Food and Dietary AllowanceIV IntravenousIL Inter LeukinLFTs Liver Function TestsMMPs Matrix MetalloproteasesMCH Major Histocompatibility ComplexMTP MetatarsophalangealMCP MetacarpophalangealMCV Muted Citrullinated VimentinMRI Magnetic Resonance ImageMTX Methotrexate

IX

NIH National Institute of HealthNHIS National Health Interview SurveysNSAIDs Non Steroidal Anti Inflammatory DrugsPIP proximal interphalangealPOCT Point of Care TestRA Rheumatoid ArthritisRF Rheumatoid FactorROM Range of MotionSA Subjective AssessmentSC SubcutaneousSSZ SulfasalazineSLE Systemic lupus erythematosusTB TuberculosisTCM Traditional Chinese MedicinesTNF Tumor necrosis factorT IAs Transient Ischemic AttackVDR Vitamin D ReceptorWBC White Blood CellWHM Western Herbal MedicinesWHO World Health Organization

X


XI


CHAPTER - 1

1.1 COMPLEMENTARY AND ALTERNATIVE MEDICINES:

General Considerations.

Definition CAM is defined by the Nation Institutes of Health (NIH) as a group of diverse health care systems, practices, and products that are not presently considered to be part of conventional medicine. CAM therapies may be used along an alternative to conventional therapies or in addition to conventional, mainstream medicine to treat condition and promote will being.

Classification CAM modalities have been classified by NIH into five major categories.

Include botanicals, dietary supplements, probiotics, vitamins, minerals, certain diets and nutritional practices, and more.

Energy medicine involves the use of energy fields, such as magnetic fields or biocides (energy fields that some believe surround and penetrate the human body).Examples include Raieki, external qigong and therapeutic touch.

Manipulative and body-based practices. Use manipulation or movement of one or more body parts (e.g., massage, chiropractic, Feldenkrais method and other "body work” systems).

Mind-body medicine uses a variety of techniques design to enhance the integration between mind and body, such as biofeedback, meditation, art and music therapy, hypnosis and guided imagery.

Whole medical systems are built on complete systems of theory and practice that have evolved apart from and often earlier than the conventional medical approach used in the United States. Systems such as traditional oriental medicine, acupuncture, homeopathy, naturopathy, Ayurvede, and Tibetan medicine often use one or more of the methods listed above.

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The Centers for Disease Control and Prevention conducted National Health interview Surveys (NHIS) in 2002 and 2007.Overall, 23,000 American adults from diverse populations were asked about their use of CAM in the 2007survey. Thirty-eight present reported using some form of CAM in the previous 12 months, essentially unchanged form 36% in 2002. The most commonly used CAM therapies were non- vitamin,nonmineral nature products (17.7%), with fish oil, gluscosamine, Echinacea, flaxseed and ginseng being most common; deep breathing exercises (12.7%); meditation (9.4%). Chiropractic or osteopathic manipulation (8.6%); massage (8.3%); and yoga (6.1%).CAM use was higher levels of educations, who were not poor, who live in the West and who have quit cigarette smoking.

The most common conditions for which and adults used CAM were similar to those seen in most primary care offices; musculoskeletal complaints, such as back, neck, and joint pain.

Funding for biomedical research in this filed increased when the NIHestablished the Office of alternative Medicine in 1992 with an annual budget of $2 million. In 1998, its role was expanded as the National Center for Complementary and Alternative Medicine (NCCAM).NCCAM’s budget for fiscal year 2009 was $2 million. Although some CAM modalities are not easily evaluated using randomized control trial methodology, the 2005 Institute of Medicine report recommends that conventional and CAM treatments both be held to similar standards of safety and efficacy.

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1.2 Alternative Medicine

Orthodox and holistic approaches to medicine

Alternative medicine is based on holistic principles.

Conventional medicine is based on very detailed and specific scientific knowledge.

Health is seen as simply an absence of symptoms, ill-health as a malfunction in the body or mind system that has to be corrected.

The emphasis is on fighting, conquering and destroying disease with use of drugs, surgery or sometimes hard treatment of the mind.

The mind and body are seen as separate entities and are treated by different disciplines, the spirit is ignored.

The focus is on symptoms of disease and it is the symptoms that will be treated while other needs of the person will largely ignored.

An imbalance in the relationship between doctor and patient may be created’

Aims to deal with the patient as a whole, not merely with physical symptoms.

Holistic Practioners:

They assume a person exists on many levels and take into account not only the body but also the mind and spirit (the animating vital principle) of an individual. The mind and spirit are not seen simply as part of the body; each is considered to be a complete system, constantly interacting with one another and of equal importance. The three systems, that is mind body and spirit, can be said to be integrated principles of the whole. Holistic practitioners believe the mind, body and spirit of an individual tend naturally towards a state of balance, known in the West as homeostasis.

For example, prolonged stress may unbalance the mind that causes the body to react with various symptoms, such as pain or fatigue. The spirit, too, may become unbalanced and depression may occur.

3

Holistic practitioners tend to focus on the underlying cause rather than on symptoms of an aliment.

When there is a problem

Any treatment provided aims

Holistic practitioners would almost certainly suggest that to control symptoms would not be able to deal with the underlying disturbances that are creating these symptoms. Not only do drugs prevent elimination of impurities but that they might add toe toxins already prevalent.Surgery is thought to destroy homeostasis and is seen as necessary only in the last resort. While it is accepted that a vieus may trigger an illness, it is thought there is probably a state of susceptibility to disease already prevalent n the individual owing to an imbalance in the mind, which cannot be treated with surgery.

Alternative Therapies in the west

Alternative therapies come from all over the world. Some, such as Ayurveda, from India, acupressure, acupuncture and Chinese herbal medicine from China, known collectively as Traditional Chinese Medicine (TCM), and Western Herbal Medicine (from Europe).

Homeopathy from Germany osteopathy from USA, aromatherapy (from France),Bach flower remedies (from England).Biofeedback (from the USA).Until about the mid-1970s alternative therapies were collective known as “fringe” and labeled unconventional or unorthodox practices.

Alternative, however, embraces all practices that are not orthodox and it is the word used to describe therapies that are not part of conventional medical practice in USA.

Australia

4


About half the total population of Australia is reckoned to use at least one non-medically prescribed remedy each year and one-quarter of the total population consult and alternative therapy.It is not permitted to treat certain diseases, such as cancer, by any alternative therapy. The three most popular therapies are probably massage, naturopathy, Chinese and Western herbal, medicine.

New Zeeland

Chiropractors and osteopaths in New Zeeland are registered as medical auxiliaries.

South AfricaAn act in 1982 in South Africa incorporated all alternative practitioners into a register supervised by the Associated Health Service Professional Board. It has the same status as the orthodox practitioners’ register.

United Kingdom

In the UK chiropractic and osteopathy are registered therapies and members of the registering boards are allowed to practice. Practitioners of almost any therapy have the right to practice under common law as except they cannot be involved with dentistry, midwifery, veterinary surgery or treat venereal, disease. No treatment or remedies for cancer can be advertised but anyone is allowed to treat the disease.In 1995 a consumers Association survey showed healing, osteopathy, chiropractic, homeopathy, aromatherapy and acupuncture to be the most popular alternative therapies, while aromatherapy is the fastest growing.

In the USA each of the 50 states decides its own policy regarding alternative medicine. In most states alternative techniques are described. Chiropractic, the most popular alternative therapy, is registered by all states and doctors refer to and receive referrals chiropractors.

While herbal medicine is banned in many states. New York State however recognizes all therapies and supports freedom of choice in health. Ayurveda, chiropractic and TCM are very popular therapies, aromatherapy and homoeopathy less so.

Health is perceived to be not merely the absence of disease but a positive quality of living.

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Patients demand to be more actively involved knowledgeable about, their own health.

There is a fear of conventional drug treatment and surgery.Patients are becoming aware of the limitations of orthodox medicine.Patients want more communication with, and more information from, their doctors than they receive.

CHAPTER - 2

2.1 INTRODUCTION TO RHEUMATIOD ARTHRITIS:

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Definition:

Rheumatoid arthritis is a chronic symmetrical polyarthritis of unknown cause and is

characterized by chronic inflammatory synovitis of mainly peripheral joints along with

systemic disturbances and extra-articular features. Course of disease is prolonged with

exacerbations and remission. Characterized by:

Symmetrical inflammatory polyarthritis

Extra-articular involment e.g. in lungs and many other organs

Progressive joint damage causing severe disability

General consideration:

Rheumatoid Arthritis (RA) is a chronic, systemic inflammatory disorder that may

effect many tissues and organs, but principally attacks flexible (sensorial) joints. The process

produces an inflammatory response of the capsule around the joints (synovium) secondary

to swelling (hyperplasia) of synovial cells, excess synovial fluid, and the development of

fibrous tissue (pannus) in the synovium.The pathology of the disease process often leads to

the destruction of articular cartilage and ankylosis of the joints. Rheumatoid arthritis can also

produce diffuse inflammation in the lungs, membrane around the heart (pericardium), the

membranes of the lung (pleura), and white of the eye (sclera), and also nodular lesions, most

common in subcutaneous tissue.

Although the cause of rheumatoid arthritis is unknown, autoimmunity

plays a pivotal role in both its chronicity and progression, and RA is considered a systemic

autoimmune disease. About 1% of the world’s population is afflicted by rheumatoid arthritis,

women three times more often than men. Onset is most frequent between the ages of 40 and

50, but people of any age can be affected.

It can be a disabling and painful condition, which can lead to substantial loss of

functioning and mobility if not adequately treated. It is a clinical diagnosis made on the basis

of symptoms, physical exam, radiographs (X-rays) and labs, although the American College

7

of Rheumatology (ACR) and the European league Against Rheumatism (EULAR) publish

classification criteria for the purpose of research. Diagnosis and long-term management are

typically performed by a rheumatologist, an expert in joint, muscle and bone diseases.

Various treatments are available. Non-pharmacological includes physical, orthoses,

occupational therapy and nutritional but these do not stop the progression of joint

destruction. Analgesia (painkillers) and anti-inflammatory drugs, including steroids are

used to suppress the symptoms, while disease-modifying antirheumatic drugs (DMARDs)

are required to inhibit or halt the underlying immune process and prevent long-term

damage. In recent times, the newer group of biologics has increased treatment options.

The name is based on the term “rheumatic fever”, an illness which includes joint pain

is derived from the Greek word pebua-rheuma (nom.),pebuaro - rheumatos (gen.) ( “flow,

current”).The suffix-oid ( “resembling”) gives the translation as joint inflammation that

resembles rheumatic fever. The first recognized description of rheumatoid arthritis was

made in 1800 by Dr.Augustin Jacob Landre-Beauvais (1772-1840) of Paris.

Signs and symptoms

While rheumatoid arthritis primarily affects joints, problems involving other of the body

are known to occur. Extra-articular (“outside the joints”) manifestations other than anemia

(which is very common) are clinically evident in about 15-25% of individuals with rheumatoid

arthritis. It can be difficult to determine whether diseases manifestation are directly caused

by the rheumatoid process itself, or from side effects of the medications commonly used to

treat it – for example, lung fibrosis from methotrexate or osteoporosis from corticosteroids.

CHAPTER - 3

8


3.1 Signs and Symptoms of Rheumatoid arthritis

The types and severity of symptoms of rheumatoid arthritis varies between individuals. At the onset of the disease, the symptoms of rheumatoid arthritis can be vague and develop slowly. They may not include the classic symptom of joint pain that people often associate with arthritis. These indistinct, early symptoms may include fatigue, loss of appetite, and weakness. Other early symptoms include muscle achiness throughout the body and stiffness that lasts more than one hour after rising in the morning. Ultimately, joint pain develops and can be accompanied by inflammation and swelling in the joints. Joint pain generally affects wrists, fingers, knees, feet, and ankles on both sides of the body. Joint destruction may develop within 1-2 years after the onset of the disease.

Other symptoms may include problems with the eyes, deformities in the hands and feet, fever, paleness, anemia, nodules under the skin, swollen glands, and redness and inflammation of the skin. Because of the generalized inflammatory nature of rheumatoid arthritis, it can affect almost any organ in the body and lead to life threatening complications. These include rheumatoid vasculitis, a type of inflammation of the blood vessels, which can lead to atherosclerosis, stroke, heart attack and other cardiac conditions. Skin ulcerations and infections, bleeding stomach ulcers, and nerve problems that cause pain, numbness, or tingling may also occur. The eyes can also be affected and the neck bones can become instable

The list of signs and symptoms mentioned in various sources for Rheumatoid arthritis includes the 29 symptoms listed below: Joint pain Joint swelling Joint stiffness Morning joint stiffness Joint stiffness after inactivity Joint tenderness Warm joints Ankle arthritis Foot arthritis Finger arthritis Wrist arthritis

Symmetrical joint pattern - both sides of the body afflicted. Morning stiffness Weight loss Fatigue

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http://www.rightdiagnosis.com/f/fatigue/intro.htm

http://www.rightdiagnosis.com/sym/fatigue.htm

http://www.rightdiagnosis.com/sym/weight_loss.htm

http://www.rightdiagnosis.com/sym/stiffness.htm

http://www.rightdiagnosis.com/sym/joint_symptoms.htm

http://www.rightdiagnosis.com/sym/wrist_symptoms.htm

http://www.rightdiagnosis.com/sym/finger_symptoms.htm

http://www.rightdiagnosis.com/sym/foot_symptoms.htm

http://www.rightdiagnosis.com/sym/joint_pain.htm

http://www.rightdiagnosis.com/sym/joint_symptoms.htm

http://www.rightdiagnosis.com/sym/joint_tenderness.htm

http://www.rightdiagnosis.com/sym/stiff_joints.htm



http://www.rightdiagnosis.com/sym/joint_swelling.htm

http://www.rightdiagnosis.com/sym/joint_pain.htm

http://www.rightdiagnosis.com/r/rheumatoid_arthritis/intro.htm

http://www.rightdiagnosis.com/h/heart_attack/intro.htm

http://www.rightdiagnosis.com/s/stroke/intro.htm

http://www.rightdiagnosis.com/a/atherosclerosis/intro.htm

http://www.rightdiagnosis.com/r/rheumatoid_vasculitis/intro.htm

http://www.rightdiagnosis.com/r/rheumatoid_vasculitis/intro.htm

http://www.rightdiagnosis.com/a/anemia/intro.htm

http://www.rightdiagnosis.com/symptom/loss-of-appetite.htm

Decreased appetite Occasional fever Bouts of mild fever Malaise Episodic flares with remissions Variable symptoms - different people experience different effects Skin bumps (rheumatoid nodules) - about 25% of cases get these Anemia Neck pain Dry eyes Dry mouth Tiredness Afternoon fatigue Afternoon malaise

3.2 Joints

The arthritis of joints known as synovitis is inflammation of the synovial membrane that

lines joints and tendon sheaths. Joints become swollen, tender and warm, and stiffness limits

their movement. With time RA nearly affects multiple joints (it is a polyarthritis), most

commonly small Joints of the hands, feet and cervical spine, but larger joints like the

shoulder and knee can also be involved. Synovitis can lead to tethering of tissue with loss of

movement and erosion of the joint surface causing deformity and loss of function.

Rheumatoid arthritis typically manifests with signs of inflammation, with the affected joints

being swollen, warm, painful and stiff, particularly early in the morning on waking or following

prolonged inactivity. Increased stiffness early in the morning is often a prominent feature of

the disease and typically lasts for more than an hour. Gentle movement may relieve

symptoms in early stages of the disease.

These signs help distinguish rheumatoid from non-inflammatory problems of the joints,

often referred to as osteoarthritis “wear-and tear” arthritis. In arthritis of non-inflammatory

causes, signs of inflammation and early morning stuffiness are less prominent with stiffness

typically less than 1 hour, and movements induce pain caused by mechanical arthritis. In RA,

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http://www.rightdiagnosis.com/sym/malaise.htm

http://www.rightdiagnosis.com/sym/fatigue.htm

http://www.rightdiagnosis.com/sym/tiredness.htm

http://www.rightdiagnosis.com/sym/dry_mouth.htm

http://www.rightdiagnosis.com/sym/dry_eyes.htm

http://www.rightdiagnosis.com/sym/neck_pain.htm

http://www.rightdiagnosis.com/sym/anemia.htm

http://www.rightdiagnosis.com/sym/skin_bumps.htm

http://www.rightdiagnosis.com/sym/malaise.htm

http://www.rightdiagnosis.com/sym/mild_fever.htm

http://www.rightdiagnosis.com/sym/fever.htm

http://www.rightdiagnosis.com/sym/poor_appetite.htm


the joints are often affected in a fairly symmetrical fashion, although this is not specific, and

the initial presentation may be asymmetrical.

As the pathology progresses the inflammatory activity leads to tendon tethering and

erosion and destruction of the joint surface, which impairs range of movement and leads to

deformity. The fingers may surfer from almost any deformity depending on which joints are

most involved.

Although any joint may be affected in RA,the proximal interphalangeal and

metacarpophalangeal joints of fingers as well as the wrist, knee ankles and toes are most

often involved. Distal interphalangeal joints are characteristically spared.

3.3 Deformities

As the disease advances (after months or year) pain, muscle spasm and joints

destruction results in limitation of joint movement, joint instability,subluxation(partially

dislocation) and deformities.

3.3.1 Hands and wrists

Spindling of fingers: In early stages, swelling of metacarpophalangeal joints produces

spindling of fingers

Anterior subluxation of the metacarpophalangeal joints along with ulnar deviation of fingers

develops due to weakening of joint capsule and muscle wasting.

Swan neck deformity: Characterized by hypertension at the proximal interphalangeal joints

and fixed flexion at the distal interphalangeal joints

Button hole deformity: Characterized by fixed flexion of the proximal interphalangeal joint

and extension of the distal interphalangeal joint

Z deformity of thumb: Characterized by hypertension of the first interphalangeal joint and

flexion of the first metacarpophalangeal joint with consequent loss of thumb mobility

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Carpal tunnel syndrome: Tenosynovitis at the wrist can entrap the median nerve and

produce carpal tunnel syndrome

Extra-articular features in hands may be palmer erythema and vasculitic lesions in nail

beds, nail folds, and digital pulp.

3.3.2 Feet and ankles

Lateral deviation of the toes and subluxation (partially dislocation) of the

metacarpophalangeal joints, so that the heads of the metatarsals become palpable in the

soles of the feet and patient often describes as sensation of walking on pebbles. Ankle

develops valgus deformity.

3.3.3 Knee

Synovial effusions and quadriceps wasting are early features:

Later on flexion, valgus (bent outwards) or varus (bent inwards) deformity appear with

joint instability.

Synovial effusion (demonstrated with patellar tap by fixing the knee fingers and thumb

of left hand, then sharply tapping the patella downwards produces a dip when effusion

is present.

Baker’s Cyst: It is an extension of inflamed synovium into the popliteal space, causing

pain and swelling. High pressure generated by flexion of knee can cause rupture of

cyst into calf, manifesting as calf swelling, tenderness and pitting edema.

3.3.4 Cervical Spine

Synovitis of upper cervical spines leads to bone destruction, damage of ligaments that

causes atlantoaxial subluxation which may damage the spinal cord.

3.4 Skin

The rheumatoid nodule, which is often subcutaneous, is the coetaneous feature most

characteristic of rheumatoid arthritis. It is a type of inflammatory reaction known to

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pathologists as a “necrotizing glaucoma”. The initial pathologic process in nodule

formation is unknown but may be essentially the same as the synovitis, since similar

structural features occur in both. The nodule has a central area of fibrinoid necrosis that

may be fissured and which corresponds to the fibrin-rich necrotic material found in and

around an affected synovial space. Surrounding the necrosis is a layer of palisading

macrophages and fibroblasts, corresponding to the intimal layer in synovium and a cuff of

connectives tissue containing clusters of lymphocytes and plasma cells, corresponding to

the suboptimal zone in synovitis.

The typical rheumatoid nodule may be a few millimeters to a few centimeters in diameter

and is usually found over bony prominences, such as the colcannon, the calcaneal

tuberosity.the metacarpophalangeal joints, or other areas that sustain repeated

mechanical stress.

Nodule is associated with a positive RF (rheumatoid factor) titer and severe erosive

arthritis. Rarely, these can occur in internal organs or at diverse sites on the body.

Several forms of vasculitis occur in rheumatoid arthritis. A benign form occurs as micro

infarcts around the manifolds. More severe forms include livedo reticular is, which is a

network (reticulum) of erythematous to purplish discoloration of the skin caused by the

presence of an obliterative coetaneous capillaropathy. Other, rather rare, skin associated

symptoms include:

Pyoderma gangrenosum, a necrotizing,ulcerative,noninfectious neutrophilic

dermatosis.

Sweet’s syndrome, a neutrophilic dermatosis usually associated with

myeloproliferative disorders.

Drug reactions.

Erythematic nodoseum

Lobular panniculitis

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Atrophy of digital skin

Palmar erythema

Diffuse thinning (rice paper skin),and skin fragility (often worsened by corticosteroid

use).

3.5 Lungs.

Fibrosis of the lungs is a recognized response to rheumatoid

disease. It is also a rare but well recognized consequence of therapy (for example with

methotrexated and leflunomide) Caplan,s syndrome describes lung nodules in

individuals with rheumatoid arthritis and additional exposure to coal dust. Pleural

effusions are also associated with rheumatoid arthritis. Another complication of RA is

Rheumatoid lung Disease. It is estimated that about one quarter of Americans with

develops Rheumatoid Lung Disease.

3.6 KIDNEYS

Renal amyloidosis can occur as a consequence of chronic inflammation. Rheumatoid

arthritis may affect the kidney glomerulus's directly through a vasculopathy or a

mesangial infiltrate but this is less well documented (though this is not surprising,

considering immune complex-mediated hypersensitivities are known for pathogenic

deposition of immune complexes in organs where blood is filtered at high pressure to

form other fluids, such as urine and synovial fluid) Treatment with Penicillamine and gold

salts are recognized causes of membranous nephropathy.

3.7 HEART AND BLOOD VESSELS.

People with rheumatoid arthritis are more prone to atherosclerosis, and risk

myocardial infarction (heart attack) and stroke is markedly increased.

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Other possible complications that may arise include: pericarditis, endocarditic, left

ventricular failure, valaulitis and fibrosis. Many people with rheumatoid arthritis do not

experience the same chest pain that others feel when they have angina or myocardial

infarction. To reduce cardiovascular risk, it is crucial to maintain optimal control of the

inflammation caused by rheumatoid arthritis (which may be involved in causing the

cardiovascular risk factors such as blood lipids and blood pressure. Doctors who treat

rheumatoid arthritis patients should be sensitive to cardiovascular risk when prescribing anti-

inflammatory medications, and may want to consider prescribing routine use of low doses of

aspirin if the gastrointestinal effects are tolerable

3.8 OTHER

3.8.1 Musculoskeletal

Subcutaneous nodules (In 20%): Usually seen at sites of pressure or friction such as the

exterior surfaces of the forearms below the elbow,scalp,sacrum,scapula.A chilles tendon,

as well as on the fingers and toes.

Bursitis:The olecranon and other bursae may become swollen.

Tenosynovitis: Particularly affecting the flexor tendons in the palm of the hand and may

contribute to flexion deformities.

Muscle wasting: around affected joints especially in the hands.

3.8.2 Ocular

The eye is directly affected in the form of episcleritis which when severe can very

rarely progress to perforating scleromalacia.Rather more common is the indirect effect of

keratoconjunctivitis sicca, which is a dryness of eyes and mouth caused by lymphocyte

infiltration of lacrimal and salivary glands. When severe, dryness of the cornea can lead to

keratitis and loss of vision. Preventive treatment of severe dryness with measures such as

nasolacrimal duct occlusion is important.

3.8.3 Hepatic

Cytokine production in joints and /or hepatic Kupfer cells leads to increased activity of

hepatocytes with increased production of acute-phase proteins, such as C-reactive protein,

15

and increased release of enzymes such as alkaline phosphates into the blood. In Fealty’s

syndrome, Kuppfer cell activation is so marked that the resulting increase in hepatocyte

activity is associated with nodular hyperplasia of the liver, which may be palpably enlarged.

Although Kupffer cells are within the hepatic parenchyma, they are separate from

hepatocytes.As a result there is little or no microscopic evidence of hepatitis (immure-

mediated destruction of hepatoctes).Hepatic involvement in RA is essentially asymptomatic.

3.8.4 Hematological.

Anemia is by far the most common abnormality of the blood cells.

Rheumatoid arthritis may cause a warm autoimmune hemolytic anemia.The red

cells are of normal size and colour (normocytic and normochromic).A low white

blood cell count (Neutrogena) usually only occurs in patients with Fehy’s

syndrome with an enlarged liver and spleen.The mechanism of neutropenia is

complex.An increased platelet count (thrombocytosis)occurs when inflammation is

uncontrolled,asdoes the anemia.Iron deficiency may also be present due to GIT

blood loss from analgesic ingestion.

3.8.5 Neurological

Peripheral neuropathy mononeuritis multiplex may occur. The most common problem

is carpal tunnel syndrome caused by compression of the median nerve by swelling

around the wrist.Atlanto –axial subluxation can occur, owing to erosion of the odontoid

process and or transverse ligaments in the cervical spine’s connection to the skull. Such

an erosion (>3mm) can give rise to vertebrae slipping over one another and compressing

the spinal cord. Clumsiness is initially experienced, but without due care this can

progress to quadriplegia.

3.8.6 Constitutional symptoms

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Constitutional symptoms including fatigue, low grade fever, malaise, and morning

stiffiness, loss of appetite and loss of weight are common systemic manifestations seen in

patients with active rheumatoid arthritis.

3.8.7 Osteoporosis

Local osteoporosis occurs in RA around inflamed joints.It is postulated to be partially

caused by inflammatory cytokines.More general osteoporosis is probably contribution to by

immobility, systemic cytokine effects, local cytokine release in bone marrow and corticosteroid

therapy.

3.8.8 Lymphoma

The incidence of lymphoma is increased in RA, although it is still uncommon.

CHATER - 4

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4.1 Diagnosis:

Diagnosis of RA is based on history, examination, X-Ray findings and serology (RA

factor).Rheumatoid arthritis presents initially with non specific symptoms but assume

its characteristic features with in 1-2 years of onset. The following features support

diagnosis of rheumatoid arthritis.

1 Bilateral symmetrical inflammatory polyarthritis involving small and large joints both the

upper and lower extremities with sparing of axial skeleton except cervical spine

suggest diagnosis

2 Systemic features indicative of inflammatory nature of disease such as morning

stiffness support the diagnosis

3 Presence of subcutaneous nodules is helpful diagnostic feature.

4.4.1 Physical Examination:

Joint involvement is the characteristic feature of rheumatoid arthritis. In general, the small joints of the hands and feet are affected in a relatively symmetric distribution. In decreasing frequency, the MCP, wrist, PIP, knee, MTP, shoulder, ankle, cervical spine, hip, elbow, and temporomandibular joints are most commonly affected. Affected joints show inflammation with swelling, tenderness, warmth, and decreased range of motion (ROM). Atrophy of the interosseous muscles of the hands is a typical early finding. Joint and tendon destruction may lead to deformities such as ulnar deviation, boutonniere and swan-neck deformities, hammer toes, and, occasionally, joint ankylosis. Other commonly observed musculoskeletal manifestations include tenosynovitis (defined as inflammation of the tendon and its enveloping tendon sheath ) and associated tendon rupture due to tendon and ligament involvement, most commonly involving the fourth and fifth digital extensor tendons at the wrist; periarticular osteoporosis due to localized inflammation; generalized osteoporosis due to systemic chronic inflammation, immobilization-related changes, or corticosteroid therapy; and carpal tunnel syndrome. Most patients with RA have muscle atrophy from disuse, which is often secondary to joint inflammation.

Fingers:

The boutonniere deformity, demonstrated in the image Fig N0.6 , describes nonreducible flexion at the PIP joint along with hyperextension of the distal interphalangeal (DIP) joint of the finger. This deformity occurs as a result of synovitis stretching or rupturing the PIP joint through the central extensor tendon, with concomitant volar displacement of the lateral bands. When the lateral bands have subluxed far enough to pass the transverse axis of the joint, they become flexors of the PIP joint. Hyperextension of the DIP joint occurs as the tendons shorten with time.

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A compensatory and reducible hyperextension may occur at the MCP joint. Consequences of boutonniere deformity are loss of thumb mobility and pincher grasp.Swan-neck deformity of the finger describes hyperextension at the PIP joint with flexion of the DIP joint (see the image Fig NO.7). The deformity may be initiated by (1) disruption of the extensor tendon at the DIP joint with secondary shortening of the central extensor tendon and hyperextension of the PIP joint, or (2) volar herniation of the PIP joint capsule due to weakening from

chronic synovitis with subsequent tightening of the lateral bands and central extensor tendon. The lateral bands may become shortened over time and lie dorsally, limiting PIP flexion and ineffectively extending the DIP joint.

Tightness of intrinsic muscles (eg, interossei, lumbricals) may cause major declines in mobility of the fingers. This characteristic is ascertained on examination when the PIP joint cannot be flexed while the MCP joint is fully

extended, but it can be flexed if the MCP is in flexion (Bunnell test); primary PIP joint pathology would be evident with the MCP joint in either position. To assess this accurately, the phalanx must be aligned with the metacarpal, as the intrinsic muscles on the ulnar side are slack when ulnar deviation at the MCP joint exists, thus allowing more motion.

Flexor tenosynovitis of the fingers is common and suggests a poor prognosis. "Triggering" of the finger occurs when thickening or nodule formation of the tendon interacts with the concomitant tenosynovial proliferation, trapping the tendon in a flexed position (stenosing tenosynovitis). Tendon rupture may occur due to infiltrative synovitis in the digit or bony erosion of the tendon at the wrist (especially the flexor pollicis longus). Arthritis mutilans (sometimes called opera glass hands) results if destruction is severe and extensive, with dissolution of bone. In the small joints of the hands, the phalanges may shorten and the joints may become grossly unstable. Pulling on the fingers during examination may lengthen the digit much like opening opera glasses, or the joint may bend in unusual directions merely under the pull of gravity. Aso see the image Fig NO.13 for hand deformities.

Metacarpophalangeal joints:

As seen in the image Fig NO.8 , 2 typical deformities that alter the alignment of the palmar skeletal arches and the stability of the fingers may occur at the MCP joints: volar subluxation and ulnar deviation. Most cases of ulnar deviation are accompanied by counterpoised radial deviation of the wrist, roughly proportional to the degree of ulnar deviation of the fingers. The volar plate is firmer and more substantial than other portions of the MCP joint capsule and, therefore, effectively limits extension and dorsal movement at the joint. The greater strength of the flexor muscles relative to the extensor muscles causes volar migration of the proximal phalanx after synovial-based inflammation has weakened ligament and tendon insertions about the MCP joint capsule.

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Ulnar deviation occurs after synovitis has led to stretching and attenuation of the volar plate and collateral ligaments, allowing dislocation of the flexor tendon volarward and ulnarward. The supporting structures of the extensor tendons also may become attenuated or destroyed by synovial distention and invasion, loosening the tendons so that they no longer ride centrally and dorsally over the metacarpal head but move into the cleft between the MCP joints. If the extensor tendon subluxation is beyond the transverse axis of the MCP joint, the tendon becomes a flexor at that joint, further limiting the active extension of the fingers.

Wrists:

Multiple deformities may occur in the wrist. Disruption of the radioulnar joint with dorsal subluxation of the ulna (caput ulna), as well as rotation of the carpus on the distal radius with an ulnarly translocated lunate, is common. The combination of an ulnar drift of the fingers and carpal rotation is known as a zigzag deformity. Shortening of the carpal height (noted on radiographs), due in part to cartilage loss, is seen with rotational deformities. Dorsal subluxation of the ulna often allows the ulnar styloid to be depressed volarly on examination, much like depressing a piano key. Subluxation may lead to rupture of the extensor tendons of the little, ring, and long fingers, because the end of the distal ulna is roughened secondary to erosion of bone and may abrade the tendons as they move back and forth during normal hand function, much like a rope being frayed while rubbing over a sharp rock. This process is especially likely to lead to tendon rupture if there is associated tenosynovitis. (See the image Fig No.9)

. Entrapment neuropathy may result from synovitis about the flexor tendons. Entrapment of the median nerve as it passes through the carpal tunnel leads to decreased sensation on the palmar aspect of the thumb, index finger, and long finger and on the radial aspect of the ring finger; weakness and atrophy of the muscles in the thenar eminence also occurs. The less frequent entrapment of the ulnar nerve at the wrist causes decreased sensation over the little finger and the ulnar aspect of the ring finger and decreased interosseous muscle strength and mass.

Elbow:

Elbow involvement is often detected by palpable synovial proliferation at the radiohumeral joint and is commonly accompanied by a flexion deformity, such as in contractures. Olecranon bursal involvement is common, as are rheumatoid nodules in the bursa and along the extensor surface of the ulna. Nodules are clearly seen in the image Fig NO.26.

. Shoulders:

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Rheumatoid arthritis commonly involves the shoulders and is manifested by tenderness, nocturnal pain, and limited motion. Initially, swelling occurs anteriorly, but it may be difficult to detect and is present on examination in a minority of patients at any point in time. Rotator cuff degeneration secondary to synovitis may limit abduction and rotation. Superolateral migration of the humerus occurs with complete tears. Glenohumeral damage leads to pain with motion and at rest and typically leads to severely restricted motion or "frozen shoulder syndrome." Acromioclavicular arthritis is not as frequent or as disabling as the other manifestations of this disease.

Feet and ankles:

The ankle joint itself is rarely involved without midfoot or MTP involvement. The ankle does not often deform, as it is a mortise joint. Major structural changes occur in the midfoot and foot due to the combination of chronic synovitis and weight bearing. Posterior tibialis tendon involvement or rupture may lead to subtalar subluxation, which results in eversion and migration of the talus laterally. Midfoot disease leads to loss of normal arch contour with flattening of the feet. The MTP joints are inflamed in most patients and, due to the heavy loads they bear, commonly become deformed over time. The great toe typically develops hallux valgus (a bunion); subluxation of the phalanx at the MTP joint of the other toes predominantly occurs dorsally. The toes may exhibit compensatory flexion due to a fixed length of the flexor tendons, thus resulting in hammer toes (thought to look like piano hammers). The second and third metatarsal heads commonly protrude and may become the primary weight-bearing surface at the MTP joints. Calluses and pain upon weight bearing result.

Knees:

Rheumatoid arthritic knees may develop large effusions and abundant accumulation of synovium. Knee effusions and synovial thickening are common and are easily detected during the early course of the disease. Persistent effusions may lead to inhibition of quadriceps function by spinal reflexes, resulting in subsequent atrophy. Instability may develop after progressive loss of cartilage and weakening of ligaments; deformity may include genu valgus or varus and flexion deformities. The energy expenditure to stand or walk significantly increases if there are flexion deformities of the knees.

Hips:

The hips are commonly involved in rheumatoid arthritis; however, because of their deep location, their involvement is not always readily apparent early on during the course of the disease. Hips are difficult to examine by direct inspection or palpation. Limited motion or pain on motion and weight bearing are the hallmarks of hip involvement. The Patrick maneuver (flexion, external rotation, and

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abduction) is abnormal in this situation. A flexion deformity may be demonstrable by conducting a Thomas test, which is performed by flexing one hip (with the patient supine) while restricting pelvic motion by keeping the other hip in the neutral position on the examination table. If the hip cannot be maintained in the neutral position, a contracture is present.

Cervical spine:

Neck pain on motion and occipital headache are common manifestations of cervical spine involvement (see the image Fig NO.10). Most patients with cervical spine involvement have a history of the disease for more than 10 years. Clinical manifestations of early cervical spine disease consist primarily of neck stiffness that is perceived throughout the entire arc of motion. The atlantoaxial joint is a synovial-lined joint and is susceptible to the same proliferative synovitis and subsequent instability seen in the peripheral joints. Patients with severe destruction in the hands (arthritis mutilans) are very likely to have symptomatic cervical spine abnormalities, as are those patients taking significant amounts of corticosteroids for control of rheumatoid arthritis.

. Neurologic involvement ranges from radicular pain to a variety of spinal cord lesions that may result in weakness (including quadriparesis), sphincter dysfunction, sensory deficits, and pathologic reflexes. Transient ischemic attacks (TIAs) and cerebellar signs may reflect vertebral artery impingement from cervical subluxation or basilar artery impingement from upward migration of the dens. Tenosynovitis of the transverse ligament of C1 may lead to C1-C2 instability. Myelopathy secondary to rupture of the transverse ligament may lead to neurologic deficits. Radiculopathy is most common at the C2 root, although symptomatic subluxations may occur at any level. Symptoms of cervical myelopathy are gradual in onset and are often unrelated to either the development of or accentuation in neck pain. When neck pain does occur, it frequently radiates over the occiput region in the distribution of the C1-3 nerve roots. The Lhermitte sign, in which tingling paresthesia that descends through the thoracolumbar spine occurs as the cervical spine is flexed, is typically observed. During the physical examination, it is important to assess the following signs and symptoms:

Stiffness Tenderness Pain on motion Swelling Deformity Limitation of motion Extra-articular manifestations Rheumatoid nodules

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Genetic and environmental factors play a role in pathogenesis. Although laboratory testing and imaging studies can help confirm the diagnosis and track disease progress, rheumatoid arthritis primarily is a clinical diagnosis and no single laboratory test is diagnostic. Complications of rheumatoid arthritis may begin to develop within months of presentation; therefore, early referral to or consultation with a rheumatologist for initiation of treatment with disease-modifying antirheumatic drugs is recommended. Several promising new disease-modifying drugs recently have become available, including leflunomide, tumor necrosis factor inhibitors, and anakinra. Nonsteroidal anti-inflammatory drugs, corticosteroids, and nonpharmacologic modalities also are useful. Patients who do not respond well to a single disease-modifying drug may be candidates for combination therapy. Rheumatoid arthritis is a lifelong disease, although patients can go into remission. Physicians must be aware of common comorbidities. Progression of rheumatoid arthritis is monitored according to American College of Rheumatology criteria based on changes in specific symptoms and laboratory findings. Predictors of poor outcomes in early stages of rheumatoid arthritis include low functional score early in the disease, lower socioeconomic status, early involvement of many joints, high erythrocyte sedimentation rate or Creactive protein level at disease onset, positive rheumatoid factor, and early radiologic changes. Rheumatoid arthritis is characterized by persistent joint synovial tissue inflammation. Over time, bone erosion, destruction of cartilage, and complete loss of joint integrity can occur. Eventually, multiple organ systems may be affected. Imaging:

X-rays of the hands and feet are generally performed in people with a polyarthritis.

In rheumatoid arthritis, there may be no changes in the early stages of the disease, or the X-

ray may demonstrate juxta-articular osteopenia, soft tissue swelling and loss of joint space.

As the disease advances, there may be bony erosion and subluxation X-rays of other joints

may be taken if symptoms of pain swelling occur in those joints. Other medical imaging

techniques such as magnetic resonance imaging (MRI) and ultrasound are also used in

rheumatoid arthritis.

There have been technical advances in ultrasonography.High –sfrequency

transducers(10MHz or higher) have improved the spatial resolution of ultrasound

images, these images can depict 20% more erosions than conventional

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radiography.Also, colour Doppler and power Doppler ultrasound,which show vascular

signals of active synovitis depending on the drgree of inflammation,are useful in

assessing synovial inflsmmstion. This is important, since in the early stages of

rheumatoid arthritis, the synovium is primarily affected, and synovitis seems to be the

best predictive marker of future joint damage.

4.1.2 BLOOD TESTS

When RA is clinically suspected, immunological studies are required, such as

testing for the presence of rheumatoid factor (RF,a non-specific antibody).A

negative RF does not rule out RA; rather, the arthritis is called seronegative.

This is the case in about 15% of patients.During the first year of illness, rheumatoid

factor is more likely to be negative with some individuals converting to seropositive

status over time.RF is also seen in other illnesses, for example Sjogren’s

syndrome, Hepatitis C,chronic infections and in approximately 10% of the healthy

population and therefore the test is not very specific.

Because of this low specificity, new serological tests have been

developed,which test for the presence of anticitrullinated protein antibodies

(ACPAs) or anti-CCP.Like Rf, these tests are positive in only a proportion

(67%) of all R A cases, but are rarely positive if RA is not present, giving it a

specificity of around 95%.As with RF, there is evidence for ACP as being

present in many cases even before onset of clinical disease.

The most common tests for ACP As are the anti-CCP (cyciccitrullinated peptide) test and the

Anti-MCV assay (antibodies against mutated citrullinated Vimentin).Recently a serological

point-of-care test (POCT) for theearly detection of RA has been developed. This assay

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combines the detection of rheumatoid factor and anti-MCV for diagnosis of rheumatoid arthritis

and shows a sensitivity of 72% and specificity of 99.7%.

Also, several other blood tests are usually done to allow for other causes of

arthritis, such as lupus erythematosus. The erythrocyte (te sedimentation rate

(ESR), C-reactive protein, full blood count, renal function, liver enzymes and

other immunological tests (e.g.,antinuclear antibody/ANA) are all performed at

this stage.Elevated ferritin levels can reveal hemochromatosis, a mimic RA, or

be assign of Still’s disease a seronegative,usually juvenile, variant of

rheumatoid.

Laboratory and Imaging Findings Associated with Rheumatoid Arthritis

Creactive protein* Typically increased to >0.7 picograms per mL; may be used to monitor

25

disease course.Erythrocyte sedimentation rate*

Often increased to >30 mm per hour; may be used to monitor disease course.

Hemoglobin/hematocrit* Slightly decreased; hemoglobin averages around 10 g per dL (100 g per L); normochromic anemia, also may be normocytic or microcytic.

Liver function* Normal or slightly elevated alkaline phosphatasePlatelets* Usually increasedRadiographic findings of involved joints*

May be normal or show osteopenia or erosions near joint spaces in early disease; wrist and ankle films are useful as baselines for comparison with future studies.

Rheumatoid factor* Negative in 30 percent of patients early in illness; if initially negative, can repeat six to 12 months after disease onset; can be positive in numerous other processes (e.g., lupus; scleroderma; Sjögren’s syndrome; neoplastic disease; sarcoidosis; various viral, parasitic, or bacterial infections); not an accurate measure of disease progression.

White blood count* May be increasedAnticyclic citrullinated peptide antibody

Tends to correlate well with disease progression; increases sensitivity when used in combination with rheumatoid factor; more specific than rheumatoid factor (90 versus 80 percent); not readily available in many laboratories.

Antinuclear antibody Limited value as a screening study for rheumatoid arthritisComplement levels Normal or elevatedImmunoglobulins Elevated alpha-1 and alpha-2 globulins possible.Joint fluid evaluation Consider if an affected joint can be tapped and diagnosis is uncertain;

straw-colored fluid with fibrin flecks often seen; fluid may clot at room temperature; 5,000 to 25,000 white blood cells per mm3 (5 to 25 × 109 per L) with 85 percent polymorphonuclear leukocytes a common finding; in rheumatoid arthritis, cultures are negative, there are no crystals, and fluid glucose level typically is low.

Urinalysis Microscopic hematuria or proteinuria may be present in many connective tissue diseases.

*—Recommended for initial evaluation for rheumatoid arthritis.note: Renal function, although not as likely to change as a direct effect of disease, should be followed to assess renal effects of drug therapy.

CHAPTER- 5

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5.1 RHEUMATIOD ARTHRITIS CLASSIFICATION CRITERIA:

In 2010 the 2010 ACR/EULAR Rheumatoid Arthritis Classification Criteria were

introduced. These new classification criteria overruled the “old” ACR criteria of 1987 and are

adapted for early RA diagnosis . The “new”classification criteria jointly published by the

American College of Rheumatology (ACR) and the European League Against Rheumatism

(EULAR)establish a point vvalue between 0 and 10.every patient with a point total of 6 or

higher is unequivocally classified as an RA patient, provided he has synovitis in at least

one joint and given that there is no other diagnosis better explaining the synovitis.Four areas

are covered in the diagnosis.

Joint involvement, designating the metacarpophalangeal joints,proximal interphalangeal

joints,the interphalangeal joint of the thumb, second through third metatarsophalangeal joint

and wrist as small joints, and elbows, hip joints and knees as large joints;

Involvement of 2-10 large joints gives 1point

Involvement of 1-3 small joints (with or without involvement of large joints) gives

points

Involvement of 4-10 small joints (with or without involvement of large joints) gives

points

Involvement of more than 10 joints (with involvement of at least 1 small joint) gives

5 points.

Serological Parameters-including the rheumatoid factor as well as ACPA- “ACPA”stand

for “anti-citrullinated protein antibody”

Negative RF and negative ACPA gives 0 points

Low-positive RF or low-positive ACPA gives 2 points

High-positive RF or high-positive ACPA gives 3 points

Acute phase reactants:1 point for elevated erythrocyte sedimentation rate,ESR,or

CRP value (c-reactive protient).

Duration of arthritis: 1 point for symptoms lasting six weeks or longer.

The new criteria accommodate to the growing understanding of rheumatoid arthritis and

the improvement in diagnosing RA and disease treatment. In the “new” criteria serology

and autoimmune diagnostics carries major weight, as ACPA detection is appropriate to

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diagnose the disease in an early state, before joints destructions occur. Destruction of the

joints viewed in radiological images was a significant point of the ACR criteria from 1987.

This criterion no longer is regarded to be relevant, as this is just the type of damage that

treatment is meant to avoid.

The criteria are not intended for the diagnoseis for routine clinical care; they were

primarily intended to categorize research (classification criteria).In clinical practice,the

following criteria apply:

Two or more swollen joints

Morning stiffness lasting more than one hour for at least six weeks

The detection of rheumatoid factors or autoantibodies against ACPA such as

autoantibodies to mutated citrullinated vimentin can confirm the suspicion of

rheumatoid arthritis.A negative autoanibody result does not exclude a diagnosis of RA.

Revised American Rheumatism Association Criteria for Classification of Rheumatoid Arthritis

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Percentage with rheumatoid arthritis if sign or symptom is*:

Sign or symptom Definition LR+ LR- Present Absent

Morning stiffness

Stiffness in or around the affected 1.9 0.5 39 14

joints for at least one hour after initiating movement

Arthritis of three or more joint areas

Three or more of the following joints noted to be fluid-filled or have soft tissue swelling: wrist, PIP, MCP, elbow, knee, ankle, MTP

1.4 0.5 32 13

Hand joint involvement

Wrist, MCP, or PIP joints among the symptomatic joints observed

1.5 0.4 33 12

Symmetric arthritis

Right and left joints involved for one or more of following: wrist, PIP, MCP, elbow, knee, ankle, MTP†

1.2 0.6 29 17

Rheumatoid nodules

Subcutaneous nodules in regions surrounding joints, extensor surfaces, or bony prominences

3.0 0.98 50 25

Serum rheumatoid factor positive

Positive result using any laboratory test that has a positive predictive value of 95 percent or more (i.e., is positive in no more than 5 percent of patients without rheumatoid arthritis)

8.4 0.4 74 13

Radiographic changes

Hand and wrist films show typical changes of erosions or loss of density adjacent to affected joints

11 0.8 79 21

*—Assumes overall probability of rheumatoid arthritis of 30 percent.†—PIP, MCP, and MTP joints need not be absolutely symmetrical.LR+ = positive likelihood ratio; LR-= negative likelihood ratio; PIP= proximal interphalangeal; MCP= metacarpophalangeal; MTP= metatarsophalangeal.

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5.2 Types Of Rheumatoid Arthritis:

Rheumatoid arthritis is an autoimmune, progressive disease in which the immunity of our body is confused and starts attacking our own healthy tissues. The disease mainly affects joints. But it can also affect ligaments, tendons, and other systemic organs. There are various types of rheumatoid arthritis.Juvenile Rheumatoid Arthritis is the RA occurring in children below the age of 16. In this too, there are three types, viz. polyarticular, pauciarticular and systemic juvenile rheumatoid arthritis. In polyarticular JRA, five or more joints are affected. It is one of the most dangerous types of rheumatoid arthritis and needs to be controlled as soon as possible by aggressive treatment. Pauciarticular JRA or oligoarthritis attacks four or less joints and occurs more in girls than in boys. Systemic JRA or Still’s disease is the type which starts with high fever and rashes which occur and go suddenly and involve the internal organs too. In all types of JRA, pain, stiffness and swelling of joints are the common symptoms and it is good to detect and treat JRA early so that the child won’t suffer more in future.Another type of rheumatoid arthritis is ankylosing spondylitis. It involves intense back pain and inflammation of spine and larger joints. The joints like elbows and knees are mostly affected in this type. The occurrence of this RA is thrice in men than in women.Polymyalgia rheumatica is a type which shows symptoms like aching and stiffness. This type of RA affects ligaments, muscles, tendons and tissues around the joints.One of the types of rheumatoid arthritis is hip rheumatoid arthritis, which affects normally the smaller joints and tendons and usually occurs at a later stage of life. Another is knee rheumatoid arthritis in which joints of knees become tender, swollen, stiff and obviously painful.

Cervical spondylosis is one more type of rheumatoid arthritis which is more commonly can be referred to as age-related wear and tear. It mainly affects joints in the neck.

One more type of rheumatoid arthritis is lupus. In medical terminology it is called systemic lupus erythematosus. It is a chronic inflammatory disease. Joint pain and inflammation occur in this, along with symptoms in other body organs too. Kidney disorder, lung and heart impairment, neurological symptoms, lesions and rashes are some of the symptoms. It is strange that the patients suffering from this type of RA generally don’t have to face any joint destruction. However, in the long run, bone deformities occur without erosion. This is also an autoimmune disorder.

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Whichever is the type of rheumatoid arthritis, barring a few exceptions, joint pain, inflammation, swelling and tenderness are its common symptoms. It is a complicated disease in terms of diagnosis. No decisive test is available to ensure its presence. Therefore, you should know all the types and their symptoms in detail. So that when some of the symptoms occur in yourself or anybody you know, you can get the diagnosis done and start the treatment in time.

Typically, this disease occurs anywhere between the age of 30 and 70 or more. But children too suffer from this disease and if they are left untreated, they can suffer much in future. Therefore you should know all types of rheumatoid arthritis thoroughly, so as to remain careful about yourself and your dear ones.

5.3 Juvenile Rheumatoid Arthritis:

Juvenile rheumatoid arthritis is the most prevalent form of arthritis occurring in children. It can occur between the age of 6 months and 16 years. The exact cause of the disease is not known. Research tells us that it is an autoimmune disease. Autoimmune disease occurs when the white blood cells fail to identify the difference between a foreign intruder like bacteria and virus and body’s own healthy tissue and produce chemicals to kill them, which causes pain and inflammation. It is very important to diagnose the disease in its initial stage and treat it before it becomes uncontrollable.

There are three types of juvenile RA and in all of them, joints are the common sites of inflammation. More than one joint can be inflamed and the more the number of affected joints, the more severe is the disease. In that case, the symptoms rarely go in remission.

The first type of juvenile RA is oligoarticular JRA, which occurs in four or fewer joints. Its symptoms are pain, swelling or stiffness in the joints. Commonest joints which are inflamed are of wrist and knee. Sometimes, joint symptoms are not seen, but inflammation of iris, i.e. the colored portion of the eye, occurs, which is called iridocyclitis, uveitis, or iritis. Early detection of this can be done by an ophthalmologist.

In another form of juvenile RA, called polyarticular JRA, five or more joints are affected. This is more common in girls than boys. Small joints, like that in hands and weight-bearing joints, like that in hips, knees, ankles, neck and feet are affected more. Low-grade fever and bumps or nodules may also be associated. The nodules appear on the spots where more pressure is applied while leaning or sitting.

Third type is systemic juvenile rheumatoid arthritis. This affects whole body. Its symptoms include high fever which increases often in the evenings and may suddenly come to normal. When the fever starts, the child looks pale, feels very ill or develops rashes. The rash may come and go suddenly. Sometimes spleen and lymph nodes get enlarged. Consequently, several of the joints get swollen, painful and stiffened.

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An initial sign of juvenile RA is limping fingers, wrists or knees. Sudden swelling may occur in the joints, which can persist. Neck, hips and other joints too can become stiffened. Suddenly appearing and disappearing rashes may also occur in one after another area. Major symptom is the high fever appearing in the evening and suddenly dropping to normal.

The treatment of juvenile RA often includes medication, physiotherapy and exercise, but in some specific situations, the child has to take injections of corticosteroids into the joints or even surgery. It is the job of the general physician, rheumatologist and the physiotherapist to develop the best treatment plan for the child.

Treatment is mainly focused on symptom relief, i.e. relief from pain and inflammation, and slow down or stop the further damage to the joints and remove the limitations on the mobility as far as possible.

The medicines primarily contain non-steroidal anti-inflammatory drugs (NSAIDs), like ibuprofen. They are for restricting the harmful chemicals released from the white blood cells and thus reducing pain and inflammation. If they cannot control the pain and inflammation, the doctor may start other medicines, like methotrexate.

5.4 Palindromic Rheumatoid Arthritis:

Palindromic rheumatoid arthritis has much similarity in symptoms and appearance with rheumatoid arthritis, but is different in that, it hardly causes permanent joint damage. Recurring attacks of pain and swelling in the joints of knees, fingers and large joints are the main characteristics of the disease. Nodules, quite same as those produced in RA, are produced on the affected joints, which usually a rheumatologist can identify and does further testing to confirm the presence of palindromic RA. The patient may or may not suffer from weakness and fever, during the repeated flares which make the joints swollen and painful and are, therefore, often confusing the disease with rheumatoid arthritis. It occurs equally in men and women, unlike RA, which occurs more prominently in women. Also, it can occur at any age between 20 and 70; however, the disease as such is rare.

Though in 40% patients of palindromic arthritis, the attacks become more frequent, x-rays of the affected joints do not generally show any narrowing of joints, which occurs in RA. A very less percentage of sufferers develops a full-scale rheumatoid arthritis from palindromic arthritis and may test positive also for the rheumatoid factor.

The patients of palindromic arthritis may show high sedimentation rates during blood tests and also may show high levels of C-Reactive Protein in the blood. Some studies have inferred the connection of anti-malarial drugs, like Plaquenil, to high risk of developing palindromic arthritis, which later develops into full-scale rheumatoid arthritis.

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Diagnosis of palindromic rheumatoid arthritis is difficult and may take time. It is usually based on elimination of other conditions and finally concluding about the occurrence of the disease. This is because there is no specific test for the diagnosis of this disease. Also it becomes more difficult with the possibility of presence of other auto-immune diseases. However, it is interesting to note that presence of rheumatoid factor indicates high chances of developing rheumatoid arthritis in future.

The flares of palindromic rheumatism may last from a few hours to a few days and then suddenly subside and may not show for a long time. They form a pattern with the symptom-free periods. More commonly 2 to 3 joints are involved and the soft tissue surrounding the joints may also be involved with swelling at particular spots. Particularly finger pads and heel pads are affected.

This is a disease caused by unknown factor. An opinion says that it is an abortive form of RA, indicated by the raised levels of antikeratin antibodies (AKA) and anti-cyclic citrullinated peptide antibodies (anti-CCP), which is the characteristic of rheumatoid arthritis.

Initial treatment includes pain-killers and anti-inflammatory drugs. The physician may also start an anti-depressant. As the attacks are highly unpredictable, the treatment is quite difficult. If the attacks are very frequent, long-term treatment with the disease-modifying anti-rheumatoid drugs (DMARDs), which is administered in rheumatoid arthritis patients, may have to be started.

To adopt a diet, free of pain-causing prostaglandins and arachidonic acid, may help quite a lot. It includes lots of vegetables, fruits, cold water fish, nuts and soy products. It is a must to keep away from weight-gaining foods and oils containing omega-6 fatty acids, namely, sesame oil, sunflower oil, corn oil, wheat germ oil and soybean oil. Palindromic rheumatoid arthritis is thus a disease which rarely causes any harm and you have to manage the pain attacks, by which it is characterized.

5.5 Pannus Rheumatoid Arthritis:

Pannus in rheumatoid arthritis is defined as thickened synovial tissue which covers articular cartilage, i.e. the cartilage present in joints. Synovial tissue is the tissue of synovium i.e. the lining of the joints. With the thickening and proliferation of synovium, the joint is filled by the thickened tissue and the tissue thus abnormally proliferated, spreads across the articular cartilage and subsequently causes erosions. There is also a risk of the pannus to penetrate into the bone and bone marrow and harm the surrounding parts such as joint capsule and tendons.

In patients of rheumatoid arthritis, pannus formation is an unavoidable situation in the long run. Pannus triggers destruction of bone and cartilage. Continuous progression of

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the disease normally coincides with the process of pannus formation. Pannus is generally a membrane of vasuclarised granulated tissue and is formed of mesenchyme and bone marrow derived cells. It is rich in fibroblasts, macrophages and lymphocytes, received from synovial tissue. It overgrows the bearing surface of the arthritic joint and is connected to the breakdown of the articular surface

Pannus formation also triggers macrophges to discharge IL-2, prostaglandins, platelet-derived growth factor, and substance P. All these, in turn, stimulate destruction of cartilage and bone erosion.

Rheumatoid arthritis is an autoimmune, inflammatory, systemic, progressive disease. Though its principal site of occurrence is joints, it may become systemic too, meaning other organs of the body too may be involved.

The ways of joint destruction caused in rheumatoid arthritis vary more than in case of osteoarthritis. Being an autoimmune disease, the rheumatoid arthritis is characterized by impaired immune system which eats up body’s own healthy tissues, the process of which takes place in three phases of inflammation. First is inflammation of synovial lining, second is spread of pannus membrane into the joint and third is release of certain enzymes by the inflamed cells which start digesting cartilage and bone, thereby joint destruction takes place.

Studies, done regarding similarities and differences between the progression of these three processes, and especially, formation of pannus in rheumatoid arthritis and osteoarthritis, show that there is much similarity in the pannus formation of both the conditions. But the osteoarthritis pannus, after invading the cartilage does not give rise to marginal erosions, which happens in rheumatoid arthritis.

MMPs (matrix metalloproteases) are some enzymes belonging to a large proteolytic enzyme group. They degrade the extracellular matrix. In the early stages of RA, MMPs increase in pannus and partake in the invasion of cartilage. They do that by destroying extracellular matrix and by stimulating other proteinases. Some of these stimulated proteinases may either directly degrade the cartilage, thereby causing joint destruction or they may degrade extracellular matrix and thus helps pannus invasion. The proteinases can be released by synovial fibroblast and cells resembling macrophages and are capable to digest the contents of the cartilage matrix and the destruction process takes place mainly in areas near inflamed pannus tissue.

Panuus also occurs in the cornea of the eye from the conjunctiva as a response to inflammation and the condition is called chronic superficial keratitis.

Pannus in rheumatoid arthritis is a quite dangerous condition and if left untreated, may even lead to sudden death and therefore needs immediate attention.

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5.6 Seronegative Rheumatoid Arthritis:

Seronegative rheumatoid arthritis is the rheumatoid arthritis in which the blood doesn’t contain Rheumatoid Factor (RF or RhF). While diagnosing RA, doctors get a range of laboratory tests done and also evaluate the physical symptoms. Testing of blood for rheumatoid factor is the most common way to help determine the presence of disease. But some patients, though they show all the arthritic symptoms, are negative for rheumatoid factor. Despite a negative rheumatoid factor test result, various other tests, to detect the presence of rheumatoid arthritis, can be done, such as, the erythrocyte sedimentation rate (ESR), X-rays, complete blood count (CBC), C-reactive protein (CRP) and antinuclear antibodies. Rheumatoid arthritis is a disease which cannot be diagnosed easily. Therefore, performing a series of tests is usual to reach its diagnosis. This type of rheumatoid arthritis is more common in men.

Common symptoms of seronegative RA are same as those of seropositive RA and they are swollen, painful and tender joints, flu-like symptoms, stiffness in the morning, muscle pain and limitations on movements. Other symptoms are fatigue, weakness and general stiffness of the body. The disease has a tendency to flare up in the mornings after long time of rest. During this time, pain and limited movement of joints, especially in wrists, ankles and back, are often seen.

It is difficult to monitor the progress of seronegative rheumatoid arthritis. When the rheumatoid factor is present in the blood, doctors can know how far and intense the disease has developed. The severity of the disease is easy to identify which is indicated by increased number of rheumatoid factor. This becomes impossible in the seronegative RA patients because of the absence of rheumatoid factor.

A remedy for this is suggested to these patients by the doctor and it is observing and documenting the ongoing of the flares. This is very essential for these patients. It is best to keep a calendar of flares. It will help the doctor by providing necessary information about the condition that takes place between the periods of remission. Evaluating the severity and frequency of flare-ups will help the doctor to determine whether the condition is getting more serious, because s/he cannot successfully perform a rheumatoid factor test.

Just like seropositive rheumatoid arthritis, treatment of seronegative rheumatoid arthritis too focuses on relief from pain, inflammation and slowing down the destruction of joints. The most common medicine is NSAID, i.e. non-steroidal anti-inflammatory drugs, analgesic drugs, DMARDs, i.e. disease modifying antirheumatic drugs and biologic response modifiers.

A major (and relieving) difference which medical studies have observed is that patients with seronegative RA have comparably less joint erosion and destruction than patients

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having seropositive RA. Also the tendency for developing rheumatoid nodules under the skin is less in this disease than the positive population. Moreover, though the other symptoms are same as in the positive group, their severity is less, which too is a bit relieving.

5.7 Seropositive Rheumatoid Arthritis:

Seropositive rheumatoid arthritis is nothing but the same rheumatoid arthritis, the blood test done for which shows presence of rheumatoid factor, or RF, in it. Rheumatoid arthritis stealthily enters the body, when our immune system goes haywire and attacks its own healthy tissues, considering them to be foreign invaders, major amongst them being the joints. During this process of attack of immune system on healthy tissues, rheumatoid factor is produced. It is not necessary that individuals who do not show rheumatoid factor in their blood test, i.e. they are seronegative, do not have rheumatoid arthritis. They too may have the disease, but it is somewhat milder.

Whether you are seropositive or seronegative, does not make much difference in the situation that you have caught the disease and you will have to live with it. The disease mainly attacks the joints, though it affects other parts of the body too. It is an autoimmune disease, and occurs when the immune system is disturbed. It can occur at any age between 20 and 70. It is more prevalent in women. It is not definite that you will suffer from flares of pain and stiffness continuously or at particular time intervals. Different patients show wide variety in this. In some patients, the disease is continuously disturbing, while in some other patients flares may last for only a short period, after which there is a long period of remission.

In any case, you will have to observe certain care so as not to let the pain and inflammation worsen. There is no definite cure for this disease and the treatment is mainly based on symptom relief.

In seropositive rheumatoid arthritis, it can only be said that the patient definitely has the disease, which is not certain with the seronegative counterpart. And in that case, you will have to take the necessary medicines, take proper diet and exercise, take plentiful rest and try to minimize the symptoms, mainly pain and joint stiffness.

You should remain active as far as possible. But it should not be done at the cost of increased pain. In most people, morning stiffness is experienced. You should find out what gives you relief from the pain and stiffness. And for that you have to educate yourself well about the disease. During a fight, if you know whom you are fighting with, you can win the fight. So get more and more knowledge and information about the disease. You can do this by regularly discussing with your health care provider, monitoring your symptoms and symptom relief, telling it to the doctor, reading about the disease and also, discussing with other patients suffering from same disease.

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In this disease, nothing can be said definitely and everything is based on trial and error, to which medicines too are not exceptions. Regarding medicine you have to depend on your doctor, who knows better than you which medicine acts well for you. But there are certain things that you can monitor and manage on your own. You can observe carefully, which activity increases the flare, which food and medicine brings about relief, which time of the day, month or year the flare is worst, and so on. Based on these observations, you can learn more and more how to live with your seropositive rheumatoid arthritis happily.

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CHAPTER – 6

6.1 DIFFERENIAL DIAGNOSES.

Several other medical conditions can resemble RA, and usually need to be

distinguished from it at the time of diagnosis.

Crystal induced arthritis(gout, and pseudo gout)

usually involves particular joints (knee,MTPI,heels) and can be distinguished with

aspiration of joint fluid if in doubt. Redness (RAdoesn't have redness at the joints),

asymmetric distribution of affected joints, pain occurs at night and the starting pain

is less than an hour with gout.

Osteoarthritis- distinguished with X-rays of the affected joints and blood tests, age

(mostly older patients),

Starting pain less than an hour, a-symmetric distribution of affected joints

and pain worsens when using joint for longer periods.

Systemic lupus erythematosus (SLE)- distinguished by specific clinical

symptoms and blood tests (antibodies against double-stranded DNA).s

One of the several types of psoriatic arthritis resembles RA- nail changes

and skin symptoms distinguish between them.

Lyme disease causes erosive arthritis and may closely resemble RA- it may

be distinguished by blood test in endemic areas.

Reactive arthritis (previously Reiter's disease) - asymmetrically involves

heel, sacroiliac joints, and large joints of the leg. It is usually associated with

arthritis, conjunctivitis, iritis, painless buccal ulcers, and keratoderma

blennorrhagica.

Ankylosing spondlitis- this involves the spine, although a RA –like

symmetrical small-joint polyarthritis may occur in the context of this

condition.

Hepatitis C- RA- Like symmetrical small-joint polyarthritis may occur in the

context of this codition.Hepatitis C may also induce Rheumatoid Factor

auto-antibodies.

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Rarer causes that usually behave differently but may cause joint pains:

Sarcoidosis, amyloidosis,and Whipple’s disease can also resemble RA.

Hemochromatosis may cause hand joint arthritis.

Acute rheumatic fever can be differentiated from RA by a migratory pattern

of joint involvement and evidence of antecedent streptococcal infection.

Bacterial arthritis (such as streptococcus) is usually asymmetric, while RA

usually involves both sides of the body.

Gonococcal arthritis (another bacterial arthritis) is also initially migratory and

involves tendons around the wrists and ankles.

Differential Diagnosis of Rheumatoid Arthritis

Diagnosis Comments

Connective tissue diseases Such as scleroderma and lupusFibromyalgia Evaluate for trigger points.Hemochromatosis Iron studies and skin coloration changes may guide diagnosis.

Infectious endocarditis Rule out murmurs, high fever, and history of intravenous drug use.

Polyarticular gout Joints often erythematous; podagra commonly found; gout and rheumatoid arthritis rarely coexist, but calcium pyrophosphate deposition disease can accompany rheumatoid arthritis.

Polymyalgia rheumatica Rheumatoid arthritis, unlike polymyalgia rheumatica, rarely presents with pain in the proximal joints of the extremities only.

Sarcoidosis Granulomas likely, as are hypercalcemia and chest film findings.Seronegative spondyloarthropathies, reactive arthritis

Tend to be more asymmetric than rheumatoid arthritis. More commonly involve the joints of the spine. Evaluate for history of psoriasis, Reiter’s comorbidities, inflammatory bowel disease. Reactive arthritis can be postinfective, sexually acquired, or related to gastrointestinal disorders.

Still’s disease Tends to present with fever, leukocytosis with left shift, sore throat, splenomegaly, liver dysfunction, and/or rash.

Thyroid disease Consider thyroid-stimulating hormone level depending on symptoms.Viral arthritis Consider parvovirus, hepatitis B.

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6.2 Diseases with Symptoms Similar to Rheumatoid Arthritis

Diseases with Symptoms Similar to Rheumatoid Arthritis

Disease Specific Subtypes

Osteoarthritis

Infectious Arthritis Lyme disease, septic arthritis, bacterial endocarditis, mycobacterial and fungal arthritis, viral arthritis

Postinfectious or Reactive Arthritis

Reiter syndrome (a disorder characterized by arthritis and inflammation in the eye and urinary tract), rheumatic fever, inflammatory bowel disease

Crystal Induced Arthritis

Gout and pseudogout

Other Rheumatic Autoimmune Diseases

Systemic vasculitis, systemic lupus erythematosus, scleroderma, Still's Disease (also called juvenile rheumatoid arthritis), Behcet's disease

Other Diseases Chronic fatigue syndrome, hepatitis C, familial Mediterranean fever, cancers, AIDS, leukemia, Whipple's disease, dermatomyositis, Henoch-Schonlein purpura, Kawasaki's disease, erythema nodosum, erythema multiforme, pyoderma gangrenosum, psoriatic arthritis

6.3 MONITORING PROGRESSION;

The progression of rheumatoid arthritis can be followed using scores such as Disease

Activity Score of 28 joints (DAS 28). It is widely used as an indicator of RA disease activity and

response to treatment, but is not always a reliable indicator of treatment effect. The joints

included in DAS28 are (bilaterally): proximal interphalangeal joints (10 joints),

metacarpophalangeal joints (10), wrists (2), elbows (2), shoulders (2) and knees(2). When

looking at these joints both the number of joints with tenderness upon touching (TEN 28) and

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swelling (SW 28) are counted. In addition, the erythrocyte sedimentation rate (ESR) is measure.

Also, the patient makes a subjective assessment (SA) of disease activity during the preceding 7

days on a scale between 0 and 100, where 0 is “no activity” and 100 is “highest activity

possible”. With these parameters, DAS 28 is calculated as:

DAS28 = 0.56 X √TEN28 + 0.28 X √SW28 + 0.70 X In (ESR) – 0.014 X SA

From this, the disease activity of the patient can be classified as follows:

Current DAS28 DAS 28 difference from initial value

≤3.2 Inactive >1.2 >0.6 but ≤ 1.2 ≤ 0.6

Good

improvement

Moderate

improvement

No improvement

>3.2 but ≤5.1 Moderate Moderate

improvement

Moderate

improvement

No improvement

> 5.1 Very

active

Moderate

improvement

No improvement No improvement

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CHAPTER – 7

7.1 PATHOPHYSIOLOGY AND CAUSES

Rheumatoid arthritis is a form of autoimmunity, the causes of which are still incompletely

known. It is a systemic (whole body) disorder principally affecting synovial tissues.

The key pieces of evidence relating to pathogenesis are:

A genetic link with HLA-DR4 and related all types of MHC Class II and the T cell-

associated protein PTPN 22.

An undeniable link with cigarette smoking and the pathogenesis of rheumatoid

vasculitis,a typical feature of this condition.

A remarkable deceleration of disease progression in many cases by blockade of

the cytokine TNF (alpha).

A similar dramatic response in many cases to depletion of B lymphocytes, but no

comparable response to depletion of T lymphocytes.

A more or less random pattern of whether and when individuals predisposed are

affected.

the presence of auto antibodies to 1gGFc, known as rheumatoid factors (RF), and

antibodies to citrullinated peptides (ACPA)

These data suggest that the disease inv loves abnormal B cell-

T cell interaction, with presentation of antigens by B cells to T cells via HLA-DR

eliciting TCell help and consequent production of RF and ACZPA. Inflammation is

then driven either by B cell or T cell products stimulating release of TNF and other

cytokines. The process may be facilitated by an effect of smoking on citrullination

but the stochastic (random)epidemiology suggest that the rate limiting step in

genesis of disease in predisposed individuals may be can inherent stochastic

process within the immune response such as immunoglobulin or T cell receptor

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gene recombination and mutation.(See entry under autoimmunity for general

mechanisms.)

If TNF release is stimulated by B cell products in the form of RF or ACPA-

containing immune complexes, through activation of immunoglobulin Fc receptors

then RA can be seen as a form of Type III hypersensitivity.

If TNF release is stimulated by T cell products such as inerleukin-17 it might be

considered closer to type IV hypersensitivity although this terminology may be

getting some what dated and unhelpful. The debate on the relative roles of

immune complexes and T cell products in inflammation in RA has continued for 30

years. There is little doubt that both B and T cells are essential to the disease.

However, there is good evidence for neither cell being necessary at the site of

inflammation. This tends to favor immune complexes (based on antibody

synthesized elsewhere) as the initiators, even if not the sole perpetuators of

inflammation,. Moreover, work by Thurlings and others in Paul-Peter Take’s group

and also by Arthur Kavanagh’s group suggest that if any immune cells are relevant

locally they are the plasma cells, which derive from B cells and produce in bulk the

antibodies selected at the B cell stage.

Although TNF appears to be the dominant, other cytokines (chemical mediators)

are likely to be involved in inflammation in RA .Blockade of TNF does not benefit

all or all tissue (lung disease and nodule may get worse).Blockade of II, 1. IL- 15

and IL-6 also have, beneficial effects and II-17 may be important.Constitutional

symptoms such as fever, malaise, loss of appetite and weight loss are also caused

by cytokines released in to the blood stream.

As with most autoimmune diseases, it is important to distinguish between the

causes (S) that trigger the process, and those that may permit it to persist and

progress.

7.2 POSSIBLE INFECTOUS TRIGGERS.

It has long been suspected that certain infections could be triggers for

this disease. The “mistaken identity” theory suggests that an infection triggers an

immune response, leaving behind antibodies that should be specific to that

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organism. The antibodies are not sufficiently specific, though, and set off an

immune attack against part of the host. Because the normal host molecule “Looks

like” a molecule on the offending organism that triggered the initial immune

reaction – this phenol neon is called molecular mimicry. Some infections organism

suspected of triggering rheumatoid arthritis include Mycoplasma, Erysipelothrix,

parvovirus B19 and rubella, but these associations have never been supported in

epidemiological studies. Nor has convincing evidence been presented for other

type’s triggers such as food allergies.

Epidemiological studies have confirmed a potential association between RA and

two herpes virus infections: Epstein-Bar virus (EBV) and Human Herpes Virus 6

(HHV-6). Individuals with RA are more likely to exhibit an abnormal immune

esponse to the Epstein –Barr virus. The allele HLA –DRB1 x0404 is associated

with low frequencies of T cells specific for the EBV glycoprotein 110 and

predisposes one to develop RA.

7.3 PSYCHOLOGICAL FACTORS:

There is no evidence that physical and emotional effects or stress could be a

trigger for the disease. The many negative findings suggest that either the trigger

varies, or that it might in fact be a chance event inherent with the immune

response, as suggested by Edwards et al.

7.4 CONTINUED ABNORMAL IMMUNE RESPONSE:

The factors that allow an abnormal immune response, once initiated, to

become permanent and chronic, are becoming more clearly understood. The

genetic association with HLA-DR4,as well as the newly discovered associations

with the gene PIPN22 and two additional genes, all implicate altered thresholds in

regulation of the adaptive immune response. It has also become clear from recent

studies that that these genetic factors may interact with the most clearly defined

environmental risk factor for rheumatoid arthritis, namely cigarette smoking .

Other environmental factors also appear to modulate the risk of acquiring

RA, and hormonal factors in the individual may explain some features of the

disease, such as the higher occurrence in women, the not –infrequent consent

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after child-birth, and the (slight) modulation of disease risk by hormonal

medications. Exactly how altered regulatory threshold allow the triggering of a

specific autoimmune response remains uncertain. However, one possibility is that

negative feedback mechanisms that normally maintain tolerance of self are

overtaken by aberrant positive feedback mechanisms for certain antigens

such as 1gG Fc (bound by RF) and cirtrullinated fibrinogen (bound by ACPA)(see

entry on autoimmunity).

Once the abnormal immune response has become established (which may

take Several years before any symptoms occur), plasma cells derived from

lymphocytes produce rheumatoid factors and ACPA of the 1gG and 1gM classes in

large quantities. These are not deposited in the way that they are in systemiclupus.

Rather, they appear to activate macrophages through Fc receptor and perhaps

complement binding. This can contribute to inflammation of the synovium,in terms

of edema, vasodilation and infiltration by activated T-cells (mainly CD4 in nodular

aggregates and DC8 in diffuse infiltrates).Synovial macrophages and dendritic

cells further function as antigen presenting cells by expressing MHC class II

molecules, leading to an established local immune reaction in the tissue. The

disease progresses in concert with formation of granulation tissue at the edges of

the synovial lining (pannus) with extensive angiogenesis and production of

enzymesthat cause tissue damage.Modern pharmacological treatment of RA target

these mediators. Once the inflammatory reaction is established, the synovium

thickens,the cartilage and the underlying bone begins to disintegrate and evidence

of joint destruction accrues

7.5 ROLE OF VITAMIN D:

The discovery of the vitamin D receptor (VDR) in the cells of the immune

system and the fact that activated dendrites cells produce the vitamin D

hormone suggested that vitamin D could have immunoregulatory properties. VDR,

a member of the nuclear hormone receptor super family, was identified in

mononuclear cells,dendritic cells, antigen –presenting cells, and activated T-B

lymphocytes. In synthesis, the most evident effects of the D-hormone on the

immune system seem to be in the down regulation of the Th1-driven autoimmunity.

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Low serum levels of vitamin D3 might be partially related, among other factors, to

prolonged daily darkness (reduced activation of the pre vitamin D by the ultra violet

B sunlight), different genetic background (i.e vitamin D receptor polymorphism) and

nutritional factors, and explain the latitude-related prevalence of autoimmune

diseases such as rheumatoid arthritis ( RA), by co considering the potential

immunosuppressive roles of vitamin D.25(OH)D3 plasma levels have been found

inversely correlated at least with the RA disease activity showing a circannual

rhythm (more severe in winter). Recently, greater intake of vitamin D was

associated with a lower risk of RA, as well as a significant clinical improvement

was strongly correlated with the immunomodulating potential vitamin D-treated RA

patients.

In patients with rheumatoid arthritis measuring vitamin D is a level seems

particularly pertinent as deficiency is highly prevalent in the group. Vitamin D is

already known to be important in preventing osteoporosis and fracture falls, which

are also common in RA.It is too early to tell whether administering vitamin D

directly affects disease activity.

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CHAPTER - 8

8.1 Complications of Untreated Rheumatoid Arthritis :

Complication Comments

Anemia Correlates with erythrocyte sedimentation rate and disease activity; three fourths of patients have anemia of chronic disease; one fourth of patients respond to iron therapy.

Cancer May be secondary to treatments; lymphomas and leukemias two to three times more common in patients with rheumatoid arthritis; increased risk for various solid tumors; genitourinary cancer risk is reduced in rheumatoid arthritis, perhaps because of nonsteroidal anti-inflammatory drugs.

Cardiac complications

Pericarditis—one third of patients may have asymptomatic pericardial effusion at diagnosis; atrioventricular block—rare; myocarditis—diffuse inflammation can occur, may or may not be symptomatic.

Cervical spine disease

Tenosynovitis of transverse ligament can lead to instability of atlas on axis. Caution must be used during endotracheal intubation; may see loss of lordosis of the neck and decreased range of motion; C4-C5 and C5-C6 subluxations are possible; may see joint space narrowing on lateral cervical spine films; avoid flexion films until odontoid fracture ruled out if injury is suspected; myelopathy can occur, with gradual onset of upper extremity weakness and paresthesias.

Eye problems Episcleritis rarely occurs.

Fistula formation

Cutaneous sinuses form near affected joints, connecting bursa to the skin.

Increased infections

More likely to be an effect of rheumatoid arthritis treatment.

Hand joint deformities

Ulnar deviation at metacarpophalangeal joints; boutonniere deformity—flexed PIP and hyperextended DIP; swan neck deformity—the reverse of

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Complication Comments

boutonniere, with flexed DIP and hyperextended PIP; thumb hyperextension; increased risk of tendon rupture

Other joint deformities

Frozen shoulder may develop; popliteal cysts can arise; carpal and tarsal tunnel syndromes common.

Respiratory complications

Lung nodules can coexist with cancers and form cavitary lesions; cricoarytenoid joint inflammation can arise, with hoarseness and laryngeal pain; pleuritis—present in 20 percent at onset of disease; not usually associated with pleuritic pain; interstitial fibrosis—rales may be noted on lung examination.

Rheumatoid nodules

Often have necrotic tissue in their centers; found in 20 to 35 percent of patients with rheumatoid arthritis; usually found on extensor surfaces of the limbs or other pressure points; may form nearly anywhere, including on the sclera, vocal cords, sacrum, or Vertebral bodies.

Vasculitis Forms include distal arteritis, pericarditis, peripheral neuropathy, cutaneous lesions, arteritis of viscera, and coronary arteritis; increased risk of developing if male sex, high rheumatoid factor titers, treatment with steroids, number of disease-modifying antirheumatic drugs prescribed; associated with increased risk of myocardial infarction.

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CHAPTER - 9

9.1 RHEUMATOID ARTHRITIS AND PREGNANCY

Pregnancy alters the immune state, possibly contributing to change in the course of rheumatoid arthritis. For decades, the ameliorating effects of pregnancy on disease activity in women with RA have been observed. No specific guidelines address obstetric monitoring in patients with RA.Because little available data suggest a significant risk for preterm birth, preeclampsia, or fetal growth restriction in pregnant patients with this disease, no special obstetric monitoring is indicated beyond what is performed for usual obstetric care.

It is important to counsel patients about the teratogenicity adverse effects of the medications used to treat rheumatoid arthritis before starting therapy, patients may need a reminder about the importance of using contraception during DMARD therapy and that some of these medications may need to be discontinued several months before conception is planned. In addition to discontinuation, some patients who take DMARDs may require treatment with other medications to enhance their clearance.

Patients with rheumatoid arthritis must be monitored closely following delivery, because they the potential to have arthritis flare-ups during the postpartum period.

9.2 Rheumatoid Arthritis Makes It Difficult to Conceive

A study done in Denmark on about 68,120 women who became pregnant between 1996 and 2002 has come to the conclusion that presence of Rheumatoid Arthritis makes it difficult for the women to conceive.Women with Rheumatoid Arthritis Find It Hard To Get PregnantAccording to the study, published in the journal Arthritis and Rheumatism, it was found that almost 25% women suffering from RA tried unsuccessfully for a year to conceive before finally getting pregnant as compared to 16% women who did not have RA. 10% of women with RA were treated for infertility as compared to 8% women without RA. 41% of women with RA got pregnant within 2 months of trying as compared to 48% women who did not suffer from RA. Thus it was concluded that rheumatoid arthritis makes it difficult for the women to conceive. Though the disease does not affect the fertility rate, it seems to increase the time to pregnancy.

49

It is difficult to say whether the time to pregnancy increases because of the rheumatoid arthritis or because of the various medicines taken to counter RA. There is no evidence till date to suggest that RA hinders pregnancy. However, the patients of RA trying to conceive are asked to stop their medications beforehand as these may have deleterious effect on the fetus. Medicines like methotrexate are known to roduce birth defects whereas newer disease modifying anti-rheumatic drugs (DMARDs) like etanercept and infliximab have not been studied enough for their effect on the developing embryo.

It has been hypothesized that this sudden stoppage of treatment for RA results in the flaring up of the disease which may somehow be related to difficulty in conceiving. Rheumatoid Arthritis has different effects on the different stages of pregnancyRheumatoid Arthritis is an autoimmune disease commonly affecting the women, wherein the body’s immune system fails to recognize its own tissue and starts damaging the joints resulting in pain, inflammation and subsequent destruction of the joints. Women suffering from RA may take longer to conceive because of inconsistent ovulation; and fatigue and pain leading to a decrease in sex drive.

Before trying to conceive, it is better to consult the doctor so that any harmful medication is tapered off or is replaced by some other safe alternative. Different medications for RA take different time to be completely washed away from the system. RA has different effects on the different stages of pregnancy. During the first trimester of pregnancy, women suffering from RA tend to get more fatigued. Almost 70 to 80% women report an improvement in their symptoms during the second trimester of pregnancy. This is especially true in women who are negative for the rheumatoid factor and anti CCP autoantibody. The fatigue worsens once again with the onset of the third trimester though now it is more related to the growing weight of the baby. RA increases the chances of an early labor and delivery of a premature baby. The likelihood of undergoing a cesarean s to deliver the baby is also more. This is because of the involvement of the hip joint by the arthritis. RA tends to flare up in the post partum period. Getting back with the old medication that the patient was taking before pregnancy should be discussed with the doctor in view of breast feeding.

Though women with RA take slightly longer to conceive, the delay is not very significant. It is advisable for such women not to put their plans of having a baby on hold as it will be more difficult to conceive in the late reproductive years.

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CHAPTER – 10

10.1 Management of Rheumatoid Arthritis under various therapies:

There is no known cure for rheumatoid arthritis, but many different types of

treatment can alleviate symptoms and or modify the disease process. Recommendations

of the American College of Rheumatology (ACR), published in 2008, followed a trend in

supporting earlier, more aggressive treatment of RA, and reflected heightened

expectations of treatment effectiveness, including remission or substantial alleviation of

symptoms for a rising percentage of patients.

The goal of treatment is twofold: alleviating the current symptoms, and preventing the

future destruction of the joints with the resulting handicap if the disease is left

unchecked.These two goals may not always coincide:while pain relievers may achieve

the first goal, they do not have any impact on the long –term consequences. For these

reasons,the ACR recommends that RA should generally be treated with at least one

specific anti-rheumatic medication, also named DMARD(see below), to which other

medications may be added depending on how long a person has had RA, how active the

disease is, and prognostic factors (such as X-ray evidence of bone erosion; elevation of

blood factors such as rheumatoid factor, anti-cyclic citrullinated peptide, C-reactive

protein, and erythrocyte sedimentation rate; age and gender; physical functioning; and

smoking, for example).Cortisone therapy has offered relief in the past, but its long-term

effects have been deemed undesirable. However, cortisone injections can be valuable

adjuncts to a long-term treatment plan, and using low dosages of daily cortisone

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(e.g,prednisone or prednisolone,5-7.5 mg daily)can also have an important benefit if

added to a proper specific anti-rheumatic treatment.

The management of Rheumatoid Arthritis includes:

A-Pharmacological Treatment

B-Non-Pharmacological Treatment

Pharmacological Treatment

Medical management of RA involves three general approaches:

Disease Modifying Anti-Rheumatic Drugs(DMARs)

Biological Agents/Immunosuppressive drugs

Non Steroidal anti-inflammatory drugs(NSAIDs)

Low dose corticosteroids

10.2 DISEASE MODIFYING ANTI-RHEUMATIC DRUGS (DMARDs)

The term Disease-modifying anti-rheumatic drug (DMARD) originally meant a drug

that affects biological measures such as ESR and haemoglobin and autoantibody levels,

but is now usually used to mean a drug that reduces the rate of damage to bone and

cartilage.DMARDs have been found both to produce durable symptomatdelay or halt

progression.This is important as such damage is usually irreversible. Anti-inflammatories

and analgesics improve pain and stiffness but do not prevent joint damage or slow the

disease progression.There is an increasing recognition among rheumatologists that

permanent damage to the joints occurs at a very early stage in the disease. In the past it

was common to start with just an anti-inflammatory drug, and assess progression

clinically and using X-rays.If there was evidence that joint damage was starting to occur

then a more potent DMARD would be prescribed.Ultrasound and MRI are more sensitive

methods of imaging the joints and have demonstrated that joint damage occurs much

earlier and in more sufferers than was previously thought.People with normal X-rays will

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often have erosions detectable by ultrasound that X-rays could not demonstrate. The aim

now is to treat before damage occurs.

There may be other reasons why starting DMARDs early is beneficial as well as

prevention of structural joint damage. From the earliest stages of the disease, as well as

prevention of the immune system that signal to one another in ways that may involve a

variety of positive feedback loops (it has long been observed that a single corticosteroid

injection may abort synovitis in a particular joint for long periods).Interrupting this process

as possible with an effective DMARD (such as methotrexate) appears to improve the

outcome from the Ra for years afterwards.

Delaying therapy for as little as a few months after the onset of symptoms can

result in worse outcomes in the long term. There is therefore considerable interest in

establishing the most effective therapy with early arthritis, when they are most responsive

to therapy and have the most to gain.

Disease-modifying anti-rheumatic drugs have been used in the treatment of

rheumatic arthritis for a long time now. Over 90% of rheumatologists now use

combitination therapy of multiple disease modifying drugs for rheumatoid arthritis as it

has become apparent that using combination of these drugs does not increase their

relative toxicity profiles. Common combinations of DMARDs include methotrexate-

hydroxychloroquine,methrexate-sulfasalazine,sulfasalazine-hydroxychloroquine, and

methotrxate- hydroxychloroquine –sulfasalazine.

In order to be effective, disease –modifying anti-rheumatic drugs must be

administered before the deformaities appear or the erosive disease

occurs.Usually,Rheumatologists do not wait for the fulfillment of the criteria for

classification of RA as published by the American College of Rheumatology (ACR) and

start treatment with this type of drugs if the pain and synovitis persist and the function is

compromised.

10.3 TRADITIONAL SMALL MOLECUAR MASS DRUGS.

Chemically synthesized DMARDs:

53

Azathioprine

Ciclosporin (cyclosporine A)

D-penicillamine

Gold salts

Hydroxychloroquine

Leflunomide

Methotrexate (MTX)

Minocycline

Sulfasalazine (SSZ)

Cytotoxic drugs:-

Cyclophosphamide

The most important and most common adverse events relate to liver and bone marrow

toxicity (MTX,SSZ, leflunomide, azathioprine,gold compounds, D-penicillamine ), renal

toxicity (cyclosporine A, parenteral gold salts, D-penicillamine),peneumonitis (MTX),allergic

skin reactions (gold compounds,SSZ),autoimmunity (D-penicillamine,SSZ,minocyciline) and

infections (azathioprine,cyclosporine A).

Hydroxychloroquine may cause ocular toxicity, although this is rare, and because

hydroxchloroquine does not affect the bone marrow or liver it is often considered to the

DMARD with the least toxicity. Unfortunately hydroxychloroquine is not very potent, and is

usually insufficient to control symptoms on its own.

Methotrexate is considered by many rheumatologists to be the

Most important and useful DMARD, largely because of lower drop-out rates for reasons of

toxicity. Nevertheless, methotrexate is often considered as a very “toxic”drug.This reputation

is not entirely justified, and at times can result in people being denied the most effective

treatment for their arthritis.

Although methotrexate does have the potential to suppress bone marrow or cause

hepatitis, these effects can be monitored using regular blood tests, and the drug withdrawn at

an early stage if the tests are bnormal before any serious harm is done(typically the blood

tests return to normal after stopping the drug).In clinical trials, where one of a range of

different DMARDs were used, people who were prescribed methotrexate stayed on their

medication the longest (the others stopped because of either side-effects or failure of the

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drug to control the arthritis). Methotrexate is often preferred by rheumatologists because if it

does not control arthritis on its own then it works well in combination with many other drugs,

especially the biological agents. Other DMARDs may not be as effective or as safe in

combination with biological agents.

Sulphasalazine: Although it appears to be a highly efficient drug in the treatment of

rheumatoid arthritis, sulphasalazine may cause side effects that can range in severity from

mild to serious.Mild side effects that may arise from treatment with sulphasalazine include

nausea and skin rash. Generally, nausea that appears as a result of treatment with this

DMARD occurs in the first days of treatment and then it tends to diminish to disappearance.

To avoid nausea, specialists recommend starting with low doses and then gradually

increasing them until the usual dosage is achieved. Skin rash has been reported in nearly 5%

of the patients and it may present pruritues.Rare side effects include Stevens-Johnson

syndrome and reduced fertility due to reversible oligospermia. Severe side effects that can

appear from therapy with sulphasalzine, through rare, aplastic anemia and neutropenia which

may result in the death of the patient. The latter is estimated to have occurred in

approximately 2% of the patients but death and further complications were avoided by

removing the drug from the patients therapy.Also according to WHO, there have been

approximately 700 of patients in whom this medicine caused blood dyscrasis,Leukopenia

has also been reported therapies with sulphasalazine, but in very rare cases.

Anti-malarials such as chloroquine and hydropchloroquine have been used to treat

rheumatoid arthritis.It has been pointed out, through clinical studies, that chloroquine has a

higher toxicity compared to

hydroxychloroquine.Although hydroxyxhloroquine appears to be more efficient in treating

rheumatoid arthritis than placebo, it is also inferior to sulphasalazine, especially in what may

also produce side effects.Mild side effects from hydroxychloroquine include nausea and skin

rash. More serous, bone marrow suppression may occur, though rare.Also, aplastic anemia

and agranulocytosis can develop as a result of anti-malarial therapy and may potentially

cause the death of the patient.A much more worrisome side effect from treatment with anti-

malarials is the damage that these drugs seem to be causing to the cornea and retina.

Recent studies have however shown that if the dosage of hydroxychloroquine given to the

patients dose not exceed 6.5 mg/kg, the risks of developing ocular complications are minimal.

55

Gold compounds are also options in treating this type of disease. Specialists agree that

injectable gold is much more effective in the treatment of rheumatoid arthriris than

auranofin.Yet,this type of drug has been shown to be more efficient than placebo and even

though its level of toxicity is quite low , auranofin seems to be causing more side effects than

any other type of DMARD.Auranofinent is therefore not considered efficient in the treatment

of rheumatoid arthritis because of its poor resultsand because it is intolerable for most

patients.Sodium aurothiomalate (Myocrisin)on the other hand is another type of gold

compound that is injected and which appears to be as efficient as sulphasalazine,d-

penicillamine and methotrexate.

Given that there is not enough proof that gold compounds are indeed efficient in preventing

the progression of erosions and the high toxicity of these drugs, they are usually not included

in the treatment plan for rheumatoid arthritis.

A Cochrane systematic review has determined that Abatacept was an effective treatment for

rheumatoid arthritis. Against placebo, it was found to increase monbility and make patients

twice as likely to achieve a 50% improvement in symptoms. However Cochrane has called for

more studies to be conducted, given the lack of evidence to distinguish between the biologics

available rheumatoid arthritis.

10.4 BIOLOGICAL AGENTS.

Biological agents (biologics ) include:

Tumor necrosis factor alpha (TNFa) blockers-etanercept (Enbrel), infliximab (Remicade),

adalimumab (Humira),certolzumab pegol (Cimzia),golimumab (simponi)

Interleukin 1 (1L-1 ) blockers- anakina (Kineret)

Monoclonal antibodies against B cells- rituximab (Rituxan)

T cell costimulation blocker – abataacept (Orencia)

Interleukin 6 (1L-6) blockers –tocilizumab (an anti-1L-6 receptor antibody) (RoActemra

Actemra).

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10.5 DMARDs for Treatment of Rheumatoid Arthritis

DMARD Dosage

Time to benefit Adverse effects Monitoring† Comments

Adalimumab (Humira)

40 mg SC every two weeks

A few days to four months‡

Infusion reactions; increased infection risk, including TB reactivation Rare: demyelinating disorders

Monitor for TB, histoplasmosis, and other infections; CBC and ALT at baseline and monthly until dose is stable; may continue every two to three months thereafter.

Monoclonal antibody to TNF-3; shown to reduce disease activity with acceptable safety.

Anakinra (Kineret)

100 to 150 mg SCper day

Within 12 weeks; lasting effects by 24 weeks

Infections and decreased neutrophil counts; headaches, dizziness; nausea Rare: hypersensitivity

CBC at baseline, monthly for three months, then every three months

Interleukin-1 receptor antagonist; used when treatment with another DMARD has failed.

Auranofin (Ridaura)

3 mg orally twice per day or 6 mg orally per day

Four to six months

Diarrhea Rare: leukopenia

CBC and urine protein (by dipstick) every one to three months

Has modest effects compared with other DMARDs.

Azathioprine (Imuran)

50 to 150 mg orally per day

Two to three months

Nausea Rare: leukopenia; sepsis; lymphoma

CBC every one to two weeks until dose is stable, then every one to three months

Has greater toxicity and is used less commonly than other DMARDs.

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DMARD Dosage


Cyclosporine (Gengraf, Neoral, generic)

2.5 to 5 mg per kgorally per day

Two to four months

Nausea; paresthesias,

Creatinine every

two weeks until

Significantclinical benefit

tremor; headaches; gingival hypertrophy; hypertrichosis Rare: hypertension; renal disease; sepsis

dose is stable, then monthly; consider CBC, LFTs, and potassium level tests

up to one year; adverse effects limit use.

D-Penicillamine (Cuprimine)


Three to six months

Nausea; loss of taste; rash; reversible platelet decrease Rare: proteinuria; late autoimmune disease

CBC and urinary protein by dipstick every two weeks until dose is stable, then every one to three months

Used less commonly than other DMARDs.

Etanercept (Enbrel)

25 mg SC twice per week or 50 mg SC per week

A few days to 12 weeks

Contraindicated in infection; mild injection site reactions Rare: demyelination

CBC and ALT at baseline and monthly until dose is stable; may continue every two to three months thereafter.

Combination of TNF receptor and portion of IgG1; inhibits TNF-3; slows joint damage.

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DMARD Dosage


Hydroxychloroquine (Plaquenil)


Two to six months

Nausea; headaches Rare: abdominal pain; myopathy; retinal toxicity

Eye examinations every 12 months in patients older than 40 years and those with previous eye disease

Can be used when diagnosis uncertain; moderate effect but relatively low toxicity.

Gold sodium thiomalate (Myochrysine) Aurothioglucose (Solganal)

25 to 50 mg IM every two to four weeks

Six to eight weeks

Mouth ulcers; rash; vasomotor symptoms after injection Rare: leukopenia; thrombocytopenia; proteinuria; colitis

CBC and urinary protein by dipstick every two weeks until dose is stable, then with each injection

Has significant withdrawal rate in trials because of toxicity.

Infliximab (Remicade)

3 mg per kg IV at weeks zero, 2, and 6, then every eight weeks§

A few days to four months‡

Infusion reactions; increased infection risk, including TB reactivation Rare: demyelinating disorders

Monitor for TB, histoplasmosis, and other infections; CBC and ALT at baseline and monthly until dose is stable; may continue every two to three months thereafter.

Monoclonal antibody to TNF-3; reduces disease activity with acceptable safety.

Leflunomide (Arava)

100 mg orally per day for three days,

Four to 12 weeks (tending

Nausea, diarrhea; rash; alopecia; highly teratogenic,

Hepatitis B and C serology in high-risk

Inhibits pyrimidine synthesis and

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DMARD Dosage


then 10 to 20 mg orally per day

toward four)

even after discontinuation Rare: leukopenia; hepatitis; thrombocytopenia

patients; CBC, creatinine, and LFTs monthly for six months, then every one to two months; repeat AST or ALT in two to four weeks if initially elevated, and adjust dose as needed.

may suppress T-cell activation; improves multiple clinical outcomes and delays radiographic changes; can be eliminated from system with cholestyramine in patients wishing to conceive.

12 to 25 mg orally, IM, or SC per week

Methotrexate One to two months

Nausea, diarrhea; fatigue; mouth ulcers; rash, alopecia; abnormal LFTs Rare: low WBC and platelets; pneumonitis; sepsis; liver disease; Epstein-Barr virus–related lymphoma; nodulosis

CBC, creatinine, and LFTs monthly for six months, then every one to two months; repeat AST or ALT in two to four weeks if initially elevated, and adjust dose as needed; liver biopsy if no resolution on discontinuation.

Rapid onset (six to 10 weeks); tends to produce more sustained results over time than other DMARDs and lowers all-cause mortality; can be used when cause of polyarthritis uncertain; often combined with newer DMARDs.

Minocycline (Minocin)

100 mg orally twice per day

One to three

Dizziness; skin pigmentation

None needed Effective in combination

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DMARD Dosage


months with prednisone for management of new-onset rheumatoid arthritis.

Staphylococcal protein A immunoadsorption (Prosorba column)

Extracorporeal; weekly for 12 weeks

Three months

Hypotension and anemia during procedure; catheter site infection, joint pain, fatigue

Follow CBC Used only in refractory patients when many other treatments have failed.

Sulfasalazine (Azulfidine)

2 to 3 g orally per day in divided doses

One to three months

Nausea, diarrhea; headache; mouth ulcers; rash, alopecia; contact lens staining; reversible oligospermia; abnormal LFTs Rare: leukopenia

CBC every two to four weeks for three months, then every three months

Rapid onset (eight to 13 weeks); enteric, coated forms available; can be used when diagnosis uncertain; modest effects compared with other medications.

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10.6 ANTI-INFLAMMATORY AGENTS AND ANALGESICS.

Anti-inflammatory agents include:

Glucocorticoids

Non-steroidal anti-inflammatory drug (NSAIDs, most also act as analgesics)

Analgesics include:

Paracetamol (acetaminophen in US and Canada)

Opiates

Diproqualone

Lidocaine topical

Historic treatments for RA have also included: rest, ice, compression and elevation, apple diet,

nutmeg, some light exercise every now and then nettles, bee venom, copper bracelets, rhubarb

diet, extractions of teeth, fasting, honey, vitamins, insulin, maggents, and electroconvulsive

therapy (ECT). Most of these have either had no effect at all, or their effects have been modest

and transient, while not being generalizable.

NSAIDs used in the treatment of RA include:

Aspirin - though not recommended for children due to side effects and the risk of Reye's syndrome. Salicylate medications Buffered aspirin Ibuprofen (Advil, Motrin IB) Ketoprofen (Orudis) Naproxen (Naprosyn) NSAID COX-2 inhibitors Celecoxib (Celebrex) Rofecoxib (Vioxx) Disease-modifying antirheumatic drugs (DMARDs) Gold salts (Myochrysine, Ridaura) - oral or injected Antimalarials Hydroxychloroquine (Plaquenil) Penicillamine (Cuprimine, Depen) Sulfasalazine (Azulfidine) Arava® (leflunomide)

Immunosuppresssive medications Methotrexate (Rheumatrex) Azathioprine (Imuran)

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http://www.rightdiagnosis.com/treat/azathioprine.htm

http://www.rightdiagnosis.com/treat/immunosuppressive_drugs.htm

http://www.rightdiagnosis.com/treat/antimalarials.htm

http://www.rightdiagnosis.com/treat/ibuprofen.htm

http://www.rightdiagnosis.com/treat/aspirin.htm


Cyclosporine (Sandimmune, Neoral) Lefluomide (Arava) Corticosteroids (glucocorticoids) Prednisone (Deltasone, Orasone) Methylprednisolone (Medrol) Biologic Response Modifiers Etanercept (Enbrel) Kineret® (anakinra) - an IL-1 blocker Remicade® (infliximab) - in combination with methotrexate. Antibody blood filtering - for severe rheumatoid arthritis. Prosorba Column® (apheresis) ibuprofen, naproxam, etodolac nabumetone, sulindac, tolementin, choline magnesim salicylate,

diclofenac,difiusinal,indometticin, ketoprofen, oxaprozin, and piroxoicam.

Cortisone therapy become a controversial medical solution become even through it can provide

great relief; there are some questions as to the usefulness of the procedure over a long period of

time.

Corticosreroids

Corticosteroids usually produce an immediate and dramatic anti-inflammatory affect in RA.They

can be used on short –term basis for the following indication:

Severe exacerbation which are not remitting with NSAIDs and DMARs.

Severe extra-articular manifestation e.g. pericarditis,perforating eye lesion.

Active and progressive disease that does not respond favorably to conservative

management.

When there is contraindication to or therapeutic failure of methotrexate or other DMARs.

When other measures fail to control persistently disabling symptoms in breadwinners,young

mothers who have to return to work.

*Low dose(< 7.5 mg/day) prednisolone is effective to achieve desired clinical effect.

*Recent evidence suggests that low dose corticosteroid therapy retard the progression of bone

erosion.

*Intra-articular corticosteroid may be helpful if one or two joints are the chief source of

difficulty.Injection Triamcinolone 10-20 mg depending on size of the joint may be given for

symptoms relief,but not more than 4-times/year.

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http://www.rightdiagnosis.com/treat/prednisone.htm

http://www.rightdiagnosis.com/treat/corticosteroids.htm

http://www.rightdiagnosis.com/treat/cyclosporine.htm

10.7 SURGERY.

In early phases of the disease, an arthroscopic or open synovectomy may be

performed. It consists of the removal of the inflamed synovia and prevents a quick destruction of

the affected joins. In older patients, the strum synovectomy may be performed. It is successful in

approximately half of patients. The surgery is mostly done on knee, elbow, shoulder, ankle or

tarsal joints.Ithas to be performed before the destruction of the cartilage. Severely affected

joints may require joint replacement surgery, such as knee replacement. Postoperatively,

physiotherapy is always necessary.

108 Non-Pharmacological Treatment:

Lifestyle treatments Rest Exercise Adequate nutrition Joint care Joint splinting Avoid alcohol - may interact with some RA medications. Rehabilitation treatments Splinting - of the hands Physiotherapy Occupational therapy Mobility aids Stress relief Relaxation therapy Biofeedback Support groups Weight loss

Regular exercise is important for marinating joint mobility and making the joint

muscles stronger. A Cochrane Review of studies determined that exercise programs

designed to improve strength and stamina were safe and led to moderate benefits for RA

sufferers.

10.9 OTHER THERAPIES

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http://www.rightdiagnosis.com/treat/support_groups.htm

http://www.rightdiagnosis.com/treat/biofeedback.htm

http://www.rightdiagnosis.com/treat/rest.htm

http://www.rightdiagnosis.com/treat/stress_reduction.htm

http://www.rightdiagnosis.com/treat/occupational_therapy.htm

http://www.rightdiagnosis.com/treat/physiotherapy.htm

http://www.rightdiagnosis.com/treat/splints.htm

http://www.rightdiagnosis.com/treat/reduce_alcohol.htm

http://www.rightdiagnosis.com/treat/adequate_nutrition.htm

http://www.rightdiagnosis.com/treat/exercise.htm

http://www.rightdiagnosis.com/treat/rest.htm

http://www.rightdiagnosis.com/treat/lifestyle_treatments.htm


Other therapies are weight loss, orthoses, occupational therapy, podiatry,

physiotherapy, immunoadsorption therapy, joint injections, and special tools to improve

hand movements (e.g. special tin-openers).

Ayurvedas, mostly in southern India, is another source of treatment, and

while it is popular in India there are no studies to show that it benefits patients with RA.One

survey in the United Kingdom between 1998and 2002 found that arthritis, in its various

forms, was among the five most common reasons for the medicinal use of cannabis.

The Prosorba column blood filtering device (removing 1gG) was approved

by the FDA in 1999 for treatment of RA.However it was discontinued at the end of 2006.

The effectiveness of treating RA with acupuncture is inconclusive, and

“more rigorous research seems to be warranted” according to one study. One study of 873

patients with RA found that those who drank some alcohol (none drank more than 10 units

of alcohol a week) had reduced severity of symptoms compared to those who drank no

alcohol. However a spokeswoman for the Arthritis Research UK (who co-funded the study)

warned that some RA treatments, like methotexate, could damage the liver when taken

with large amounts of alcohol. Experimental chemicals capable to lower secretion of

inflammatory cytokines linded to arthritis include Dimethyl sulphoxide and dimethyl

sulphone (Kloesch et al,.Life Seiences Volume 89 ,Issues 13-14).However, it is important to

safeguard liver against potential toxicity (Brayton,Cornell Vet.,76-61.

10.9.1 Homeopathic Treatment of Rheumatoid Arthritis:

65

Homoeopathy

The word homoeopathy is derived from the Greek homeos meaning like and pathos

meaning suffering.

Principal of Homoeopathy

Homoeo therapy is based on thee principals.

Like Cures Like

That is, a substance that produces the symptoms of a disease may also cure it. This is

known as law of similar that which makes sick shall heal.

Minimum Dose

It is believed that more a substance is diluted, the more potent it becomes.

Uniquencess of the Remedy

Which is regarded as specifies to a particular patient at a particular time.

Mechanism of Action

Stimulate the body immune system and strengnthens it against illness

Stimulate the body own vital force(hemostasis),the mechanism that generate self healing

and helps to achieve equilibrium

Several other mechanisms are under investigation.

Repertory

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Is an index to the symptoms of diseases and their remedies, in which thy are arranged in an

orderly manner so that they can be found easily

Remedy

Is something as a medicine that cures or relieves a disease or bodily disorder

Types of Remedy

Classical Remedy: That is named after the single remedy product it contains

Indicated or Combined Remedy: That is usually a combination of three or four remedies

that are suitable for treating a particular problem

Clinical Uses

Chronic Conditions:Arthritis,Allergies,Autoimmune Diseases

Non life Threatening Conditions: Viral infections, Minor Trauma

Recurrent Conditions:Otitis media

Dynamic Conditions:Hydrocele,FibriodUterus,Benign enlargement of prostate

Currently FDA considers these medicines as non prescription products. WHO state

that Homoeopathy is the second most used medical system internationally Non

physician may practice Homoeopathy within the scope of practice of their specific

profession.

Homeopathy offers a wider range of options than Conventional medicine.

Constitutional Homeopathic treatment with the management of an experienced and

professional Homeopath is an excellent choice for Rheumatoid Arthritis. The

Constitutional approach of Homeopathy, which considers mind and body together as one,

bestows a lot of significance to emotions, and believes that emotional factors are vital in

the development of most of the diseases, including Rheumatoid Arthritis. It can even be

the cause of Rheumatoid Arthritis. Heredity plays an important role in Rheumatoid

Arthritis. However, a study conducted at the Stanford University School of Medicine,

67

suggested that emotions can overcome genetics. The study showed that even those who

are genetically predisposed to Rheumatoid Arthritis can avoid the disease by staying

emotionally healthy. If you are at risk for Rheumatoid Arthritis, you can avoid getting the

disease if you stay in good condition psychologically.

In conclusion, for every patient suffering from Rheumatoid Arthritis Classical Homeopathy treatment must be given a serious consideration for long term and lasting relief. Homeopathy is often helpful for relieving pain and stiffness. A constitutional remedy, with the guidance of an experienced homeopath, is often the best approach for dealing with chronic conditions. Following are the Drugs available for Rheumatoid Arthritis.

Arnica

Chronic arthritis with a feeling of bruising and soreness may be helped by this remedy. The painful parts feel worse from being moved or touched. (Herbal Arnica gels and ointments may also help to soothe arthritic pain when applied externally to areas of inflammation and soreness.)

Aurum metallicum

Wandering pains in the muscles and joints that are better from motion and warmth, and worse at night, suggest a need for this remedy. Deep pain may be felt in the limbs when the person tries to sleep, or discomfort may wake the person up. People who need this remedy are often serious and focused on work or career, with a tendency to feel depressed.

Bryonia

This remedy can be helpful for stiffness and inflammation with tearing or throbbing pain, made worse by even the smallest motion. The condition may have developed gradually, and is worse in cold dry weather. Discomfort is aggravated by being touched or bumped, or from any movement. Pressure brings relief (if it stabilizes the area) and improvement also comes from rest. The person may want to stay completely still and not be interfered with.

Calcarea carbonica

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This remedy may be useful for deeply aching arthritis involving node formation around the joints. Inflammation and soreness are worse from cold and dampness, and problems may be focused on the knees and hands. Weakness in the muscles, easy fatigue from exertion, and a feeling of chilliness or sluggishness are common. A person who needs Calcarea is often solid and responsible, but tends to become extremely anxious and overwhelmed when ill or overworked.

Causticum

This remedy may be indicated when deformities develop in the joints, in a person with a tendency toward tendon problems, muscle weakness, and contractures. The hands and fingers may be most affected, although other joints can also be involved. Stiffness and pain are worse from being cold, and relief may come with warmth. A person who needs this remedy often feels best in rainy weather and worse when the days are clear and dry.

Calcarea fluorica

This remedy is often indicated when arthritic pains improve with heat and motion. Joints become enlarged and hard, and nodes or deformities develop. Arthritis after chronic injury to joints also responds to Calcarea fluorica.

Dulcamara

If arthritis flares up during cold damp weather, or after the person gets chilled and wet, this remedy may be indicated. People needing Dulcamara are often stout, with a tendency toward back pain, chronic stiffness in the muscles, and allergies.

Kali bichromicum

When this remedy is indicated, arthritic pains may alternate with asthma or stomach symptoms. Pains may suddenly come and go, or shift around. Discomfort and inflammation are aggravated by heat, and worse when the weather is warm.

Kali carbonicum

Arthritis with great stiffness and stitching pains, worse in the early morning hours and worse from cold and dampness, may respond to this remedy-especially if joints are becoming thickened or deformed. People who need this remedy often have a rigid moral code, and tend to feel anxiety in the stomach.

Kalmia latiflora

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Intense arthritic pain that flares up suddenly may responds to this remedy-especially when problems start in higher joints and extend to lower ones. Pain and inflammation may begin in the elbows, spreading downward to the wrists and hands. Discomfort is worse from motion and often worse at night.

Ledum palustre

Arthritis that starts in lower joints and extends to higher ones may respond to this remedy. Pain and inflammation often begin in the toes and spread upward to the ankles and knees. The joints may also make cracking sounds. Ledum is strongly indicated when swelling is significant and relieved by cold applications.

Pulsatilla

If rheumatoid arthritis pain is changeable in quality or the flare-ups move from place to place, this remedy may be useful. The symptoms (and the person) feel worse from warmth, and better from fresh air and cold applications. People who need this remedy usually are emotional and affectionate, sometimes having teary moods.

Rhododendron

This remedy is strongly indicated if swelling and soreness flare up before a storm, continuing until the weather clears. Cold and dampness aggravate the symptoms. Discomfort is often worse toward early morning, or after staying still too long. The person feels better from warmth and gentle motion, and also after eating.

Rhus toxicodendron

Rheumatoid arthritis, with pain and stiffness that is worse in the morning and worse on first motion, but better from continued movement, may be helped with this remedy. Hot baths or showers, and warm applications improve the stiffness and relieve the pain. The condition is worse in cold, wet weather. The person may feel extremely restless, unable to find a comfortable position, and need to keep moving constantly. Continued motion also helps to relieve anxiety.

Ruta graveolens

Arthritis with a feeling of great stiffness and lameness, worse from cold and damp and worse from exertion, may be helped with this remedy. Tendons and capsules of the joints can be deeply affected or damaged. The arthritis may have developed after overuse, from repeated wear and tear.

Dosage

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Homeopathy Dosage Directions

Select the remedy that most closely matches the symptoms. In conditions where self-treatment is appropriate, unless otherwise directed by a physician, a lower potency (6X, 6C, 12X, 12C, 30X, or 30C) should be used. In addition, instructions for use are usually printed on the label.

Many homeopathic physicians suggest that remedies be used as follows: Take one dose and wait for a response. If improvement is seen, continue to wait and let the remedy work. If improvement lags significantly or has clearly stopped, another dose may be taken. The frequency of dosage varies with the condition and the individual. Sometimes a dose may be required several times an hour; other times a dose may be indicated several times a day; and in some situations, one dose per day (or less) can be sufficient.If no response is seen within a reasonable amount of time, select a different remedy.

10.9.2 Acupuncture for Rheumatoid Arthritis

Rheumatoid arthritis and Osteoarthritis, also known as degenerative joint disease, is commonly referred to as the wear and tear disease. Fortunately today, there are many safe and effective alternatives to ease the pain and suffering. Acupuncture doctors decrease pain by increasing the release of endorphins (morphine-like chemicals) that block pain especially during times of stress or pain.

How does it work

Acupuncture is routinely used to relieve pain such as low back, knee, arthritis, sciatica, headaches, tennis elbow, facial and chronic pain where the underlying cause has yet to be discovered. Chinese Medicine considers pain to be a stagnation of energy, blood or body fluids. By inserting very fine needles along the energy pathways called meridians, acupuncture harmonizes and enhances the bodies own natural restorative powers. And, it works well with other alternative healing therapies. People are typically void of exercise which maintains the flow of our bodily fluids and keeps our muscles and joints limber. Acupuncture is very effective for the treatment of arthritic pain and the results are usually felt immediately.

A general guide for the treatment of rheumatoid arthritis

When applying acupuncture treatment for example, there are main points and secondary points. Because there are different causes for Rheumatoid Arthritis, the following acupuncture points will vary according to the symptom.

Mainly caused by pathogenic wind: Fengmen (B12), Kanshu (BL 18), Leshu ( BL 17)

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Mainly caused by pathogenic cold: Dazhui (GV 14), Guanyuan (CV 4) Mainly caused by pathogenic dampness: Pishu (BL 20), Chungwan (CV 12), Yinlingquan

(SP 9) Mainly caused by heat transformed by exogenous pathogen: Quchi (LI 11), Hoku (LI 4)

Treatment for Rheumatoid Athritis using acupuncture prevents and cures this condition by stimulating the human body through the role of meridians and acupuncture points. Joints have a complex structure and rely on the surrounding muscles, ligaments, bursa and other structures so that joints are vulnerable to aute and chronic injury due to the invasion of exogenous pathogens. Meridians become blocked by exogenous pathogens resulting in blood stasis which leads to pain. Acupuncture treatment of Rheumatiod arthritis works to expel cold-dampness and promote blood circulation. Once the Qi flow and blood are flowing smoothly, rheumatoid symptoms will disappear accordingly.

Clinical Trials for Rhematoid Arthritis

1. A recent study from China shows that both traditional acupuncture and electroacupuncture – a type in which pulsating electrical currents are sent through the needles to stimulate target areas – may reduce tenderness. All 36 participants had a standardized treatment, whether they received traditional acupuncture or electroacupuncture. During a total of 20 sessions throughout a 10-week period, needles were placed at a depth of about 10 to 20 millimeters and left in place for 30 minutes.

2. In a German study, 304,674 people with knee osteoarthritis who received 15 sessions of acupuncture combined with their usual medical care had less pain and stiffness, improved function and better quality of life than their counterparts who had routine care alone. The improvements occurred immediately after completing a three-month course of acupuncture and lasted for at least another three months, indicating osteoarthritis is among conditions treated with acupuncture.

CONCLUSION:

Acupuncture is both a viable and popular alternative to effectively help you with your rheumatoid arthritis or osteoarthritis – without side effects.

10.9.3 Ayurveda Treatment of Rheumatoid Arthritis.

Ayureda is a comprehensive andinterative health science origination in India.Ayureda, commonly translated as the knowledge of life is part of the Vedas an ancient Hindu text written in the Sanskrit language. Ayurvedic medicine has been practiced continuously for more than 5,000 years and is respected world wide as a safe, effective and holistic approach to lifelong health.Ayurveda has particular application to those suffering with the chronic pain and inflammation of arthritis, a condition known as amavata in Ayurvedic medicine. Ama is the toxin that builds up in the body usually as a result of improper digestion. These toxins circulate throughout the body and typically deposit in weaker area such as the joints. This leads to the arthritis symptoms of pain and inflammation. The vata, as

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identified in Ayurveda medicine, is one of three basic energetic forces that vitalize the body.

Aynrveda distinguishes three categories of arthritis, corresponding to the three energetic forces vata, pitta and kapha.

Principle of ayurdic healing.

The Ayurvedie approach to healing first takes into account the unique circumstances of the individual seeking relied.Ayurvedie treatment depends upon an individual's basic energy and body type and the external environment in which they live.Ayurveda identifies three basic energetic forces, called doshas,or body humors, that underlie all bodily proceses. The relative balance of energy of these doshas is a determining factor in the overall health of an individual and in her susceptibility to illness and degenerative disease.The three doshas of Ayurvedic Medicine are:

Vata:- This vital energy regulates blood circulation, breath, heartbeat, and even the blinking of the eyes.

Pitta:- This vital energy regulates the metabolic systems including body temperature, digestion, and absorption of nutrients.

Kapha;- This vital energy is responsible for physical growth, maintaining the immune system, and providing body parts with the necessary moisture.

Ayurveda treatment of arthritis.

It is important to engage the services of a qualified Ayurveda practitioner who can provide an accurate assessment of one's individual condition and of the specific dosha imbalance and type of arthritis that may be causing the distress.A qualified Ayurveda practitioner can identify specific treatments appropriate for one's unique needs and characteristics.

Ayurveda treatment for arthritis may include a combination of the following:-

Dietary and lifestyle adjustments

Specific Yoga asanas, or exereises, including the Sun Salute

Breathing techniques to alleviate stress and anxiety

Oil massage and heat therapy

Short periods of fasting to help eliminate toxiety

Panchkarma, a specific detoxifying regime in Ayurveda

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Detoxifying and nutritive herbs or herbal combinations

Enemas and colonies

Ingesting fresh juices, such as carrot, beet, cucumber, grapes, apples, oranges and papaya, and castor oil.

Successful treatment of arthritis with Ayurveda may require that one reduce or eliminate use of certain aggravating dietary substances such as nicotine, caffeine, white sugar, and alcohol. In addition, one may be required to minimize dietary intake of certain gas producing foods such as potatoes, broccoli and cabbage, and maintain an environment sheltered from cold winds and damp conditions.

Ayurveda approach for the treatment of Rheumatoid Arthritis.Some of the more frequently used berbs and herbal combinations for Ayurvedic

treatment of arthritis include many plants native to India. Most are available for purchase through your local Ayurvedic practitioner or health food supplier. Western scientific research has confirmed the effectiveness of many herbs used in Ayurvedic medicine in the of ostco-and rheumatoid arthritis.

Asafetida (Ferula Assafoetida)- Known in Ayurveda medicine as Hing,this herb can be combined with coconut oil or ginger paste to provide relief from inflammation.

Garlic (Allium Sativium)-Known in Ayurveda medicine as Lehsun,this herb helps to strengthen the immune system and cleanse toxins,or ama, from the system.

Ginger root (Zingiber officinale)-Known as Sunthi in Ayurveda, this herb relives pain and inflammation of arthritis.

Guggul (Commiphora mukul)-a resin from the guggul tree, native to India.This substance helps eleeanse and rejuvenate the body,especially the blood vessels and the joints.

Licorite (Glycyrrhiza Glabra)- Known in Ayurveda medicine as Yashimadhu, acts effectively as an anti-inflammatory to reduce arthritis pain in the joints.

Turmeric (Circuma Longa ) – Known in Ayurveda medicine as Haldi, this pungent herbis an anti-inflammatory agent and alleviates pain,particularly in osteoarthritis,response modififying agents such as anti-TNF antibody therapy, may present with serious infections and /or malignancies.

Additionally, adverse events from RA medications may include liver toxicity, renal toxicity, bone narrow depression, lung inflammation, and skin manifestations.

Patients taking anti-TNF agents must avoid live-virus vaccines.

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10.9.4 Reflexology.

Reflexology, or zone therapy, is an alternative medicine involving the physical act of applying pressure to the feet, hands, or ears with specific thumb, finger, and hand techniques without the use of oil or lotion.

It is based on what reflxologists claim to be a system of Zones and reflex areas that say an image of the body on the feet and hands, with premise that such work effects a physical change to the body. A 2009 systematic review of randomized condomised controlled trials concludes that “The best evidence available to date dose not demonstrate convincingly that reflexology is an effective treatment for any medical condition.

There is no consensusnreflexologists on how reflexology is supposed to work: a unifying theme is the idea that areas on the food correspond to areas of the body, and that by manipulation these one can improve health trough one’s.Reflexologists divide the body into ten equal vertical zones, five on the right and five on the left. Concerns have been raised by medical professional that treating potentially serious illnesses with reflexology, which has no proven efficacy, could delay the seeking of appropriates medical treatmenent

MechanismThe Reflexology Association of Canada defines reflexology as;“A natural healing art based on the principle that there are reflexes in the feet,

hands and ears and their referral areas within zone related areas. Which correspond to every past, gland and organ of the body. Through application

of pressure on these reflexes without the use of tools, crimes or lotions, improves circulation and helps promote the natural function of the related areas of the body.

Reflexologies posit that the blockage of an energy filed, invisible life force, or Oi can prevent healing.

Another tenet of reflexology is the belief that practitioners can relieve stress and pain in other parts of the body through the manipulation of the feet. One claimed explanation is that the pressure received in the feet that balance the nervous system or release chemicals such endorphins that reduce stress and pain. These hypotheses are rejected by general medical community who cite a lack of scientific evidence and the well tested germ theory of diseas.

Common criticisms of reflexology are the lack of evidence for its claimed effects, or of a scientific or demonstrated basis for its theories, of central regulation, acereditation and licensing or of medical training provided to reflexologists, and the short duration of training programmes.As with other pseudoscience’s without any proven effect beyond placebo, if patients rely on them and delay or even reject effective medical treatment there can be significant health risks.

Reflexology’s claim to manipulate energy (Qi) has been high controversial, as there is no scientific for the existence of life energy (Qi) energy balance.

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Use by population. An example of a reflexology chart of the Hand, demonstrating the areas of hand

that practitioners believe correspond with organs in the “zones” of the body.Reflexology is one of the most used alternative therapies in Denmark’s national

survey from 2005 showed that 21.4 % of the Danish population had used reflexology, at some point in the life and 6.1% had used reflexology within the previous year. A study from Norway showed that 5.6 % the Norwegian population in 2007had used reflexology with the last 12 months.

RegulationIn the United Kingdom,refexology is coordinated on a voluntary basis by the

Complementary and Natural Healthcare Council (CNHC) Registrants are required to meet Standards of Proficiency outland by profession Specific Bosrds,as CNHC is voluntary any one practicing can describe themselves as reflexologies. When the CNHC began admitting efflexologists, a sceptic search for and found 14 of them claiming efficacy on illnesses. Once pointed out.

The CNHC had the claims retracted as it conflicted with their Adverting stadtising Standards Authority.

HistoryReflexology was introduced to the United States in 1913 by William

II .Fitzgerald.M.D (1872-1942), ear nose, and throat specialist, and Dr.Edwin Bowers.Fitzerald claimed that applying pressure had an anesthetic effect on other areas of the body.

Reflexology was modified in the 1930s and 1940s by Eunice D.Ingham (1889-1974), nurse and physiotherapist. Ingham claimed that the feed and hands especially sensitive, and mapped the entire body into “reflexes” on the feed renaming “zone therapy” to refexology.Ingham’s theories are in the United States and United Kingdom, Although modern methods also exist.

Reflexology has had several clinical trials dedicated to it over the years with mixed results. One systematic review found, “The best evidence available to date not demonstrates convincing that reflexology is effective treatment for any medical

10.9.5 Yoga Treatment of Rheumatoid Arthritis.

Continuing research shows the therapeutic benefits that yoga has on rheumatoid arthritis. As long as you take gentle approach, yoga can provide relief for body and soul.

By Dennis Thompson JanMedically reviewed by pat F bass iii MD, MPH.

The practices of yoga might seem daunting to a person with rheumatoid arthritis (RA). The thought of bending stretching into and then holding pretzel-like poses while your joints are inflamed may sound impossible. However research has shown that gentle yoga can be of great benefit as rheumatoid arthritis treatment.

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Yoga movements can help the body by increasing strength and flexibility while meditative parts of the practice help mind allowing you to sleep better and feel more energetic and happy RA patients also report reduced pain as a result of regular yoga practice.

Some patients may have trouble doing all the things in yoga, but anything that keeps range of motoring in the joints will keep the joints flexible” says Scott Zashin MD clinical assistant professor of internal medicine in the rhemutolog division at University of taxes Southwestern medical School at Dallas and a rhematiogist at Presbyterian Hospitals of dalais and Plano.

Yoga Benefits for RA symptoms.

Scientific in major medical journals have found that yoga can help arthritis patients by;

Building muscle strength

Increasing flexibility

Promoting better balance

Reducing body aches and pains

Creating a better sense of well-being

Reducing feelings of anxiety and depression

These findings continue to be supported by new research. According to a study presented at a recent annual meeting of the American CollegeRheumatology, 30 sedentary adults with rheumatoid arthritis reported reduced joint pain and swelling after participating in an eight, week yoga program modified to accommodate their reduced flexibility and other symptoms.

The results of a study appearing in the Indian journal of Rheumatology found that the 26 RA patients who followed an eight –week yoga program experienced considerable improvement in their arthritis symptoms and some were able to stop taking arthritis medications they had been presented.

In another study published in Alternative therapies, the benefits for a group of 16 women with rheumatoid arthritis who participated in three yoga classes a week over 10 week arthritis. According to research in the journal Psychosomatic Medicine, a study of 50 healthy women found that those who were expert yoga practitioners had a reduced inflammatory response to stressful conditions compared with yoga novices.

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The Safe Approach to Yoga.

People interested in pursuing yoga as a rheumatoid arthritis treatment should follow some basic guideline basic guidelines to make sure that practice will provide relief without any exercise injury.

Get the go -ahead. Before starting yoga, ask your doctor about any specific limitations or restrictions you should observe given your specific arthritic condition.

Choose an appropriate class. Find a gentle or beginner’s yoga class that will accommodate any limitations in your range of motion flexibility. Many gyms and yoga studios offer classes specially designed for people with arthritis. Make sure your teacher is certified.

React to any pain.” physically, if there’s a type of movement or stretch that causes pain or if you hart more, the day after you do yoga, then its either not the right activity for you or you need to modify it “Zashin says.

Be mindful of your neck. “If someone with rheumatoid arthritis has neck involvement,[Yoga] might not be the best therapy, “ Zashin says.” With yoga, you can sometimes put the neck into strange positions. You want to avoid positions that would aggravate neck issues.”

Practicing yoga that suits your body’s abilities may bring welcome relief; a gentle of this ancient therapy can not only help with your rheumatoid arthritis pains, but should relax you and enable you to better enjoy daily activities.

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CHAPTER – 11

11.1 Prognosis:

Rheumatoid arthritis prognosis is compromised if there is a delay in the diagnosis and proper treatment. The prognosis is either exacerbation or remission. It varies highly from person to person. However, it is generally observed that nearly 40% patients with rheumatoid arthritis are disabled after 10 years. Some patients show a comparatively self-limited disease, while others show a chronic progressive disease.

An unfavourable prognosis is correlated with signs like high serum titer of autoantibodies, such as, RF and anti-cyclic citrullinated peptide (CCP), an increased number of affected joints, extra-articular manifestations, female sex, age younger than 30 and systemic symptoms. This unfavourable prognosis is in terms of joint damage and disability. One more unfavourable sign is insidious onset.

Much worsened prognosis of rheumatoid arthritis is seen in patients with positive RF (Rheumatoid Factor) results. However, the absence of RF does not always indicate a good prognosis.

Other laboratory test findings indicating a poor prognosis are early radiological evidence of bone injury, high levels of C1q component of complement, persistent anemia of chronic disease and the presence of anti-CCP antibodies.

If the disease remains persistent for more than 1 year, it is likely to cause joint deformities and disability. Whereas if the symptoms last for a few weeks or months, followed by remission, better prognosis is indicated.

General mortality rate in RA patients is 2.5 times more than that in common population. Much of this increased mortality results from infection, poor nutrition and vasculitis. RA is also related to cardiovascular risk factors.

Rheumatoid arthritis prognosis, along with other factors, is based more importantly on how prominent the disease is currently, i.e. if it is in a flare, a remission or can it be managed well with treatment.

Nearly 10 to 20% of the patients show sudden onset of the disease, which is followed by a long period of no symptoms. This is called a prolonged remission. Some patients of RA show coming and going symptoms, occurring between flares, which can last for months and are referred to as intermittent symptoms of rheumatoid arthritis. Majority of the patients have chronic, progressive type of RA and need long-term medical treatment.

Factors that affect the prognosis so as to make the patients more vulnerable to a

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progressive and bad form of rheumatoid arthritis are intense flares lasting for a long time, disease diagnosed at young age and being active for years and presence of rheumatoid nodules. It is better to assess and reassess all the influencing factors and get the tests, like x-rays and other laboratory tests, done and see if physical results have improved.

If it is evident from the tests that the disease is very active, the doctor may need to change the course of treatment for a more aggressive one so as to slow down or stop the disease progression. Biologic, combined with traditional, DMARDs have been proven to be very effective in the management of rheumatoid arthritis.

Rheumatoid arthritis prognosis regarding the daily activities can be monitored by taking HAQ, i.e. Health Assessment Questionnaire, periodically, which helps you to determine whether your functions are improving or deteriorating and if they are deteriorating, your doctor needs to change to better

About 15% of all RA patients will have symptoms for a short period of time and will ultimately get better, leaving them with no long-term problems. A number of factors are considered to suggest the likelihood of a worse prognosis. These include:

race and gender (female and Caucasian). more than 20 joints involved. extremely high erythrocyte sedimentation rate. extremely high levels of rheumatoid factor. consistent, lasting inflammation. evidence of erosion of bone, joint, or cartilage on x rays. poverty. older age at diagnosis. rheumatoid nodules. other coexisting diseases. certain genetic characteristics, diagnosable through testing.

Patients with RA have a shorter life span, averaging a decrease of three to seven years of life. Patients sometimes die when very severe disease, infection, and gastrointestinal bleeding occur. Complications due to the side effects of some of the more potent drugs used to treat RA are also factors in these deaths.

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11.1.2 PROGNOSTIC FACTORS:

Poor prognostic factors include persistent synovitis, early erosive

disease,extra-articular findings(including subcutaneous rheumatoid nodules),positive

serum RF findings, positive serum anti-CCP auto antibodies, carrier ship of HLA-DR4

“Shared Epitope” alleles, family history of RA, poor functional status, socioeconomic

factors, elevated acute phase response (erythrocyte sedimentation rate [ESR], C-

reactive protein [CRPL], and increased clinical severity.

High titers of rheumatoid factor

Insidious onset of disease

More than a year of active disease without remission

Early development of nodules or erosion

Extra-articular manifestation

Severe functional impairment

11.1.3 MORTALITY.

Estimates of the life –shortening effect of RA vary; most sources cite a

lifespan reduction of 5 to 10 years. According to the UK’s National Rheumatoid Arthritis

Society, “Young age onset, long disease duration, the concurrent presence of other

health problems (called co-morbidity), and characteristics of severe RA ---such as poor

functional ability or overall health status, a lot of joint damage on x-rays, the need for

hospitalization or involvement of organs other than the joints ---have been shown to

associate with higher mortality. Positive response to treatment may indicate a better

prognosis. A 2005 study by the Mayo clinic noted that RA suffers suffer a doubled risk of

heart disease, independent of other risk factors such as diabetes, alcohol abuse, and

elevated cholesterol, blood pressure and body mass index.

The mechanism by which RA causes this increased risk remains unknown; the

presence of chronic inflammation has been proposed as a contributing factor.

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CAHPTER -12

12. EPIDEMIOLOGY.

The incidence of RA is in the region of 3 cases per 10,000 populations per

annum. Onset is uncommon under the age of 15 and from then on the incidence rises

with age until the age of 80. The prevalence rate is 1 %, with women affected three to five

times as often as men. It is up to three times more common in smokers than non-

smokers, particularly in men, heavy smokers, and those who are rheumatoid factor

positive. A study in 2010 found that those who drank modest amounts of alcohol regularly

were four times less likely to get rheumatoid arthritis than those who never drank. Some

Native American groups have higher prevalence rates (5-6%) and people from the

Caribbean region have lower prevalence rates. First –degree relatives prevalence rate is

2-3% and disease genetic concordance in monozygotic is approximately 15-20%.It is

strongly associated with the inherited tissue type Major histocompatibility complex (MHC)

antigen HLA-DR4 (most specifically DR0401 and 0404)- hence family history is an

important risk factor.

The risk of first developing the disease (the disease incidence) appears to

be greatest for women between 40 and 50 years of age, and for men somewhat later. A is

a chronic disease, and although rarely, a spontaneous remission may occur, the natural

course is almost invariably one of persistent symptoms, waning intensity, and a

progressive deterioration of is joint structures leading to deformations and disability.

CHAPTER - 13

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13. HISTO.RY

The first known traces of arthritis date back at least as far as 4500BC.A text

dated 123 AD first describes symptoms very similar to rheumatoid arthritis. It was noted in

skeletal remains of Native Americans found in Tennessee. In the Old World the disease is

ravishingly rare before the 1600s, and on this basis investigators believe it spread across

the Atlantic during the Age of Exploration. In 1859 the disease acquired its current name.

An anomaly has been noticed from investigation of Pre-Columbian bones.

The bones from the Tennessee site show no signs of tuberculosis even though it was

prevalent at the time throughout the Americas.

Jim Mobley, at Pfizer, has discovered a historical pattern of epidemics of

tuberculosis followed by a surge in the number of rheumatoid arthritis cases a few

generations later.Mobley attributes the spikes in arthritis to selective pressure caused by

tuberculosis’s hyper vigilant immune system is protective against tuberculosis at the cost

of an increased risk of autoimmune disease.

The art of peter Paul Rubens may possibly depict the rheumatoid arthritis.

In his later paintings, his rendered hands show, in the opinion of some physicians,

increasing deformity consistent with the symptoms of disease. Rheumatoid arthritis

appears to some to have been depicted in 16 th century paintings. However, it is generally

recognized in art historical circles that the painting of hands in the sixteenth and

seventeenth century followed certain stylisedconventions, most clearly seen in the

Mannerist. It was conventional, for instance to show the up help right hand of Christ in

what now appears adeformed posture.These conventions are easily misinterpreted as

portrayals of disease. They are much too widespread for this to be plausible.

The fist recognized description of rheumatoid arthritis was in 1800 by French physician Dr Augustin Jacob Landre-Beauvais (1772-1440) who was based in the famed Salpetriere Hospital in Paris.The name “rheumatoid arthritis”itself was coined in 1859 by British rheumatologist Dr.Alfred Baring Garrod.

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CHAPTER – 14

PHOTOGRAPHS

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Fig- 1 HUMAN SKELETON ANTERIOR VIEW

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http://en.wikipedia.org/wiki/File:Human_skeleton_front_en.svg

Fig – 2 HUMAN SKELETON POSTERIOR VIEW

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http://en.wikipedia.org/wiki/File:Human_skeleton_back_en.svg


Fig – 3 CROSS SECTION VIEW OF BONE

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Fig – 4 PANNUS FORMATION

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Fig – 5 BOUTONNIERE DEFORMITY.

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Fig -6 RHEUMATOID CHANGES IN THE HAND

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Fig – 7 SUBLUXATION IN THE METACARPOPHALANGEAL JOINTS, WITH ULNAR DEVIATION, IN A PATIENT WITH RHEUMATOID ARTHRITIS OF THE HANDS.

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Fig - 9 Fig-8 CORONAL, T1-WEIGHTED MAGNETIC RESONANCE IMAGING SCAN SHOWS CHARACTERISTIC PANNUS AND EROSIVE CHANGES IN THE WRIST IN A PATIENT WITH ACTIVE RHEUMATOID ARTHRITIS.

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Fig -9 LATERAL VIEW OF THE CERVICAL SPINE IN A PATIENT WITH RHEUMATOID ARTHRITIS SHOWS EROSION OF THE ODONTOID PROCESS

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Fig -10 A COMMON FEATURE IN RA IN THE FEET IS PROMINENCE Of THE METATARSAL HEADS DUE TO METATARSOPHALANGEAL SUBLUXATION

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Fig – 11 RHEUMATOID ARTHRITIS HANDS DEFORMITIES

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Fig-12 IMAGE OF HAND SHOWING LATE STAGE OF RA, WITH BOUTONNIERE DEFORMITY, ULNAR DEVIATION OF METACARPOPHALANGEAL JOINTS AND SWAN–NECK DEFORMITY OF FINGERS.

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Fig -13 PSORIATIC ARTHRITIS OF FOURTH TOE

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Fig -14 RHEUMATOID ARTHRITIS HAND DEFORMITY

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Fig-15 Photos show examples of RA with inflammation in the joints and

surrounding tissue.

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Fig -16 Bilateral ulnar deviation of hands

.

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http://dermimages.med.jhmi.edu/images/RHEUMATOID_ARTHRITIS_2_110114.jpg

http://dermimages.med.jhmi.edu/images/RHEUMATOID_ARTHRITIS_2_110114.jpg


Fig-17 RHEUMATOID VASCULITIS

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Fig -18 KNEE NODULE IN RA

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Fig -19 CORONAL, T1-WEIGHTED MAGNETIC RESONANCE IMAGING SCAN SHOWS CHARACTERISTIC PANNUS AND EROSIVE CHANGES IN THE WRIST IN A PATIENT WITH ACTIVE RHEUMATOID ARTHRITIS.

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Fig - 20 SOFT-TISSUE SWELLING AND EARLY EROSIONS IN THE PROXIMAL INTERPHALANGEAL JOINTS IN A PATIENT WITH RHEUMATOID ARTHRITIS OF THE HANDS.

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Fig -21 SAGITTAL FAT-SATURATED T2-WEIGHTED MAGNETIC RESONANCE IMAGE (MRI) SCAN OF THE RING FINGER SHOWS FLUID WITH HIGH SIGNAL INTENSITY AROUND THE FLEXOR TENDONS RESULTING FROM TENOSYNOVITIS IN A PATIENT WITH RHEUMATOID ARTHRITIS OF THE HANDS

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.

Fig – 22 SAGITTAL T1-WEIGHTED MRI SHOWS EROSIVE CHANGES IN THE LUNATE, CAPITATE, AND METACARPAL BASES IN A PATIENT WITH RHEUMATOID ARTHRITIS OF THE HANDS.

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Fig-23 POWER DOPPLER IMAGE SHOWS HYPEREMIC BLOOD FLOW IN THE FLEXOR TENDON SHEATH IN A EUMATOID ARTHRITIS OF THE HANDS.

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Fig -24 RHEUMATOID NODULES AT THE ELBOW.

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Fig -25 A 78-YEAR-OLD MAN HAD RHEUMATOID ARTHRITIS DIAGNOSED 4 YEARS AGO. RHEUMATOID NODULES WERE EVIDENT ON BOTH ELBOWS. THERE WAS SWELLING OF THE METACARPAL- PHALANGEAL AND PROXIMAL-INTERPHALANGEAL JOINTS OF BOTH HANDS AS WELL AS WASTING OF THE SMALL MUSCLES AND CONTRACTURE OF THE PALMAR APONEUROSIS.

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http://dermimages.med.jhmi.edu/images/Rheumatoid_arthritis_4_100218.jpg

Fig -26 SUBLUXATION IN THE METACARPOPHALANGEAL JOINTS, WITH ULNAR DEVIATION, IN A PATIENT WITH RHEUMATOID ARTHRITIS OF THE HANDS.

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Fig-27 NEEDLES BEING INSERTED INTO A PATIENT'S SKIN

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http://en.wikipedia.org/wiki/File:Acupuncture1-1.jpg

Fig-28 LATERAL VIEW OF THE CERVICAL SPINE IN A PATIENT WITH RHEUMATOID ARTHRITIS SHOWS EROSION OF THE ODONTOID PROCESS

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Fig – 29 RHEUMATOID CHANGES IN THE HAND..

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References

1. Essential of Complementary Alternative Medicine, Jonas W. Levin(editors). Lippincott William & Wilkins,1999.

2. Alternative Medicine by Loulou Brown.

3. Complementary & Alternative Medicine by Kevin Barrows,MD

Complementary and Alternative Medicine use among adults and Childern: United State 2007.

CDC National Health Statistics Report Number 12 Dec 2008.

4. Clinical Medicine by Parveen Kumar and Micheal Clark( 7th Edition) Pag.523-532.

5. Medical Diagnosis and Management by Dr.Mohammad Inam Danish (4th Edition 1992) pag.514-525.

6. Current Medical Diagnosis & Treatment(1982) by Marcus A. Krupp,MD ,Pag.487-493.

7. Renger F, Bang H, Fredenhagen G, Natusch A, Backhaus M, Feist E, Egerer K, Burmester GR. "Anti-MCV Antibody Test for the Diagnosis of Rheumatoid Arthritis Using a POCT-Immunoassay". American College of Rheumatology, 2008 Annual Scientific Meeting, poster presentation

8. Albano, Shirley A., Weisman, Michael H., "Cigarette Smoking and Rheumatoid Arthritis," Seminars in Arthritis and Rheumatism. Volume 31. Issue 3. December 2001. Pages 146-159.)

10. American College of Rheumatology Subcommittee on Rheumatoid Arthritis Guidelines (February 2002). "Guidelines for the management of rheumatoid arthritis: 2002 Update " . Arthritis & Rheumatism 46 (2): 328–346.

11. Luime JJ, Colin EM, Hazes JM, Lubberts E. (2009). "Does anti-MCV has additional value as serological marker in the diagnostic and prognostic work-up of patients with rheumatoid arthritis? A systematic review " . Ann Rheum Dis. 2009 Mar 15. [Epub ahead of print] 69 (2): 337–44.

12.Saag KG, Gim GT, Nivedita M et al (June 2008). "American College of Rheumatology 2008 Recommendations for the Use of Nonbiologic and Biologic Disease-Modifying Antirheumatic Drugs in Rheumatoid Arthritis". Arthritis & Rheumatism 59 (6): 762–784.

114

http://www3.interscience.wiley.com/journal/119635887/abstract?CRETRY=1&SRETRY=0



http://ard.bmj.com/cgi/rapidpdf/ard.2008.103283v1



http://doi.wiley.com/10.1002/art.10148

http://doi.wiley.com/10.1002/art.10148


13. Leventis P, Patel S (2008). "Clinical aspects of vitamin D in the management of rheumatoid arthritis". Rheumatology (Oxford) 47 (11): 1617–21.

14. Alamanos Y, Voulgari PV, Drosos AA (2006). "Incidence and prevalence of rheumatoid arthritis, based on the 1987 American College of Rheumatology criteria: a systematic review". Semin. Arthritis Rheum. 36 (3): 182–8.

15.Chris Deighton, Rachel O’Mahony, Jonathan Tosh, Claire Turner, Michael Rudolf, and Guideline Development Group (March 2009). "Management of rheumatoid arthritis: summary of NICE guidance". British Medical Journal 338: 710–712.

16.Lee1 MS, Shin B-C, Ernst E (2008). "Acupuncture for rheumatoid arthritis: a systematic review". Rheumatology 47 (12): 1747–53.

17.Newsome G. Guidelines for the management of rheumatoid arthritis: 2002 update. J Am Acad Nurse Pract 2002; 14(10):432-437.18.Hochberg MC, Altman RD, Brandt KD, Clark BM, Dieppe PA, Griffin MR et al. Guidelines for the medical management of osteoarthritis. Part II. Osteoarthritis of the knee.American College of Rheumatology. Arthritis Rheum 1995; 38(11):1541-1546.19.Bearne LM, Scott DL, Hurley MV. Exercise can reverse quadriceps sensorimotor dysfunction that is associated with rheumatoid arthritis without exacerbating disease activity. Rheumatology (Oxford) 2002; 41(2):157-166.20. Dash M, Telles S. Improvement in hand grip strength in normal volunteers and rheumatoid arthritis patients following yoga training. Indian J Physiol Pharmacol 2001; 45(3):355-360.21. US Department of Health and Human Services. Physical Activity and Health: A Report of the Surgeon General. 1996. Atlanta, GA, US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion.22. Lyngberg K, Danneskiold-Samsoe B, Halskov O. The effect of physical training on patients with rheumatoid arthritis: changes in disease activity, muscle strength and aerobic capacity. A clinically controlled minimized cross-over study. Clin Exp Rheumatol 1988; 6(3):253-260.23. Clincal Practice of Acupuncture by A.L .Agrawal, G.N Sharma (2nd Edition)24. Homoeopathic Materia Medica and Repertory by William Boericke, MD

25. Bratman, MD, Steven (1997). The Alternative Medicine Sourcebook. Lowell House. p. 7.

26. Walter R., PhD. Frontera; DeLisa, Joel A.; Gans, Bruce M.; NICHOLAS E. WALSH (2005). Physical medicine and rehabilitation: principles and practice. Hagerstwon, MD: Lippincott Williams & Wilkins. pp. Chapter 19.

27. Shen AC, Whitehouse MJ, Powers TR et al. A pilot study of the effects of acupuncture in rheumatoid arthritis. Arthritis Rheum 1973;16:569–70.

115

http://books.google.com/?id=1sWk1GYCvKoC&printsec=frontcover

http://rheumatology.oxfordjournals.org/content/47/11/1617.long

http://rheumatology.oxfordjournals.org/content/47/11/1617.long

28. Struthers GR, Scott DL, Scott DGI. The use of `Alternative treatments' by patients with rheumatoid arthritis. Rheumatol Int 1983;3:151–2

29. Ayurvedic Trust. World Health Organization/Indian Council for Medical Research Collaborative Study on the Efficacy of Ayurvedic Treatment in Rheumatoid Arthritis. Coimbatore, India: The Ayurvedic Trust; 1984.

30. Ropes M, Bennett GA, Cobb S, Jacox R, Jessar RA. 1958 Revision of diagnostic criteria for rheumatoid arthritis. Bull Rheum Dis 1958;9:175-6.

31. Hardy M, Coulter I, Venuturupalli S, et al. Ayurvedic Interventions for Diabetes Mellitus: A Systematic Review. Evidence Reports/Technology Assessments, No. 41. Rockville (MD): Agency for Healthcare Research and Quality (US); 2001 Sep.

32. Chopra A, Lavin P, Patwardhan B, Chitre D. Randomized double blind trial of an Ayurvedic plant derived formulation for treatment of rheumatoid arthritis. J Rheumatol 2000;27:1362-5.

33. Kulkarni RR, Patki PS, Log VP, Gandage SG, Patwardhan B. Efficacy of an Ayurvedic formulation in rheumatoid arthritis: A double blind, placebo controlled, cross-over study. Indian J Pharmacol 1992;24:98-101.

34. Sander O, Herborn G, Rau R. Is H15 (extract of Boswellia serrata,"incense") an efficient supplementation to established drug therapy in RA? Results of a double blind pilot trial. Z Rheumatol 1998;57:11-6.

35. Hardy ML. Research in Ayurveda: Where do we go from here? Altern Ther Health Med 2001;7:34-5.

36. Firestein GS, Budd RC, Harris ED, McInnes IB, Sergent JS. Kelley's Textbook of Rheumatology. 8 th ed. Philadephia PA: WB Saunders; 2008.

37. Venkatraman M, Assefi N. Ayurveda: General Principles and Treatment of Rheumatoid Arthritis. Alt Med Alert 2002;5:144-7.

38. Furst DE, Venkatraman MM, McGann M, Manohar PR, Booth-Laforce C, Sarin R, Sekar PG, Raveendran KG, Mahapatra A, Gopinath J, Kumar PR. Double-blind, randomized, controlled, pilot study comparing classic Ayurvedic medicine, methotrexate, and their combination in rheumatoid arthritis. J Clin Rheumatol. 2011 Jun;17:185-92.

39. Varier KS. Ayurvedic Treatment of Rheumatoid Arthritis. Swasth Hind 1980;5:334-6.

40. Banerji D. The place of indigenous and western systems of medicine in the health services of India. Soc Sci Med 1981;15A:109-14

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