Reumatoid ArthritisFDH2013.ppt

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RHEUMATOID ARTHRITIS RHEUMATOID ARTHRITIS D r. F A I Z A LD R I S S A H A S I B U A N , S pP D B a gi a nPe nya k it D a l a m FKU N IV. YA R S I J A K A R TA 2013

Transcript of Reumatoid ArthritisFDH2013.ppt

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 Artritis Reumatoid :

 Tersebar luas, semua kelompok, ras, etnik di dunia

 Penyakit inflamasi sistemik autoimun

 Inflamasi yg kronik pd sendi

 Suatu poli artritis progresif Sendi dan organ tubuh lain

 Gejala penyakit kronis yang hilang timbul

  kerusakan sendi deformitasdisabilitas

 Etiologi pasti ????

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 Autoimmune Diseases Autoimmune Diseases

 Autoimmune diseases occur Autoimmune diseases occur

when the immune systemwhen the immune system

mistake self tissue for non-mistake self tissue for non-

self and mounths anself and mounths an

inappropriate attackinappropriate attack

Most autoimmune disordersMost autoimmune disorders

affect women moreaffect women more

frequentlyfrequently

RA-3: 1RA-3: 1

 Autoimmune disorders may Autoimmune disorders mayresult from multipleresult from multiple

interactions of genes andinteractions of genes and

environmental factorsenvironmental factors

 Autoimmune diseases can affectdifferent systems within the ody

!ervous system

Multiple sclerosis

"lood

 Autoimmune

haemolyticanaemia

#kin

$soriasis

%ndocrine system

&ype 1 diaetes

Multiple organs

#ystemic lupus%rythematosus

"ones and 'oints

Arthritis

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Penyakit autoimun :Penyakit autoimun :

Sistem imun teraktivasiSistem imun teraktivasi 

Menyerang 'aringan yg sehatMenyerang 'aringan yg sehat

(nflamasi dan kerusakan 'aringan ) organ(nflamasi dan kerusakan 'aringan ) organ

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$roses autoimun meliatkan :$roses autoimun meliatkan :

Sel limfosit T & sel Messenger molecules

 Antiodi *R+,

 Anti cyclyc citrullinated -peptic antiody *anti-$-a, er!a"ai sitokin

- (nterleukin-1β *(.-1β,

- &umor necrosis factor α *&!+- α,

- /emokin dan Reseptornya

#ignalling and co stimulatory molecules

#el mast

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#inoviosit#inoviosit

%ctopic lymphoid neogenesis%ctopic lymphoid neogenesis

 Angiogenesis Angiogenesis

0.A-class ((0.A-class ((

!on-M0 risk genes!on-M0 risk genes

 Arthritogenic antigen Arthritogenic antigen MacrofagMacrofag

#el dendrit#el dendrit

"lys *"-lymphocytes stimulator,"lys *"-lymphocytes stimulator,

 A$R(. *a proliferating inducing legand, A$R(. *a proliferating inducing legand,

MerokokMerokok

enderender

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"anyak sekali faktor yg terliat"anyak sekali faktor yg terliat

 Ada interaksi diantara faktor-faktor ts Ada interaksi diantara faktor-faktor ts

# !reak$o%n of self tolerane# !reak$o%n of self tolerane

# inflamasi y" merusak 'arin"an# inflamasi y" merusak 'arin"an

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%pidemiology%pidemiology

ommon disease: affects 21 of the populationommon disease: affects 21 of the population

$redominantly affects women$redominantly affects women

4nset of disease is usually etween 56 and 764nset of disease is usually etween 56 and 76

years of age8 ut can start at any ageyears of age8 ut can start at any age

4ccurs in all races and ethnic groups8 ut is rare in4ccurs in all races and ethnic groups8 ut is rare in

less developed and more rural parts of the worldless developed and more rural parts of the world

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 Aetiology)pathogenesis Aetiology)pathogenesis

Rheumatoid arthritis *RA, is a chronic8 inflammatory8Rheumatoid arthritis *RA, is a chronic8 inflammatory8

systemic8 autoimmune diseasesystemic8 autoimmune disease

Mainly a polyarticular diseaseMainly a polyarticular disease

hronic inflammation in the synovial memrane ofhronic inflammation in the synovial memrane of

affected 'ointsaffected 'oints

&he specific cause of RA is unknown8 ut the immune&he specific cause of RA is unknown8 ut the immune

response is well characterisedresponse is well characterised

 

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PATOGENESIS ETIOLOGIK

Perubahan berupa :

Kerusakan mikrovaskuler, oedem jarinan sinovial, proli!erasi

linin sel pada sinovial"

  Terdapa# sel leukosi# polimor!onuklear pada permukaan

sinovial"

 

Terjadi obli#erasi pada pembuluh darah ke$il akiba# adan%ain!lamasi dan #rombi %an #eroranisir"

  &airan sinovial menandun ban%ak sel mononuklear leukosi#

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PATOLOGI SEL'LE( 

Tampak adan%a :

  Oedema sinovial

  )iperplasia dan hiper#ropi sel linin sinovial %an dapa#

menebal oleh karena peninka#an sel A *re#i$uloendo#helial

like+ dan sel #ipe

  Lisosom merusak

Obs#ruksi kapiler

  in!il#rasi sel neu#ro!il pada dindin ar#eri

  -aerah #rombosis

 

Perdarahan perivaskuler

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%tiopathogenese RA%tiopathogenese RA

/ominasi eragai faktor genetik/ominasi eragai faktor genetik

Respon imun atau inflamasi akiat infeksiRespon imun atau inflamasi akiat infeksi

 Autoimunitas terhadap eragai komponen sendi8 Autoimunitas terhadap eragai komponen sendi8

seperti sinovium dan rawan sendi8 akiat auto antiodiseperti sinovium dan rawan sendi8 akiat auto antiodipatogen atau sel & yg mengalami auto reaksipatogen atau sel & yg mengalami auto reaksi

/elainan pengaturan produksi eragai sitokin yg/elainan pengaturan produksi eragai sitokin yg

erfungsi seagai sitokin proinflamasi atau dlmerfungsi seagai sitokin proinflamasi atau dlm

kerusakan sendikerusakan sendi

&ransformasi komponen seluler sinovium men'adi&ransformasi komponen seluler sinovium men'adi

autonom8 mementuk sel-sel yg dpt menginvasi 'aringanautonom8 mementuk sel-sel yg dpt menginvasi 'aringan

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#itokin $roinflamasi :#itokin $roinflamasi :

T()#T()# 

* I+#,* I+#, 

** M-#+8 M-#+ dan (.-9M-#+8 M-#+ dan (.-9

#itokin anti inflamasi :#itokin anti inflamasi :

(.-168 (.-118 &+-(.-168 (.-118 &+-ββ Antagonis reseptor (.-18 reseptor &!+ terlarut Antagonis reseptor (.-18 reseptor &!+ terlarut

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PATO-E(ESAPATO-E(ESA

Rantai .eristi%a imunolo"is

 Antigen dalam memran sinovial diproses A$ *sinoviosit

 A8 sel dendritik8 makrofag,

 0.A DR

  Ag dikenali8 diproses8 diikat oleh D5

 kompleks trimolekular; Dengan antuan (.-1

menyeakan aktivasi D5

 Ag kompleks trimolekular mengekspresikan (.-< pada

permukaan D5

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+agositosis kompleks imun disertai pementukan+agositosis kompleks imun disertai pementukandan pemeasan radikal eas8 leukotrin 8 $8dan pemeasan radikal eas8 leukotrin 8 $8

protease neutralprotease neutral  erosi rawan sendi dan tulangerosi rawan sendi dan tulang

Ra$ikal !e!asRa$ikal !e!as  depolimerasi hialuronatdepolimerasi hialuronat  viskositas cairan sendiviskositas cairan sendi ;;

Ra$ikal !e!asRa$ikal !e!as 'uga merusak kolagen dan 'uga merusak kolagen danproteoglikan rawan sendiproteoglikan rawan sendi

Masuknya sel radang ke memran sinovialMasuknya sel radang ke memran sinovial  .annus.annus *'ar; ranulasi yang terdiri dari firolas8*'ar; ranulasi yang terdiri dari firolas8mikrovaskular dan eragai 'enis sel radang,mikrovaskular dan eragai 'enis sel radang,

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P(OSES PENG('SAKAN

- Kerusakan ra.an / Kerusakan liamen#

/ Kerusakan #endon / Kerusakan #ulan

  Penipisan pro#eolikan : / Tidak normal

/ Tidak menkila#

/ Tidak ken%al

/ Kuran kua#

  Proli!erasi membran sinovial

  Pannus : jarinan ranulasi vaskuler #erdiri dari

!ibroblas %an berproli!erasi

  pembuluh darah ke$il

  sel in!lamasi

 →

  menimbulkan kerusakan

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 Primer penyakit synovial,

 Sekunder perobahan pada sinovial, fluid,cartilage, paraarticuler, tendon dan komponen

vascular.

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$athogenesis$athogenesis

 A$ = antigen presenting cell

Maini; Rheumatology

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$otential Roles of " ells in the$otential Roles of " ells in the

(mmunopathogenesis of RA(mmunopathogenesis of RA

(Dörner & Burmester, 2003; Edwards et al, 1999; Gause & Berek,

2001; Shaw et al, 2003; Takemura et al, 2001; Zhan & Br!des,19"#$

#ecretion of proinflammatory#ecretion of proinflammatory

cytokinescytokines

 Antigen presentation Antigen presentation

&-cell activation&-cell activation

 Autoantiody production Autoantiody production

and self-perpetuationand self-perpetuation

Cartilage lossCartilage loss

IL-6

B cell

T cell

Macrophage

Dendriticcell

IL-10TNF-α

TNF-αIL-10

RF

Fix complementFix complement

InamedInamed

s!no"ias!no"ia

Inammator!Inammator! 

damagedamage

TNF-α

B cell

IL-6

B cell

#lasmacell

RFRF

RF

RF

IL-1

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ompromised integrity ofompromised integrity of

the 'oint structure leading to disailitythe 'oint structure leading to disaility

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linical patternlinical pattern 

%!sk' (199"$; )l*e(199#$ 

$rogressive onset *from$rogressive onset *fromweeks to months,weeks to months,

$ain and stiffness$ain and stiffness*synovitis,*synovitis,

#wollen 'oints#wollen 'oints

#ymmetric articular pattern#ymmetric articular pattern

+lu-like symptoms+lu-like symptoms Morning stiffnessMorning stiffness

+atigue+atigue

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linical pattern *cont?d,linical pattern *cont?d,

 At onset8 RA usually affects hands8 wrists At onset8 RA usually affects hands8 wrists

and feetand feet

4ften a chronic cyclical course4ften a chronic cyclical course

During flare-ups8 new 'oints are affectedDuring flare-ups8 new 'oints are affected

and e@isting lesions are worsenedand e@isting lesions are worsened

oints ecome deformed8 leading tooints ecome deformed8 leading toadditional disailityadditional disaility

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TANGAN

• en#uk jari spindle/ shape !usi!orm ok pembenkakan PIP

• S.an ne$k de!ormi#is * hipere0#ensi PIP !le0i -IP +

• ou#onniere de!ormi#as * 1le0i PIP e0#ensi -IP+

• Ibu jari :

/ hipere0#ensi sendi in#erphalan dan !le0si 2&P

→ da%a jepi# jempol menhilan

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.ateral deviation of the M$ 'oints.ateral deviation of the M$ 'oints

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Slide 9

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/ Sime#ris

Pen#in un#uk (A

edakan denan ar#hri#is %an lain

-IP #ak kena

  mornin s#i!!ness dapa# dipakai sebaai ukuran bera#n%a

pen%aki#

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PE(GELANGAN TANGAN

*Sana# serin #erkena A"("+

3 o% s%novium

3 Pembenkakan ulnar

3 -orso!le0i perelanan #anan #eranu

3 Sindrome &arpal/#unnel * N"2edianus #er#ekan+

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SIK'

3 !leksi kon#rak#ur

3 Pembenkakan

3 -es#ruksi para/olekranon

3 -islokasi sendi

A)'

3 Sendi lenohumeralis

3 A$romio$lavi$ularis

3 Thora$os$apularis

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PANGG'LPANGG'L*jaran #erkena A"(+*jaran #erkena A"(+

3 Lankah abnormal

3 Gerak sendi #erba#as

3 (asa #ak enak pd lipa#an

paha

L'T'TL'T'T 

*serin #erkena A"(+*serin #erkena A"(+

3 )%per#ro!i sinovium

3 E!usi sendi

3 A#ro!i o#o# 4uadri$ep

3 Terben#uk kis#a aker

*bila pe$ah keluhan mirip

#hromboplebi#is+

3 Ins#abili#as sendi

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KAKI -AN PE(GELANGAN KAKI

• Gerakan !leksi dan eks#ensi #erba#as

• Saki# pada daerah #umi# a#au bursa diba.ah

#endon A$hiles dan #elapak kaki bila berjalan

• )allu0 valus *deviasi la#eral ibu jari

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&E(5I&AL&E(5I&AL

3 N%eri dan kaku leher

3 Erosi proressi! 

3 Sub lu0a#io A#lan#o a0ial"

  6 $ompressi 2ed" Spinalis

 ejala neurolois

  6 perpu#aran dan penekanan ar#eri ver#ebralis

*dp# menimbulkan sinkope se.ak#u menundukan kepala+

3 N%eri lokal

3 Spasme o#o#  erak memu#ar #erba#as

3 Saki# kepala daerah o$$ipu#

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%@tra-articular pattern%@tra-articular pattern

(n some cases8 RA has an e@tra-articular pattern(n some cases8 RA has an e@tra-articular pattern

*involvement of other organ systems,*involvement of other organ systems,

Bsually occurs in rheumatoid factor *R+,-positiveBsually occurs in rheumatoid factor *R+,-positivepatients with more severe articular diseasepatients with more severe articular disease

More common in menMore common in men

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5askuli#isKelainan Paru *Pleuri#is, Pneumoni#is+

  Perikardi#is

  Nodul (euma#ik : / bursa olekranon

/ eks#ernal lenan a#as

/ #endo A$hilles

/ #elina

Neuropa#i

Lesi kornea dan konjun$#iva

  Skleri#is

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Pembesaran kelenjar e#ah benin 

Pembesaran lim!a

  )iperpimen#asi

 

'lkus di kuli#

 

Lim! adenopa#i

  Anemia

 

Thrombosi#openia

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LAO(ATO(I'2LAO(ATO(I'2

3 S( menini

3 Anemia rinan

3 (heuma !a$#or :

(ose .aaler lebih spesi!i$ 7 la#e0 lebih sensi#i!"

3 1ak#or AP1 ama# spesi!ik 

3 -arah ru#in, urine ru#in, !aal injal, !aal hepar

3 &airan sinovial berupa e0uda#

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Dia"nosisDia"nosis

linical patternlinical pattern

"iology"iology

(magery(magery

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"iology"iology %levation of common non-specific serum markers of%levation of common non-specific serum markers of

inflammation contriutes to the assessment of diseaseinflammation contriutes to the assessment of diseaseactivity levelactivity level

%rythrocyte sedimentation rate *%#R,%rythrocyte sedimentation rate *%#R,-reactive protein *R$,-reactive protein *R$,

Rheumatoid factors *R+,Rheumatoid factors *R+,Bsually appear in the first year of the diseaseBsually appear in the first year of the disease 296 of RA patients are R+ *(gM the main isotype,296 of RA patients are R+ *(gM the main isotype, Associated with more rapidly evolving the more erosive Associated with more rapidly evolving the more erosive

disease and a higher incidence of e@tra-articulardisease and a higher incidence of e@tra-articularmanifestationsmanifestations

R+ can e detected in healthy patients during infections *5R+ can e detected in healthy patients during infections *5in aucasians,in aucasians,

R+ also associated with other chronic diseases *1,R+ also associated with other chronic diseases *1,

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(magery C conventional -ray(magery C conventional -ray

$erformed at disease onset and on a regular asis$erformed at disease onset and on a regular asis

Bsually hands and feetE other 'oints monitoredBsually hands and feetE other 'oints monitored

according to the disease patternaccording to the disease pattern "one erosions and 'oint space narrowing patterns"one erosions and 'oint space narrowing patterns

notednoted

 Appro@imately 36 of patients already have ony Appro@imately 36 of patients already have ony

erosion at disease onset *>F6 at < years,erosion at disease onset *>F6 at < years,

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Bltrasounds and MR(Bltrasounds and MR(

#ynovitis detection is mainly assessed#ynovitis detection is mainly assessed

clinicallyclinically

(n difficult cases8 ultrasound may e useful(n difficult cases8 ultrasound may e useful

to detect synovitis and tenosynovitisto detect synovitis and tenosynovitis

MR( is not used in routine practiceMR( is not used in routine practice

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 Artritis Reumatoid ( ACR, 1987 ) :1. Kaku pagi minimal 1 jam untuk jangka  waktu minimal 6 minggu

2. Bengkak 3 sendi atau lebih untuk jangka waktu minimal 6 minggu

3. Bengkak sendi pergelangan tangan,

  metacapofalangeal atau proksimal  interfalang selama 6 minggu atau lebih

4. Bengkak sendi yang simetrik

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5. Perubahan radilogik tangan yang tipikal  untuk artritis reumatoid yang harusmeliputi erosi dan dekalsifikasi tulang

  unequivocal.

6. Nodul reumatoid

7. Faktor reumatoid positif (dengan metode  dimana orang normal positif kurang dari 5 %)

 Diagnosa artritis reumatoid ditegakkan biladitemukan 4 kriteria atau lebih.

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-IAGNOSA AN-ING-IAGNOSA AN-ING

(heuma#i$ 1ever : / respons denan salis%la#e

/ $ardi#is, $horea, skin rash

/ ASTO menini

SLE : / u##er!l% rash

/ (enal disease

/ L"E posi#i! 

Os#eoar#hrosis :: / #anda in!lamasi minimal

/ Pain sore

Gou#% Ar#hri#is: / a$u#e onse#$  / r%s#al ura#e

/ #ophi

P%oeni$ Ar#hri#is : demam, mi$r" oranism didapa#

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&herapeutic goals&herapeutic goals

$rimary goals in the treatment of RA$rimary goals in the treatment of RA$revention or control of structural damage to$revention or control of structural damage to

 'oints 'oints

$revention or reversal of disaility$revention or reversal of disaility$ain relief $ain relief &o improve quality of life&o improve quality of life

&he ultimate goal is to achieve disease&he ultimate goal is to achieve diseaseremissionremission

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urrent treatment strategy in RAurrent treatment strategy in RA

The "oal is to ahieve lo% $isease ativity

or remission

Early an$ intensive treatment intervention

0ontrol effiay !y monitorin" $isease ativity

Ra.i$ s%ithin" %ith lak of im.rovement

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Treatment strate"y a..roahesTreatment strate"y a..roahes

Dramatically changed over the last decadeDramatically changed over the last decade

Moved towards anMoved towards an early .harmaolo"ialearly .harmaolo"ial

treatment interventiontreatment intervention 

To in$ue remission

To slo% /.revent1 ra$iolo"ial

.ro"ression an$ .revent $isa!ility

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AR B(D%.(!%# (! RA &R%A&M%!&AR B(D%.(!%# (! RA &R%A&M%!&

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ESTA+ISHESTA+ISH

RA DIA-(OSISRA DIA-(OSIS EvaluateEvaluateH Disease ativity5e6tent of synovitisDisease ativity5e6tent of synovitisH Strutural $ama"eStrutural $ama"eH )untional5.syhosoial status)untional5.syhosoial status

Initiate TreatmentInitiate TreatmentH Patient e$uationPatient e$uationH Physial an$ ou.ational thera.y* et7Physial an$ ou.ational thera.y* et7

H (SAIDs(SAIDsH Possi!le loal or oral steroi$s /Possi!le loal or oral steroi$s /

 ,4 m"7 Pre$nisone1,4 m"7 Pre$nisone1

Assess Disease AtivityAssess Disease Ativity

 AR B(D%.(!%# (! RA &R%A&M%!& AR B(D%.(!%# (! RA &R%A&M%!&

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AR B(D%.(!%# (! RA &R%A&M%!&AR B(D%.(!%# (! RA &R%A&M%!&

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 AR B(D%.(!%# (! RA &R%A&M%!& AR B(D%.(!%# (! RA &R%A&M%!&

Refratory Rheumatoi$ ArthritisRefratory Rheumatoi$ Arthritis

0onsult Rheumatolo"ist0onsult Rheumatolo"istH Most effetive (SAIDMost effetive (SAIDH Most effetive DMARDMost effetive DMARDH Possi!le loal or oral steroi$sPossi!le loal or oral steroi$sH Reha!ilitationReha!ilitation

$ersistent

 Active

Disease

Monitor Disease AtivityMonitor Disease Ativity

Perio$iallyPerio$ially

Mechanical oint #ymptoms

Remission or #atisfactory ontrol

Reactivation of Disease

Sur"ial InterventionSur"ial Intervention

Mechanical oint #ymptoms

Revise Treatment PlanRevise Treatment PlanH 0onsult Rheumatolo"ist0onsult Rheumatolo"istH 0han"e (SAIDs0han"e (SAIDsH 0han"e5a$$ DMARDs0han"e5a$$ DMARDsH +oal or oral steroi$s+oal or oral steroi$sH Reha!ilitationReha!ilitation

EU+AR D fi iti f I t i RAEU+AR D fi iti f I t i RA

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EU+AR Definition of Im.rovement in RAEU+AR Definition of Im.rovement in RA %B.AR response criteria are ased on DA#<9%B.AR response criteria are ased on DA#<9 DA# is divided into 3 categories:DA# is divided into 3 categories:

.ow disease activity *.ow disease activity *≤≤<;5,<;5,

Moderate disease activity *><;5 andModerate disease activity *><;5 and ≤≤3;I,3;I, 0igh disease activity *>3;I,0igh disease activity *>3;I,

(mprovement in the DA# is compared with a patient?s aseline DA#(mprovement in the DA# is compared with a patient?s aseline DA# ood response is defined as a >1;< improvement in the DA# compared withood response is defined as a >1;< improvement in the DA# compared with

aseline and a DA# attained during follow-up ofaseline and a DA# attained during follow-up of ≤≤<;5<;5

*van estel 1JJF,

*(mprovement in DA# from aseline,

≤<;5

><;5 and ≤3;I

>3;I

*DA# attained

during follow-up,

>1;<   ≤1;< and >6;F   ≤6;F

ood response

Moderate response

!o response

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Tabel ;" eberapa jenis anale#ik dan NSAI- %an umum diunakan

dalam #erapi pen%aki# reuma#ik 

(ama -enerik -olon"an Pre.arat

 

$arasetamol $anadol 766 mg

Mefenamic acid $onstant <768 766 mg

&ramadol !ovalges 76 mg

MetamiGole !ovalgin 766 mg

!eoralgin 766 mgMethampyron

Melo@icam

!imesulide

Melo@in tas I87 mg8 17 mg

!ico@ tas 166 mg

Morphin sulfate M#& continus 168178368F68166 mg

%todolac lonene 1668 366 mg+enufen yufe 366 mg

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(ama -enerik -olon"an Pre.arat

!a;Diclofenac

(ndomethasin

Diflunisal

&iaprofenic acid  (uprofen

/etoprofen

 !apro@en

$irprofen

arprofen

 eleco@i

 Acetic Acid

 Acetic Acid

aronic Acid

$ropionic Acid$ropionic Acid

$ropionic Acid

$ropionic Acid

$ropionic Acid

$ropionic Acid

 Koltaren tas <78768#RI7 mg

(ndocid caps <7 mg

Diflonid tas <768766 mg

#urgam tas <66 mgMotrin tas <668566 mg

$rofenid %768 %1668 <66 mg L supp

!a@en tas <768766 mg

Rengasil tas <66 mg

(madil tas 176 mg

 

o@ < inhiitor elere@ 1768 366 mg

$iro@icam&eno@icam

4@icam4@icam

+eldene caps 168<6 mg

&ilcotil tas <6 mg

O A O A

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• ekerja lamba# menunu kadar di darah $ukup

Khasia# baru mulai =/;< bulan

• Side e!!e$# dan #oksisi#as #ini

• -iharapkan dapa# menhen#ikan proresi!i#as7

menjadi remisi"

6 des#ruksi sendi pada masa dini *B (A erosi < #hn per#ama"

6 )asil penoba#an %an buruk munkin karena #erlamba#

memulai -2A(-

OAT/OAT (E2ITI1OAT/OAT (E2ITI1

-2A-(S-2A-(S

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• -ianosa pas#i : -2A(- seera diberi

• Tersanka (A, respons NSAI- minimal →  mulai -2A(-

•  Se#elah pakai =/9 bulan #ak memuaskan

 → Gan#i -2A(- lain

 → Kombinasi denan %an lain

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/lasifikasi oat-oat anti rematik *%dmon et al, :

1; #ymptom-modifying anti-rheumatic drugs *#MARDs,

  (ni akan memperaiki simptom dan ge'ala klinis

!#A(Ds

/ortikosteroid

4at-oat ker'a lamat : antimalaria8 #A#$8 garam emas8

D$8 oat sitotoksik

<; Disease controlling anti rheumatic therapy

4at ini meruah per'alanan penyakit RA8 dengan cara:

Memperaiki dan mempertahankan fungsi sehuungan

dengan erkurangnya peradangan sinovial

Mencegah dan mengurangi progresifitas kerusakan struktur

sendi

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DMARD yang laGim digunakan dalampengoatan AR

1; /lorokuin atau hidroksiklorokuinm1; /lorokuin atau hidroksiklorokuinm

<; #ulfasalaGine<; #ulfasalaGine

3; D-penisilamin3; D-penisilamin

5; aram emas5; aram emas

7; M&7; M&

F; #iklosporin -AF; #iklosporin -A

I; .eflunomideI; .eflunomide  ene therapyene therapy  "iological agent"iological agent

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0H+ORO8UI( PHOSPHAT : 94 # 44 M- 5 HARI

H;DRO<;0H+ORO8UI( : 944 # 244 M- 5 HARI

Tera.i AR se'ak tahun ,34#an

Di In$onesia .alin" !anyak

Men"an$un" 2#amino=uinoline7 >[email protected] ethyl* hi$roksiklorokuin ?@

hy$ro6yethyl