ABNORMAL LFT AND HEPATITIS UKM FAMILY MEDICINE TELECONFERENCE 21 JAN 2014 BY DR NURUL NADIA...
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ABNORMAL LFT AND HEPATITIS
UKM FAMILY MEDICINE TELECONFERENCE 21 JAN 2014
BY DR NURUL NADIASUPERVISOR: DR NADIAH, PHYSICIAN HOSPITAL
TUANKU JAAFAR SEREMBAN
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The aim of this teleconference is to enable the postgraduate trainees to elaborate on the clinical approach to a patient with abnormal liver function test and discuss on the latest development in management of Viral Hepatitis, particularly chronic Hepatitis B and C.
General objectives
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1. Know how to approach patients with abnormal liver function test
2. Be able to discuss the diagnostic tools/methods available for patients with abnormal liver function test (especially for viral hepatitis A, B and C and fatty liver)
3. Be able to identify the various viruses that could cause hepatitis and their peculiar course and prognosis of disease.
4. Be able to outline on the management of patients with fatty liver and hepatitis especially A,B and C.
Specific objectives
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Normal values
Liver function test (LFT)
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Formed from lysis of red cell Unconjugated bilirubin: bound to albumin,
water insoluble Conjugated bilirubin: water soluble, appears
in urine Parenchymal liver disease, biliary obstruction
LFT- bilirubin
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Causes of isolated hyperbilirubinemia
Unconjugated
Increased bilirubin production- Hemolysis- Ineffective erythropoiesis- Blood transfusion- Resorption of hematoma Decreased hepatic uptake- Gilbert’s syndrome- Drugs- rifanpicin Decreased conjugation- Criggler-Najlar syndrome- Physiological jaundice of newborn
Conjugated
Dubin-Johnson Syndrome Rotor’s syndrome
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Low level with progressive liver disease reflecting decrease synthesis
Level dependent on nutritional status, catabolism, hormonal factors, urinary/GI losses
Albumin concentration does correlate with prognosis in chronic liver disease
LFT- albumin
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LFT- aminotranferases
Aspartate transaminase (AST)
- Found in liver, cardiac muscle, kidneys, brain, pancreas, lungs, leucocytes, red cells
- Less sensitive/specific
Alanine transaminase (ALT)
- Highest concentration in liver
- More specific
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Common causes of raised transaminases
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Suggested algorithm for evaluating raised transaminases (ALT, alanine transaminase; HAV, hepatitis A virus; HCV, hepatitis C virus; PT, prothrombin time).
Limdi J K , and Hyde G M Postgrad Med J 2003;79:307-312
Copyright © The Fellowship of Postgraduate Medicine. All rights reserved.
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LFT- alkaline phosphatase
Mainly from liver and bone Also present in intestine, kidney, placenta,
leucocyte Elevation maybe physiological or
pathological GGT is a good discriminator to identify
source of ↑ALP, rise in liver but not bone disease
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Causes of ↑ALP
Physiological
Women in 3rd trimester Adolescent Benign, familial (d/t
↑intestinal ALP)
Pathological
Bile duct obstruction Primary biliary cirrhosis Primary sclerosis
cholangitis Drug induced cholestasis Adult bile ductopenia Metastatic liver disease Bone disease
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Suggested algorithm for evaluating a raised ALP (ALP, alkaline phosphatase; ERCP, endoscopic retrograde cholangiopancreatography; GGT, gammaglutamyl transferase; PT,
prothrombin time; MRCP, magnetic resonance cholangiopancreatography).
Limdi J K , and Hyde G M Postgrad Med J 2003;79:307-312
Copyright © The Fellowship of Postgraduate Medicine. All rights reserved.
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LFT- gammaglutamyl transferase
Found in hepatocytes and biliary epithelial cells
Sensitive test of hepatobiliary disease Usefulness is limited by lack of specificity Isolated ↑ GGT need to be followed up at
few months interval If still persistent with abnormal AST/ALT
further USS abd/ CT ± liver biopsy may be considered
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Causes of raised GGT
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LFT- PT / INR
Prothrombin Time
Measures rate of conversion of prothrombin to thrombin
Prolonged in vit K deficiency, warfarin therapy, liver disease, consumptive coagulapathy
Administration of vit K will reduce prolonged PT due to fat malabsorption but not due to intrinsic liver disease
International Normalised Ratio
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Recent travel Transfusion Drugs history including herbal Tattoos Unprotected sex Alcohol Occupation Medical hx: DM, obesity, dyslipidemia FHx
History
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Stigmata of chronic liver disease: icteric skin/ mucuos membrane, palmar erythema, bruising, spider naevi, gynecomastia
Hepatomegaly Splenomegaly Ascites Obesity Any clues to the underlying cause e.g.
lymphadenopathy Features suggestive of hepatic encephalopathy
Examination
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1. Unexplained liver abnormalities >1.5 time normal on 2 occasions, minimum of 6months apart
2. Unexplained liver disease with evidence of hepatic dysfunction
3. Known liver disease where treatment beyond withdrawal of the implicating agent is required
Abnormal LFT- when to refer
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1. Viral hepatitis screening2. Antinuclear antibody3. Ceruloplasmin in <40y4. Iron studies5. Ultrasound of the liver especially suspected
fatty liver
Tests to do before referal
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Acute liver infection caused by a hepatovirus of the Picornavirus family hepatitis A virus
2nd most common vaccine preventable infection Most common form of viral hepatitis Associated with poor hygiene and overcrowding HAV is shed in stool of infected persons, can survive
for weeks, can persist on hands for several hours and longer in food kept in room temperature, resistant to heat/freezing
Transmission is via fecal/oral route, and can occur through direct person-person contact, occasional transmission through sexual contact and blood transfusion
Hepatitis A
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Incubation period: 15-50 days Childhood infection is usually asymptomatic
but in adult 75% develop icteric disease 4-10days of prodromal symptoms: fever,
malaise, nausea, vomiting, weakness, anorexia
Acute infection manifest as dark urine, followed by jaundice and pale stool 1-2 days later with gradual resolution of other symptoms
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Malaise and anorexia may persist, hepatic discomfort and pruritus
LFT usually normalise within a month Complications are unusual but rarely include
fulminant hepatitis Chronic infection doesn’t occur but 10%
have prolonged or relapsing symptoms over6-9 months
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Detection of anti HAV IgM in acute phase May from 3-6months after acute illness Anti HAV IgG indicates past infection or
immunisation and likely to persist for life
Hepatitis A - diagnosis
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No specific Rx Supportive measures Usually with complete recovery
Hepatitis A - treatment
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Vaccine is recommended especially for travelers in endemic area
Education on hygiene and food and water precaution
Hepatitis A - prevention
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Globally estimated 350mil persons chronically infected by hepatitis B virus
Prevalence decrease with vaccination HBV is transmitted in blood and secretions
infectious outside the body >7days Commonly acquired from infected mother
(vertical transmission) or from family members (horizontal transmission)
Hepatitis B
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Double stranded DNA hepadnavirus HBV genome produces nucleocapsid
contains hepatitis B core antigen (HBcAg) Has outer envelope called hepatitis B surface
antigen (HBsAg) *for screening A segment of HBcAg results in production of
hepatitis B e antigen (HBeAg) associated with viral replication and high infectivity
HBV
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Hepatitis B- diagnosis
Evaluation of patient’s blood
1. HBcAg2. HBsAg3. HBeAg4. HBV DNA5. General liver
investigations
Liver biopsy- measure inflammation (current activity) and fibrosis (more chronic scarring)
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Acute infection may cause nonspecific symptoms: fatigue, poor appetite, nausea, vomiting, abdominal pain, low grade fever, jaundice, dark urine
Physical exam: hepatomegaly, splenomegaly, liver tenderness
Typically last 2-4 months Infants, child <5y, immunosuppressed adults usually
asymptomatic In adult with healthy immune system, 95% of acute
infection is self-limited and developed immunity <5% progress to chronic infection
Acute hepatitis B
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Chronic necroinflammatory disease persists longer than 6 months
Can be divided into HBeAg positive or negative
Risk inversely related to age Occult HBV infection maybe reactivated by
chemotherapy or immunosupressant Coinfection with HIV and HCV
Chronic hepatitis B
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Inactive HBsAg carrier state= persistent HBV infection of the liver without significant ongoing necroinflammatory disease
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Treatment
To reduce inflammation of the liver Prevent liver failure and cirrhosis Reduce risk of hepatocellular carcinoma by
suppressing HBV replication Treatment is based on phase of infection Finite course of interferon therapy or long
term viral suppression with neucloside/nucleotide analogue
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Hepatitis C
Leading cause for chronic liver disease Principal cause of death from liver disease
and leading indication for liver transplant in the US
Caused by hepatitis C virus single-stranded RNA virus
Transmitted through percutaneous exposure of infected blood
No vaccine
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Most patients are asymptomatic Nonspecific symptoms: fatigue, nausea,
anorexia, myalgia, arthralgia, weakness, weight loss
Chronic infection leads to cirrhosis, increased risk of complication of liver disease: portal hypertension, ascites, hemorrhage, hepatocellular carcinoma
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Factors associated with disease progression to cirrhosis
1. Male2. Age >403. HIV or HBV coinfection4. Immunosupression5. Alcohol intake6. Hepatotoxic drugs
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Natural history of hepatitis C virus infection.
Lo Re V , and Kostman J R Postgrad Med J 2005;81:376-382
Copyright © The Fellowship of Postgraduate Medicine. All rights reserved.
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HCV antibody enzyme immunoassay Recombinant immunoblot assay
(confirmatory test) Quantitative HCV RNA PCR Liver biopsy
Diagnosis
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Treatment
To slow or stop progression of fibrosis prevent complications and death recommended treatment: combination of
pegylated interferon alfa and ribavirin Sustained virologic response used to
evaluate effectiveness of therapy
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Non alcoholic fatty liver disease (NAFLD)
Definition1. evidence of hepatic steatosis by imaging or
histology2. No causes for secondary hepatic fat
accumulation3. Lack of alcohol consumption- <21 drinks per week in men- <14 in women
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NAFLD
Histologically can be divided into 1. Nonalcoholic fatty liver (NAFL) = presence
of hepatic steatosis with no evidence of hepatocellular injury
2. Nonalcoholic steatohepatitis (NASH)= presence of hepatic steatosis and inflammation with hepatocyte injury with/without fibrosis
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Treating liver disease and associated co-morbidities mainly for NASH
To reduce aminotranferases and improve hepatic steatosis
Lifestyle modification 1. Diet - hypocaloric2. Exercise 3. Weight loss
NAFLD - Management
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Metformin Thiazolidinediones Vitamin E- Decrease in aminotransferases- Improve in steatosis, inflammation,
ballooning and resolution of steatohepatitis- No effect on hepatic fibrosis
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Ursodeoxycholic acid (UCDA), omega-3 fatty acids
Bariartric surgery Statins are safe in patients with liver disease
to treat dyslipidemia Reduce alcohol consumption
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Treatment algorithm for NAFLD.
Adams L A , and Angulo P Postgrad Med J 2006;82:315-322
Copyright © The Fellowship of Postgraduate Medicine. All rights reserved.
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A 45 year-old lady comes for follow up for her Diabetes, Dyslipidaemia and Hypertension. She is asymptomatic. She is on Diamicron 80mg bd , Enalapril 10mg bd and Lovastatin 20mg ON, which she was on since 1 year ago. Her latest blood result shows HbA1c is 7%, FSL: TG is 2.1mmol/l , HDL is 1.0 mmol/l, LDL 4.1 mmol/l. Her liver function test shows ALT 66 iU/L (previously was 74). Other parameters in the liver function test are normal. How would you manage her?
Case scenario 1
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A 30 year old man presents to the casualty with nausea, vomiting and general malaise for the past 4 days. Clinically he is jaundice with tender right upper quadrant. Proceed with your management.
Case scenario 2
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Thank you!