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Indian Pediatr 2011;48: 485-486 |
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Prolonged Cholestasis due to Hepatitis A Virus
Infection |
Pawan Kumar and Vidyut Bhatia
From the Department of Pediatrics, All India Institute of
Medical Sciences, New Delhi 110 029, India.
Correspondence to: Dr Vidyut Bhatia, Senior Research
Associate, Department of Pediatrics,
AIIMS, New Delhi 110 029, India.
Email: [email protected]
Received: January 25, 2010;
Initial review: February 26, 2010;
Accepted: March 29, 2010.
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We present a 12-year old boy with jaundice for 2 weeks. The child was
deeply icteric and had hepatomegaly. IgM antibodies for hepatitis A
virus were positive. However this child had prolonged cholestasis and
cholestyramine was started. The child responded only after prednisolone
was started.
Key words: Hepatitis A, Clinical features, Cholestasis.
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A cute viral hepatitis due to
Hepatitis A virus is usually a self limiting illness in children
with complete recovery within two months of onset of symptoms [1].
Occasionally, the clinical syndrome of cholestasis, characterized by
intense pruritus and prolonged conjugated hyperbilirubinemia, may
persist for several months [2].
Case Report
A 12-year old male child was admitted with
complaints of jaundice for 6 weeks and itching for 2 weeks. The
onset of jaundice was preceded by low grade fever and nausea for 4-5
days. There was no history of bleeding from any site or any symptoms
of encephalopathy. There was no past history of jaundice. On
examination, the child was deeply icteric. Scratch marks were
present all over the body and there was no pallor. His weight was 39
kg and height was 142 cm. The vital parameters were stable, and
examination of cardiovascular, respiratory and neurological systems
was unremarkable. Liver was palpable 5 cms below costal margin with
a span of 13.5 cms.
Spleen was not palpable and there was no free
fluid. A diagnosis of acute viral hepatitis with cholestasis was
made. Hematological workup including prothrombin time were normal.
Liver biochemistry revealed AST 56 U/L, ALT 36 U/L, alkaline
phosphatase 468 U/L, total serum bilirubin 33.5 mg% with conjugated
fraction of 23.9 mg%. Total serum proteins were 7.1 g/dL; serum
albumin was 3.6 g/dL. IgM antibodies for Hepatitis A virus were
positive. HbsAg, Anti HCV and anti HEV IgM were negative. Child was
started on ursodeoxycholic acid (UDCA) but there was no improvement
in jaundice or itching. After 10 days, serum bilirubin had further
increased to 42.3 mg% (conjugated fraction, 32.1 mg%). Oral
cholestyramine was added. Ultrasound abdomen ruled out any
extrahepatic obstruction. His G6PD levels, osmotic fragility, and
coomb’s tests were (direct and indirect) negative. Liver histology
showed significant intracanalicular cholestasis, maintained lobular
architecture, mild portal triaditis and focal spotty necrosis. Over
the next six days, his total bilirubin further rose to 45.6 mg%
(conjugated, 34.6 mg%), and AST and ALT were 39 and 26 U/L,
respectively.
The child was started on 60 mg of daily oral
prednisolone. After 3 days of starting steroids, he showed
improvement in symptoms. The total bilirubin declined to 22.3 mg% in
14 days. After 2 weeks of daily prednisolone, the dose of oral
steroids was reduced to 30 mg and then tapered off over next 4
weeks. After 4 weeks of prednisolone therapy, total serum bilirubin
had declined to 2.6 mg%, and at the end of therapy, child was
asymptomatic with serum total bilirubin of 0.8 mg%.
Discussion
Though Hepatitis A is usually a self limiting
disease, atypical manifestations including prolonged and relapsing
course are well known [3,4]. Prolonged cholestasis for a period of
upto five to seven months after infection with Hepatitis A has been
reported [4,5]. Response to oral or parenteral steroids in such
cases has also been documented earlier [1,6].
The mechanism of intrahepatic cholestasis in
acute viral hepatitis is not clear. Recent in vitro and
animal studies on lymphocyte cultures of patients with alcoholic
hepatitis and acute viral hepatitis suggest that cellular or humoral
immune phenomena might be involved in the pathogenesis [7]. The
other proposed mechanism is from interruption in continuity of bile
flow secondary to periportal spotty necrosis [8]. The lympholytic
action of cortico-steroids may be the reason for their efficacy in
cholestasis due to Hepatitis A infection.
To conclude, corticosteroids should be considered
for the management of patients with prolonged cholestasis secondary
to hepatitis A.
Contributors: PK and VB were involved in
diagnosis and case management; PK: reviewed the literature and
prepared the initial draft; PK and VB: prepared the final version of
the paper.
Funding: None.
Competing interests: None stated.
References
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Ann Intern Med. 1984;101:635-7.
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2005. p. 109-25.
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