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LETTER TO EDITOR  
Year : 2012  |  Volume : 4  |  Issue : 3  |  Page : 185-186
Prolonged cholestasis following hepatitis a virus infection: Revisiting the role of steroids


Department of Pediatrics, TN Medical College and BYL Nair Hospital, Mumbai Central, Mumbai, Maharashtra, India

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Date of Web Publication4-Sep-2012
 

How to cite this article:
Saboo AR, Vijaykumar R, Save SU, Bavdekar SB. Prolonged cholestasis following hepatitis a virus infection: Revisiting the role of steroids. J Global Infect Dis 2012;4:185-6

How to cite this URL:
Saboo AR, Vijaykumar R, Save SU, Bavdekar SB. Prolonged cholestasis following hepatitis a virus infection: Revisiting the role of steroids. J Global Infect Dis [serial online] 2012 [cited 2018 Sep 20];4:185-6. Available from: http://www.jgid.org/text.asp?2012/4/3/185/100588


Sir,

A 12-year-old boy presented with complaints of progressively increasing cholestatic jaundice and intense pruritis that disturbed sleep for 6 weeks preceded by fever for 5 days. The patient was diagnosed to have hepatitis A virus (HAV) infection on the basis of raised liver enzymes and positive HAV immunoglobulin M test [Table 1] and was treated with ursodeoxycholic acid (UDCA, 30 mg/kg/day) without any success. There was no history of drug ingestion, blood transfusions, or similar episodes. He had a soft and tender liver, palpable 2cm below the right costal margin (liver span: 7cm). At presentation, the serum bilirubin level had skyrocketed to 29.9 mg/dl while serum aspartate transaminase and alanine transaminase levels had moderated [Table 1]. He had no biochemical evidence of hepatic biosynthetic defect with normal serum albumin levels, prothrombin time, and blood ammonia levels.
Table 1: Results of serial biochemical tests

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Ultrasonography showed hypoechoic liver and normal intra- and extrahepatic bile ducts. For cholestasis, in addition to UDCA, he was treated with cholestyramine (4 g BD) and rifampicin (10 mg/kg/day OD) for 12 days, which failed to elicit a clinical response. Investigations were done to detect other causes of prolonged hepatic manifestations: tests for detection of antibodies against HBV, HCV, and nuclear, smooth muscle, mitochondrial, and liver-kidney antigens were negative. The serum ceruloplasmin was 0.4 OD (normal: 0.2-0.5 OD). Oral prednisolone was then started with 40 mg/day on 55 th day of illness for recalcitrant pruritis in the absence of any other chronic cholestatic liver disease. Within a week, there was a dramatic reduction in pruritus, jaundice started regressing, and hepatic tenderness subsided with the biochemical resolution of cholestasis [Figure 1] and [Table 1]. The prednisolone dose was tapered to 30 mg/day after 6 weeks when the serum bilirubin levels halved, after which the dose was tapered by 10 mg every 2 weeks and steroids were withdrawn after 110 days. At follow-up, 4 months after the steroid therapy, the patient continues to be asymptomatic and has not shown any biochemical or clinical evidence of relapse.
Figure 1: Serial biochemistry of patient. T bili: total bilirubin, D bili: direct bilirubin, AST: aspartate transaminase, ALT: alanine transaminase, Alk Phos: alkaline phosphatase

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The presence of intense pruritus, elevated serum bilirubin for over 12 weeks of illness despite normalization of hepatic transaminases clinched the diagnosis of prolonged cholestatic jaundice (PCJ) following HAV infection in this child. This phenomenon is exceedingly rare in children. [1],[2] It is defined as a peak serum bilirubin of more than 10 mg/dl (with direct bilirubin higher than 50% of the total bilirubin), [2] and hyperbilirubinemia or jaundice lasting for more than 12 weeks in the absence of hemolysis and renal failure with the alanine transaminase level below 500 U/l. [3],[4],[5] Till date, in children, only two reports of successful treatment of HAV-associated PCJ with corticosteroids are available in English literature. This communication intends to provide a more detailed description of therapy and response that was lacking in earlier reports. [6],[7],[8] Corticosteroids alleviate cholestasis by stimulating the alternate efflux pathway for bile salts and by anti-inflammatory action, while UDCA stimulates both normal and alternate efflux pathway and even stimulates glucocorticoid receptor, underscoring the need for their combined use for maximum response. [9],[10]

It is hoped that this case would remind pediatricians that, though rare, PCJ can occur in children with HAV infection and hence extensive investigational workup, especially liver biopsy, may not be warranted. And if the child continues to have disabling symptoms even after an adequate trial of choleretic agents, oral prednisolone therapy can be tried under close supervision. This communication, being a report of a single case (without control), cannot be considered as the ultimate proof of effectiveness of corticosteroids. It is hoped that this report will spur clinicians to publish their experiences and also use various study designs to prove the efficacy of combination therapy (UDCA and corticosteroids).


   Acknowledgment Top


We thank Dr. Ravi Rananavare, Dean, TN Medical College and BYL Nair Hospital, for permitting us to publish this case report.

 
   References Top

1.Yoon EL, Yim HJ, Kim SY, Kim JH, Lee J-H, Lee YS, et al. Clinical courses after administration of oral corticosteroids in patients with severely cholestatic acute hepatitis A; three cases. Korean J Hepatol 2010;16:329-33.  Back to cited text no. 1
    
2.Molina MA, Martínez-Huguet F, Asensi Monzó M, Brines Solanes J, Codoñer Franch P. Cholestatic-type hepatitis in childhood. An Esp Pediatr 1998;49:253-6.  Back to cited text no. 2
    
3.Schiff ER. Atypical clinical manifestations of hepatitis A. Vaccine 1992;10(Suppl 1):S18-20.  Back to cited text no. 3
[PUBMED]    
4.Khalid Sakib CJ. Cholestatic variants of viral disease and alcohol. In: Lindor KD, Talwalkar JA, editors. Cholestatic Liver Disease. First ed. New Jersey: Humana Pr Inc; 2008. p. 120-6.  Back to cited text no. 4
    
5.Lee D. Other Viral Infections. In: Kleinman R, Goulet OJ, Mieli-Vergani G, Sanderson I, Sherman P, Shneider B., editors. Walker's Pediatric Gastrointestinal Disease. 5 th ed. Hamilton, Ontario: BC Decker Inc; 2008. p. 859-60.  Back to cited text no. 5
    
6.Arief S, Hernik R, Nugrohowidhi A, Hidayat B. A cholestatic type of hepatitis A in a child. Paediatr Indones 2001;41:308-10.  Back to cited text no. 6
    
7.Bhatia V, Kumar P. Prolonged Cholestasis due to Hepatitis A Virus Infection. Indian Pediatr 2011;48:485-6.  Back to cited text no. 7
    
8.Gordon SC, Reddy KR, Schiff L, Schiff ER. Prolonged Intrahepatic Cholestasis Secondary to Acute Hepatitis A. Ann Intern Med 1984;101:635-7.  Back to cited text no. 8
[PUBMED]    
9.Trauner M, Wagner M, Fickert P, Zollner G. Molecular regulation of hepatobiliary transport systems: Clinical implications for understanding and treating cholestasis. J Clin Gastroenterol 2005;39 (4 Suppl 2):S111-24.  Back to cited text no. 9
    
10.Boyer JL. Nuclear receptor ligands: Rational and effective therapy for chronic cholestatic liver disease? Gastroenterology 2005;129:735-40.  Back to cited text no. 10
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Correspondence Address:
Sandeep B Bavdekar
Department of Pediatrics, TN Medical College and BYL Nair Hospital, Mumbai Central, Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-777X.100588

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2008 Journal of Global Infectious Diseases | Published by Wolters Kluwer - Medknow
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