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 Table of Contents  
Year : 2021  |  Volume : 6  |  Issue : 1  |  Page : 56-58

Prolonged cholestatic jaundice as an atypical manifestation of acute hepatitis A virus (HAV) infection in children: Case reports

1 Department of Pediatric Gastroenterology and Nutrition, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh
2 Department of Pediatrics, Bangladesh Specialized Hospital, Dhaka, Bangladesh

Date of Submission11-Sep-2021
Date of Acceptance23-Sep-2021
Date of Web Publication29-Dec-2021

Correspondence Address:
Dr. Md Shafiul Alam
Department of Pediatric Gastroenterology and Nutrition, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pnjb.pnjb_9_21

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This article reports two cases of prolonged cholestatic type hepatitis A, a rare clinical manifestation of hepatitis A virus infection in children. Acute hepatitis A virus infection typically resolves spontaneously in 90% of the cases. In children, complete recovery usually occurs in most of the cases within two months. Occasionally, the cholestatic variety may persist for several months, characterized by intense pruritus and prolonged conjugated hyperbilirubinemia. The diagnosis is based on the presence of IgM anti-HAV, symptoms longer than 8 weeks, bilirubin concentration >10 g/dL in the absence of substantial hepatocellular and biliary damage. Use of only ursodeoxycholicacid (UDCA) rather than the combined use of UDCA and corticosteroid is sufficient.

Keywords: Children, cholestasis, hepatitis A

How to cite this article:
Alam MS, Benzamin M, Hasan S, Haq N, Mazumdar MW. Prolonged cholestatic jaundice as an atypical manifestation of acute hepatitis A virus (HAV) infection in children: Case reports. Paediatr Nephrol J Bangladesh 2021;6:56-8

How to cite this URL:
Alam MS, Benzamin M, Hasan S, Haq N, Mazumdar MW. Prolonged cholestatic jaundice as an atypical manifestation of acute hepatitis A virus (HAV) infection in children: Case reports. Paediatr Nephrol J Bangladesh [serial online] 2021 [cited 2023 Oct 4];6:56-8. Available from: http://www.pnjb-online.org/text.asp?2021/6/1/56/334122

  Introduction Top

Acute hepatitis A is an acute, usually self-limiting necroinflammatory disease of the liver caused by hepatitis A virus (HAV).[1] In developing countries, A virus infection is predominant in children in whom this disease is endemic.[1] Age is the major factor that influences the clinical course of the primary HAV infection; it is symptomatic in only 4–16% of children compared with 75–95% of adults.[2],[3] The diagnosis is based on the presence of immunoglobulin M (IgM) anti-HAV. Symptomatic patients have four main clinical presentations, i.e., classical, relapsing, cholestatic, and fulminant.[4] Acute viral hepatitis due to hepatitis A virus is usually a self-limiting illness in children with complete recovery within 2 months of onset of symptoms.[5] Cholestatic hepatitis A, a specific form, shows persistent jaundice, biochemical evidence of intrahepatic cholestasis, and absence of substantial hepatocellular disease.[6] Occasionally, the clinical syndrome of cholestasis, characterized by intense pruritus and prolonged conjugated hyperbilirubinemia, may persist for several months.[7] This variant is rare in children, and it is usually found in elderly patients, mainly in women.[8] The purpose of this case report is to make physicians aware about the cholestatic variety of acute hepatitis A infections in children, regarding its clinical presentation, management, and outcome.

  Case Report Top

In the Department of Paediatric Gastroenterology and Nutrition, BSMMU, we treated two patients who had cholestatic jaundice due to HAV infection recently. Case 1, a 16-year-old boy, presented with the history of jaundice for 2 months and itching for 7 days. Case 2, an 11-year-old boy, presented with jaundice for 1.5 months and intermittent fever for the same duration. Both of them have h/o prodorm such as low grade fever, anorexia, and nausea for 7–10 days followed by progressive deepening of jaundice; subsequently, the patient developed intense itching all over the body. There was no past history of jaundice, blood transfusion, surgery, deterioration of school performance, family H/o liver disease, or psychiatric illness, but having history of taking street food in both cases and other family members. There was no history of bleeding from any site or any feature of encephalopathy. On examination, both children were deeply icteric and there was no pallor. Scratch marks were present all over the body and stigmata of chronic liver disease were absent. Vital parameters and anthropometries were within normal limits. Liver was palpable 4 cm with a liver span of 13 cm in the first case and 5 cm with a liver span of 14 cm in the second case. Spleen was not palpable and ascites was absent in both cases. Examination of cardiovascular, respiratory, and neurological systems was unremarkable, respectively. Both the cases were diagnosed as acute viral hepatitis with cholestasis.

Laboratory findings of the patients are given below:

Both the cases were treated initially by ursodeoxycholic acid (UDCA) and subsequently fexofenadine was added for itching but there was no remarkable improvement of jaundice or itching, which was observed within the 1st week in the first case and within 10 days in the second case. They were also given lactulose for regular bowel habit. After the above-mentioned time, patients were started to improve clinically and were evident by the declining trends of laboratory parameters of serum bilirubin, serum ALT, and serum AST. After 1 month of treatment, patients were discharged with the advice for regular follow-up when serum bilirubin in the first case was 25 mg/dL and 18 mg/dL in the second case. Total serum bilirubin, AST, and ALT were found to be 1.3 mg/dL, 30 U/L, and 60 U/L, respectively, after 2.5 months in the first case and 1.1 mg/dL, 305 U/L, and 65 U/L after 2.5 months in the second case and finally they were declared cured.

  Discussion Top

Infection by HAV is mainly asymptomatic and it is usually a self-limiting disease in 90% of the cases. Symptomatic infection occurs in only 4–16% of children, and atypical manifestations including prolonged and relapsing course are well known.[9] Cholestatic hepatitis A viral infection occurs in 10% of the patients with symptomatic disease.[4],[6] Prolonged cholestasis for a period of up to 5–7 months has been reported.[9],[10] It is characterized by prolonged fever, pruritus, and jaundice for at least 8 weeks, bilirubin concentration increasing more than 10 mg/dL, absence of other hepatotrophic viral markers, no evidence of previous liver disease or previous exposure to hepatotoxic substances, and normal biliary tree in the abdominal ultrasound.[1],[7],[8] We found similar findings in our patients. The mechanism of intrahepatic cholestasis in acute viral hepatitis is not clear but a few suggest that cellular or humoral immune phenomena might be involved in the pathogenesis.[11] The other proposed mechanism of cholestasis is interruption incontinuity of bile flow secondary to periportal spotty necrosis.[12] Treatment of HAV infection is mainly supportive. A study suggested that severe cholestasis takes long duration to be improved by supportive care only.[13] Another study found following steroid administration early alleviation of symptoms and less duration of hospital stay in their studied children suffering from cholestatic Hep-A infection than the others who were treated without steroids. However, the overall time period for full recovery might have not been shortened.[14] Corticosteroids stimulate the alternate efflux pathway for bile salts, thereby alleviating cholestasis. Also by anti-inflammatory action, UDCA stimulates both normal and alternate efflux pathways and also stimulates glucocorticoid receptor. Corticosteroids have more side effects, so they are not frequently advised than the UDCA. Treatment with steroids is effective in reducing the atypical manifestations of acute HAV infection in the form of cryoglobulinemia-related symptoms.[15] In our cases, we gave only symptomatic treatment by UDCA, fexofenadine, and lactulose, and both the patients were cured within 2.5 months which was much less than the maximum time mentioned in the literature.[7] Therefore, the combined use of UDCA and corticosteroids is not needed for maximum response.[9],[10]

  Conclusion Top

Prolonged cholestatic jaundice is an atypical manifestation of acute HAV. It is common in adult patients mainly in women but can also occur in children. Persistent cholestasis generally resolves spontaneously, with clinical and biochemical recovery at 6 months.[16] This type of patients can be managed only by UDCA rather than using both corticosteroids and UDCA.


We thank Prof. ASM Bazlulkarim, Head of the Department of Paediatric Gastroenterology and Nutrition, BSMMU, Dhaka, Bangladesh, for permitting us to publish these case reports.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Sjamsu A, Retno H, Agung N, Boerhan H A cholestatic type of hepatitis A in a child. Paediatr Indones 2001;41:308-10.  Back to cited text no. 1
Jeong SH, Lee HS Hepatitis A: Clinical manifestations and management. Intervirology 2010;53:15-9.  Back to cited text no. 2
Tong MJ, el-Farra NS, Grew MI Clinical manifestations of hepatitis A: Recent experience in a community teaching hospital. J Infect Dis 1995;171(Suppl. 1):S15-8.  Back to cited text no. 3
Kemmer NM, Miskovsky EP Infection of the liver, hepatitis A. Infect Dis Clin North Am 2000;14:1-11.  Back to cited text no. 4
Rachima CM, Cohen E, Garty M Acute hepatitis A: Combination of the relapsing and the cholestatic forms, two rare variants. Am J Med Sci 2000;319:417-9.  Back to cited text no. 5
Lemon SM Type A viral hepatitis. In: Prieto J, Rodes J, Shafritz DA, editors. Hepatobiliary Diseases. Berlin: Springer Verlag; 1992. p. 495-510.  Back to cited text no. 6
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. 7
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. 8
Coppola N, Genovese D, Pisaturo M, Taffon S, Argentini C, Pasquale G, et al. Acute hepatitis with severe cholestasis and prolonged clinical course due to hepatitis A virus Ia and Ib coinfection. Clin Infect Dis 2007;44:e73-7.  Back to cited text no. 9
Ertekin V, Selimoğlu MA, Orbak Z An unusual combination of relapsing and cholestatic hepatitis A in childhood. Yonsei Med J 2003;44:939-42.  Back to cited text no. 10
Marbet UA, Shefer S, Leevy CM [Intrahepatic cholestasis: Modulation by immunological factors?]. Schweiz Med Wochenschr 1986;116:969-70.  Back to cited text no. 11
Sciot R, Van Damme B, Desmet VJ Cholestatic features in hepatitis A. J Hepatol 1986;3:172-81.  Back to cited text no. 12
Jung KM, Cho YK, Cho JW, Park SH, Kim IH, Choi CS, et al. Clinical features of cholestatic hepatitis with acute viral hepatitis A in Chunbuk province of Korea: Multicenter experience [Abstract]. Korean J Hepatol 2009;15:S175.  Back to cited text no. 13
Yoon EL, Yim HJ, Kim SY, Kim JH, Lee JH, 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. 14
Nassih H, Bourrahouat A, Sab IA Hepatitis A virus infection associated with cryoglobulinemic vasculitis. Indian Pediatr 2020;57: 71-2.  Back to cited text no. 15
Muñoz-Martínez SG, Díaz-Hernández HA, Suárez-Flores D, Sánchez-Ávila JF, Gamboa-Domínguez A, García-Juárez I, et al. Atypical manifestations of hepatitis A virus infection. Rev Gastroenterol Mex (Engl Ed) 2018;83:134-43.  Back to cited text no. 16


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