Volume 32, Issue 4 e14028
SHORT COMMUNICATION

Clinico-Pathological Spectrum of Hepatitis A Virus-Induced Autoimmune-Like Hepatitis in Children

Samannay Das

Samannay Das

Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India

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Vikrant Sood

Corresponding Author

Vikrant Sood

Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India

Correspondence:

Vikrant Sood ([email protected])

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Archana Rastogi

Archana Rastogi

Department of Pathology, Institute of Liver and Biliary Sciences, New Delhi, India

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Neha Agarwal

Neha Agarwal

Department of Pathology, Institute of Liver and Biliary Sciences, New Delhi, India

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Sanjeevani Kaul

Sanjeevani Kaul

Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India

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Deepika Yadav

Deepika Yadav

Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India

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Bikrant Bihari Lal

Bikrant Bihari Lal

Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India

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Rajeev Khanna

Rajeev Khanna

Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India

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Seema Alam

Seema Alam

Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India

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First published: 01 November 2024

Funding: The authors received no specific funding for this work.

ABSTRACT

There is limited evidence that hepatitis A virus (HAV) infection can trigger hepatic autoimmunity, but this area remains largely unexplored. This study was thus planned with the aim to compare HAV-induced autoimmune-like hepatitis (HAV-ALH) with HAV-related liver dysfunction (HAV-acute viral hepatitis or HAV-AVH) and classical autoimmune hepatitis (AIH). This was a retrospective review of 46 patients with HAV infection who underwent liver biopsy (including 17 cases of HAV-ALH: diagnosis based on histopathology), and they were compared to 46 cases of age- and gender-matched classical AIH. Overall, HAV cohort (n = 46) had higher prevalence of pruritus, higher bilirubin levels, higher proportion of cholestasis, lower IgG levels, higher seronegativity and lack of disease recurrence, while the classical AIH group had higher proportion/severity of interface hepatitis, fibrosis, necrosis and pseudorosetting (p < 0.05). In comparison to the classical HAV-AVH group, HAV-ALH group had higher AST levels, higher presence of autoantibodies, and higher prevalence of severe zone 3 perivenulitis and marked pseudorosetting on histology (p < 0.05). Also, HAV-ALH group, in comparison to the AIH group, had more pruritus (OR 7.29, p < 0.004) and more seronegativity (41% vs. 13%, p < 0.031), while duration of illness (p < 0.003), IgG (p < 0.001) levels and liver stiffness measurement (p < 0.006) were significantly higher in AIH group (versus the HAV-ALH and HAV-AVH groups). Histologically, in comparison to AIH, HAV-ALH group had significantly less interface hepatitis (OR 0.03, p < 0.001) and fibrosis (OR 0.08, p < 0.001) and significantly more cholestasis (OR 4.5, p < 0.021). HAV infection can act as a potential trigger for immune-mediated hepatic damage, akin to drug-induced autoimmune-like hepatitis. Larger multicentric studies are needed to further explore this aspect.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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