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Fibrosing cholestatic hepatitis: a report of three cases
1Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Insights
Fibrosing cholestatic hepatitis is a severe viral hepatitis complication in immunosuppressed patients. This aggressive condition, often fatal, rapidly progresses to liver failure despite antiviral therapies.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Fibrosing cholestatic hepatitis (FCH) is a severe complication in immunosuppressed individuals, particularly those with viral hepatitis.
- Hepatitis B virus (HBV) infection is a common cause of liver disease, especially in transplant recipients and immunocompromised patients.
Observation:
- This report details three cases of FCH in patients with a history of liver or renal transplantation and chemotherapy.
- Clinical presentations varied, including fever, jaundice, and elevated liver enzymes, with histological findings of disarrayed lobules, hepatocyte ballooning, fibrosis, and cholestasis.
- Hepatocytes showed diffuse positivity for Hepatitis B surface antigen (HBsAg) and Hepatitis B core antigen (HBcAg).
Findings:
- All three patients experienced rapid disease progression.
- Despite antiviral treatment, patients succumbed to liver failure within 1 to 3 months post-biopsy.
Implications:
- FCH represents a critical, often fatal, outcome in immunosuppressed HBV patients.
- Early recognition and aggressive management strategies are crucial for improving outcomes in these high-risk patients.
- Further research into the pathogenesis and novel therapeutic targets for FCH is warranted.
Abstract:
Fibrosing cholestatic hepatitis is an aggressive and usually fatal form of viral hepatitis in immunosuppressed patients. We report three cases of fibrosing cholestatic hepatitis in various clinical situations. Case 1 was a 50-year-old man who underwent a liver transplant for hepatitis B virus (HBV)-associated liver cirrhosis. Two and a half years after the transplant, he complained of fever and jaundice, and liver enzymes were slightly elevated. Serum HBsAg was positive. Case 2 was a 30-year-old man in an immunosuppressed state after chemotherapy for acute lymphoblastic leukemia. He was a HBV carrier. Liver enzymes and total bilirubin were markedly elevated. Case 3 was a 50-year-old man who underwent renal transplantation as a known HBV carrier. One year after the transplant, jaundice developed abruptly, but liver enzymes were not significantly elevated. Microscopically lobules were markedly disarrayed, showing ballooning degeneration of hepatocytes, prominent pericellular fibrosis, and marked canalicular or intracytoplasmic cholestasis. Portal inflammation was mild, but interphase activity was definite and cholangiolar proliferation was prominent. Hepatocytes were diffusely positive for HBsAg and HBcAg in various patterns. Patients died of liver failure within 1 to 3 months after liver biopsy in spite of anti-viral treatment.