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Related Concept Videos

Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...
Viral Hepatitis I: Introduction01:28

Viral Hepatitis I: Introduction

Viral hepatitis is an inflammatory condition of the liver caused by infection with hepatotropic viruses, most commonly hepatitis A, B, C, D, and E. Despite variations in structure and transmission, all viruses mentioned infect hepatocytes and provoke immune responses that can hinder liver function. Additionally, some non-hepatotropic viruses can also lead to hepatic inflammation.Hepatitis A VirusHepatitis A virus (HAV) is transmitted through the fecal–oral route, typically by ingestion of food...
Cirrhosis I: Introduction01:23

Cirrhosis I: Introduction

Cirrhosis is a chronic, irreversible liver disease characterized by the widespread replacement of healthy liver tissue with fibrotic scar tissue and the formation of regenerative nodules.Etiology of cirrhosisCirrhosis results from sustained liver injury that triggers progressive fibrosis and structural remodeling. The underlying causes are diverse, encompassing common and less frequent clinical conditions. Regardless of the origin, all causes lead to chronic inflammation, hepatocyte loss, and...
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
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Chronic Pancreatitis I: Introduction01:25

Chronic Pancreatitis I: Introduction

Chronic pancreatitis is a long-standing, relapsing inflammation of the pancreas, characterized by irreversible damage to the gland. It results in progressive destruction of the pancreatic parenchyma, fibrosis, and eventual loss of both exocrine and endocrine function. The disease may evolve gradually after multiple episodes of acute pancreatitis or develop independently.EtiologyChronic pancreatitis can arise from a variety of causes:Alcohol use is the leading cause, accounting for 70–80% of...

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Published on: February 3, 2012

Late autoimmune hepatitis after hepatitis C therapy.

Cumali Efe1, Alexandra Heurgué-Berlot, Ersan Ozaslan

  • 1aDepartment of Gastroenterology, Hacettepe University bDepartment of Gastroenterology, Numune Research and Education Hospital, Ankara, Turkey cDepartment of Hepato-Gastroenterology, CHU Reims, Reims, France dDepartment of Gastroenterology and Hepatology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.

European Journal of Gastroenterology & Hepatology
|May 1, 2013
PubMed
Summary

Autoimmune hepatitis (AIH) can develop years after interferon (IFN) therapy for hepatitis C (HCV). This study identified cases of late-onset AIH, highlighting the need for long-term monitoring in patients treated with IFN.

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Area of Science:

  • Hepatology
  • Immunology
  • Viral Hepatitis Research

Background:

  • Interferon (IFN) therapy for hepatitis C (HCV) is known to sometimes trigger autoimmune hepatitis (AIH).
  • However, AIH developing long after IFN treatment cessation is infrequently reported.

Observation:

  • This retrospective study identified five patients who developed AIH between 1 and 10 years after completing HCV treatment.
  • The onset of AIH occurred despite varying responses to antiviral therapy.

Findings:

  • AIH can manifest significantly later than previously thought, even years after interferon discontinuation.
  • No specific risk factors for developing late-onset AIH were identified in this cohort.
  • While immunosuppressive therapy was effective in most cases, one patient experienced a fatal outcome.

Implications:

  • Clinicians should consider the possibility of late-onset AIH in patients with a history of interferon therapy for HCV.
  • Long-term surveillance may be warranted for patients treated with IFN, as AIH can emerge years after treatment completion.
  • Further research is needed to elucidate risk factors and optimal management strategies for late-onset AIH.