Clinicopathological features of severe and fulminant forms of autoimmune hepatitis.
Summary of "Clinicopathological features of severe and fulminant forms of autoimmune hepatitis."
Diagnosis of the acute presentation of autoimmune hepatitis (AIH) is difficult because patients do not always show typical clinicopathological features of AIH. Although some of them progress to fulminant hepatitis, the survival rate of which is <20% without liver transplantation, their clinicopathological features have remained uncertain. We examined them for a better understanding and improvement of the prognosis of "life-threatening" severe and fulminant AIH.
Clinical, biochemical and pathological features of 28 patients with severe or fulminant AIH and treatment responses were examined retrospectively.
At the time of admission, mean immunoglobulin G was 2479 +/- 1170 mg/dl, with 7 (25%) patients showing normal levels. Anti-nuclear antibody was =1:40 in 8 (29%). Liver histology showed severe activity in 95% and acute hepatitis in 86% of the patients. Centrilobular necrosis including submassive and massive necrosis was characteristic. Of the 25 patients treated with corticosteroids, 17 responded and 8 did not. Responders to corticosteroids showed younger age and higher prothrombin time (PT) activity than non-responders at the time of corticosteroid administration. The improvement of PT activity during 2 weeks and 4 weeks and total bilirubin level during 4 weeks was statistically significant in responders, but not in non-responders.
We should diagnose and treat acute onset AIH patients before they develop into severe and fulminant disease. Performing liver biopsy at the early stage of acute onset AIH, evaluating the biopsy specimens precisely and initiating corticosteroid therapy may be essential for improving the prognosis without liver transplantation.
Department of Medicine and Clinical Oncology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
This article was published in the following journal.
Name: Journal of gastroenterology
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/20821236
- DOI: http://dx.doi.org/10.1007/s00535-010-0316-3
Medical and Biotech [MESH] Definitions
Liver Failure, Acute
A form of rapid-onset LIVER FAILURE, also known as fulminant hepatic failure, caused by severe liver injury or massive loss of HEPATOCYTES. It is characterized by sudden development of liver dysfunction and JAUNDICE. Acute liver failure may progress to exhibit cerebral dysfunction even HEPATIC COMA depending on the etiology that includes hepatic ISCHEMIA, drug toxicity, malignant infiltration, and viral hepatitis such as post-transfusion HEPATITIS B and HEPATITIS C.
Hepatitis, Viral, Human
INFLAMMATION of the LIVER in humans due to infection by VIRUSES. There are several significant types of human viral hepatitis with infection caused by enteric-transmission (HEPATITIS A; HEPATITIS E) or blood transfusion (HEPATITIS B; HEPATITIS C; and HEPATITIS D).
INFLAMMATION of the LIVER with ongoing hepatocellular injury for 6 months or more, characterized by NECROSIS of HEPATOCYTES and inflammatory cell (LEUKOCYTES) infiltration. Chronic hepatitis can be caused by viruses, medications, autoimmune diseases, and other unknown factors.
A family of hepatotropic DNA viruses which contains double-stranded DNA genomes and causes hepatitis in humans and animals. There are two genera: AVIHEPADNAVIRUS and ORTHOHEPADNAVIRUS. Hepadnaviruses include HEPATITIS B VIRUS, duck hepatitis B virus (HEPATITIS B VIRUS, DUCK), heron hepatitis B virus, ground squirrel hepatitis virus, and woodchuck hepatitis B virus (HEPATITIS B VIRUS, WOODCHUCK).
Hepatitis A Virus
A species in the genus HEPATOVIRUS containing one serotype and two strains: HUMAN HEPATITIS A VIRUS and Simian hepatitis A virus causing hepatitis in humans (HEPATITIS A) and primates, respectively.
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