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Presence of antimitochondrial autoantibodies in patients with autoimmune hepatitis
Author(s) -
Nezu Saeko,
Tanaka Atsushi,
Yasui Hideaki,
Imamura Makiko,
Nakajima Hiroshi,
Ishida Hitoshi,
Takahashi ShinIchi
Publication year - 2006
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2006.04434.x
Subject(s) - medicine , autoantibody , autoimmune hepatitis , primary biliary cirrhosis , bile duct , gastroenterology , fibrosis , hepatitis , biliary tract , pathology , cirrhosis , immunology , antibody
Background and Aim: Antimitochondrial autoantibodies (AMA) are known to be a hallmark of primary biliary cirrhosis, and it has been suggested that AMA play a crucial role in generating biliary changes. Biliary tract lesions are not uncommon in patients with autoimmune hepatitis (AIH) and previous works have demonstrated that AMA are occasionally detectable in sera of patients with AIH. Therefore, the role of AMA as a cause of bile duct lesions in AIH livers should be addressed. The aim of the present study was to determine whether the presence of AMA is associated with clinical features, especially the occurrence of bile duct lesions, in patients with AIH. Methods: Forty‐one patients diagnosed as having AIH according to the revised scoring system of the International Autoimmune Hepatitis Group were enrolled in this study. Clinical data were retrospectively reviewed, and histological findings of the liver were investigated. AMA reactivity was determined by immunoblotting using beef heart mitochondria as antigens. Results: Although not found in any enrolled patient by conventional indirect immunofluorescence, AMA were detectable in 14 out of 41 patients (34%). Clinical parameters including biochemistry, autoantibody profile, and responses to treatment were similar irrespective of AMA status. Bile duct lesions were noted in 14/14 (100%) and 23/27 (85%) of AMA‐positive and ‐negative patients with AIH, respectively ( P = 0.134). There was no statistically significant difference in the grade of inflammation or stage of fibrosis between the two groups. Conclusion: Antimitochondrial autoantibodies were found to be present in sera of patients with AIH more frequently than expected, even at very low titer. However, clinical features and histological findings of AIH were not influenced by the AMA status.