Prognosis of acute severe autoimmune hepatitis (AS-AIH): The role of corticosteroids in modifying outcome
Andrew D. YeomanRachel WestbrookYoh ZenWilliam BernalThawab Al–ChalabiJulia WendonJohn G. O’GradyMichael A. Heneghan
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Autoimmune Hepatitis
Acute hepatitis
Autoimmune Hepatitis
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Autoimmune Hepatitis
Liver disease
Hepatitis B
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We investigated clinical characteristics and incidence of patients with acute non-A-G hepatitis, who were all registered in 17 Japanese National Hospitals. Seven hundreds thirty-one (24.0%) of 3052 patients with sporadic acute hepatitis and 73 (21.2%) of 344 patients with posttransfusion acute hepatitis were diagnosed as acute non-ABC hepatitis. Patients with acute non-ABC hepatitis were older (Mean +/- SD, 44 +/- 15 years) and male/female ratio was 0.70. Although mean levels of liver function abnormality was generally mild, 4(1.8%) of 250 patients with acute non-ABC hepatitis were died of fulminant hepatitis.
Acute hepatitis
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Fulminant
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Acute hepatitis
Toxic hepatitis
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This study describes a murine model of autoimmune hepatitis: experimental autoimmune hepatitis. Experimental autoimmune hepatitis could be induced most effectively in male C57BL/6 mice by intraperitoneal immunization with the 100,000 g superantant of syngeneic liver homogenate (S–100) in complete Freund's adjuvant. BALB/C and C3H mice were less susceptible than C57BL/6 mice. Experimental autoimmune hepatitis could not be induced in Lewis rats. Intraperitoneal immunization was more effective than intramuscular or subcutaneous injections, and the amount of protein administered above a threshold was of little influence. A single intraperitoneal injection of S–100 in complete Freund's adjuvant resulted in hepatitis of at least 6 mo duration. Histological changes were most marked 4 wk after disease induction. The histological findings were characterized mainly by perivascular inflammatory infiltrates and hepatocyte necroses. The histological changes were accompanied by biochemical evidence of liver cell death. Passive transfer of experimental autoimmune hepatitis with concanavalin. A-activated splenocytes was possible. Specific T–cell reactivity against fractions of S–100 could be demonstrated in vitro. Thus experimental autoimmune hepatitis is a murine model of autoimmune hepatitis probably mediated by autoreactive T cells. It will allow studies of the pathogenesis of autoimmune hepatitis. (HEPATOLOGY 1990; 11: 24-30.)
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Autoimmune hepatitis is an unresolving, hepatocellular inflammation of unknown cause that is characterized by the presence of periportal hepatitis on histologic examination, tissue autoantibodies in serum, and hypergammaglobulinemia. By international consensus, the designation autoimmune hepatitis has replaced alternative terms for the condition. Three types of autoimmune hepatitis have been proposed based on immunoserologic findings. Type 1 autoimmune hepatitis is characterized by the presence of antinuclear antibodies (ANA) or smooth muscle antibodies (SMA) (or both) in serum. Seventy percent of patients with type 1 of autoimmune hepatitis are women. This type is the most common form and accounts for at least 80% of cases. Type 2 is characterized by the presence of antibodies to liver-kidney microsome type 1 (anti-LKM1) in serum. Patients with this type of autoimmune hepatitis are predominantly children. Type 3 autoimmune hepatitis is characterized by the presence of antibodies to soluble liver antigen (anti-SLA) in serum. There are no individual features that are pathognomonic of autoimmune hepatitis, and its diagnosis requires the confident exclusion of other conditions. The large majority of patients show satisfactory response to corticosteroid (usually prednisone or prednisolone) therapy. For the past 30 years it has been customary to add azathioprine as a "steroid sparing" agent to allow lower doses of steroids to be used and remission, once achieved, can be sustained in many patients with azathioprine alone after steroid withdrawal. Patients with autoimmune hepatitis who have decompensated during or after corticosteroid therapy are candidates for liver transplantation.
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Autoimmune hepatitis type 1 in a 8-year old girl is described. The diagnosis was established using International Autoimmune hepatitis group scoring system. In addition to characteristic histologic features of autoimmune hepatitis (periportal hepatitis, piecemeal necrosis and rozettes) prominent centrilobular necrosis was discovered. As an isolate finding in autoimmune hepatitis, this type was described only in five cases. In our unique case centrilobular necrosis is a very important parallel finding previously not detected in autoimmune hepatitis. Some experimental studies suggest that cytokines present in inflammatory cell infiltrate in the liver play a pathologic role in autoimmune liver cell damage.
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The case of a young man with hepatitis A and a chronic course is presented. The patient recived a short course of steroid therapy for recurrence of symptoms following acute hepatitis A. Thereafter liver enzymes have remained marginally elevated for 4 years and annual liver biopsies have shown evidence of chronicity. HAV IgM Ab persisted for 1034 days with subsequent development of HAV IgG Ab. The possiblity of other viruses in the aetiology and the role of steroids in the development of chronicity are discussed.
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We describe the clinical and liver biopsy morphologic features for 4 patients with minocyclineinduced autoimmune hepatitis (group 1). We compared the serum laboratory values and liver biopsy findings from group 1 with those from 10 patients with sporadic autoimmune hepatitis (group 2). All patients in group 1 had positive serum antinuclear antibody titers, but none had positive serum anti–smooth muscle antibody titers. The morphologic findings of group 1 biopsies were those of autoimmune hepatitis in all 4 patients. In addition, 1 of these biopsy specimens also had scattered single eosinophils, unlike autoimmune hepatitis. The mean histologic activity index scores for patients in groups 1 and 2, respectively, were 6.7 and 5.4. No patients in group 1 had marked bridging fibrosis or cirrhosis, compared with 4 of 10 patients in group 2. Minocycline-induced autoimmune hepatitis is usually identical to sporadic autoimmune hepatitis. The absence of eosinophils does not exclude the possibility of a minocycline cause. In the absence of clinical or morphologic differences, a recent ingestion of minocycline should be excluded before the diagnosis of sporadic autoimmune hepatitis is established. Whether the drug is unmasking latent autoimmune hepatitis is unclear.
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Twenty seven children with relapsing hepatitis have been reviewed. The characteristic clinical course and the excellent prognosis of this form of hepatitis is emphasised. After an apparently ordinary initial episode of hepatitis followed by recovery, a relapse occurs within 1--3 months that is usually more severe clinically and biochemically. The histological appearances are similar to those of acute hepatitis. A delayed but spontaneous recovery occurs. No satisfactory explanation has been proposed for this condition.
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