Immunoserological and histological differences between autoimmune hepatitis with acute presentation and chronic autoimmune hepatitis.

AimThe histological features of clinically chronic autoimmune hepatitis (AIH) have been well established, with interface hepatitis and plasma cell infiltration as hallmark lesions, however, the immunoserological and histological features of recent-onset and acute AIH remain undefined. The goal of this study was to define the immunoserological and histological differences between AIH with acute presentation and chronic AIH. MethodsThirty-two consecutive patients with well-characterized AIH who had undergone a liver biopsy were identified at our institution. These patients were divided into two groups. Sixteen patients whose liver dysfunction had persisted for at least 12months were defined as chronic AIH (C-AIH) patients, and 16 patients whose liver dysfunction had been within normal limits for >12months previously, and had only recently been found to have abnormal function for the first time, were defined as AIH with acute presentation (AIH-a) patients. Various biological and histological characteristics were compared between these two patient groups. ResultsNo significant differences were found between the groups for age, body mass index, serum levels of total bilirubin, transaminase, alkaline phosphatase, prothrombin activity, immunoglobulin, titers of antinuclear antibody, or diagnostic scores between the groups. Histologically, there was no significant difference in the degree of interface hepatitis, plasma cell infiltration, or centrilobular necrosis between AIH-a and C-AIH patients. However, histological active findings such as activity, lobular inflammation, rosette formation, spotty necrosis, seroid-laden macrophages, and single cell necrosis were significantly more frequent in AIH-a patients, whereas portal fibrosis was significantly more frequent in C-AIH patients. Only one case among the 16 AIH-a patients was confirmed as acute AIH, showing massive centrilobular necrosis with a mild degree of portal inflammation and interface hepatitis. All patients with AIH-a and C-AIH responded well to corticosteroid or ursodeoxycholic acid treatment. ConclusionsPatients with AIH-a could not be distinguished from C-AIH patients clinically or immunoserologically. Based on the histopathological findings of the liver, almost all cases of AIH-a might be exacerbations of non-symptomatic pre-existing C-AIH.