Progressive fibrosis during corticosteroid therapy of autoimmune hepatitis

• Published in: Hepatology (Baltimore, Md.) Vol. 39; no. 6; pp. 1631 - 1638
• Main Authors: Czaja, Albert J., Carpenter, Herschel A.
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01-06-2004; Wiley
• Subjects: Biological and medical sciences; Disease Progression; Female; Follow-Up Studies; Gastroenterology. Liver. Pancreas. Abdomen; Glucocorticoids - adverse effects; Hepatitis, Autoimmune - drug therapy; Humans; Liver Cirrhosis - chemically induced; Liver Cirrhosis - pathology; Liver. Biliary tract. Portal circulation. Exocrine pancreas; Male; Medical sciences; Middle Aged; Other diseases. Semiology; Prednisone - adverse effects; Retrospective Studies; Progressive; Immunopathology; Corticosteroid; Hepatitis; Therapy; Treatment; Fibrosis; Digestive diseases; Hepatic disease; Autoimmune disease
• ISSN: 0270-9139; 1527-3350
• DOI: 10.1002/hep.20235

Hepatic fibrosis and cirrhosis are possible consequences of corticosteroid‐treated autoimmune hepatitis. Our aims were to determine the frequency of progressive fibrosis and the factors associated with this progression. Two hundred seventy‐seven liver tissue specimens that had been obtained from 73 patients were interpreted in batch under code by a single pathologist. Fibrosis scores and histological activity indices were determined using the Ishak scoring system, and worsening fibrosis scores were correlated with clinical features, laboratory findings, and treatment responses. Fibrosis scores increased (2.3 ± 0.4 points to 4.2 ± 0.4 points; P < .0001) in 18 patients (25%) during 79 ± 13 months. Only five patients (7%) developed cirrhosis, and 55 patients (75%) had stable (16 patients) or decreased (39 patients) fibrosis scores. Human leukocyte antigen (HLA) DR3/DR4 occurred more frequently in patients with progressive fibrosis than others (23% vs. 2%; P = .03). Patients with progressive fibrosis had higher histological activity indices at last follow‐up than patients with stable or reduced fibrosis (3.2 ± 0.7 vs. 1.7 ± 0.2; P = .01), and these indices worsened more commonly during therapy (17% vs. 2%, P = .04). Relapse, treatment failure, and incomplete response did not affect progression of fibrosis. In conclusion, fibrosis progresses in only a minority of patients during corticosteroid therapy. Progression is associated with HLA DR3/DR4 and worsening histological activity. Exacerbations or persistence of disease activity does not increase disease progression after treatment has been instituted. (HEPATOLOGY 2004;39:1631–1638.)