Steroid therapy of chronic hepatitis: characteristics associated with response in anti-hepatitis C virus-positive and -negative patients.
OBJECTIVE
The goals of this study were to examine responses to corticosteroid-containing therapy in non-B chronic hepatitis patients with different anti-hepatitis C virus (HCV), autoantibody, and biochemical test results and to determine what factors correlate with response.


METHODS
Patients with a prior or current history of steroid therapy for putative autoimmune or chronic non-A, non-B hepatitis were assessed. Responses during the first 6 months of therapy were categorized as "complete" (normal aminotransferases for > or = 1 month), "partial" ( > 50% reduction), or "no response."


RESULTS
Sufficient data available to permit evaluation in 32 patients. Complete responses were noted in 17, partial responses in 12, and no response in three subjects. By multivariate analysis, only absence of anti-HCV and presence of cirrhosis were independent predictors of response. Nonresponders were found to have lower scores in a proposed autoimmune hepatitis scoring system, but scores of complete and partial responders were not significantly different. Despite a lower likelihood of a complete response, 80% (12/15) of patients with multiantigen positive anti-HCV tests had either partial or complete initial responses to corticosteroid-containing therapy, and, in nine patients, aminotransferases fell to < 2 times the upper limit of normal. All 15 anti-HCV-negative patients, but only three of 15 anti-HCV-positive patients, entered complete responses that were sustained (aminotransferases < twofold abnormal) on regimens containing < 20 mg/day or prednisolone or prednisone.


CONCLUSIONS
Although anti-HCV-positive patients frequently exhibit partial initial responses to immunosuppressive therapy, the absence of specific anti-HCV antibodies was better as a predictor of completeness of response than assessment of autoantibodies or degree of biochemical abnormalities.
Thiele
D L
DL
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, USA.
DuCharme
L
L
Cunningham
M R
MR
Mimms
L T
LT
Cuthbert
J A
JA
Lee
W M
WM
Combes
B
B
D000305:Adrenal Cortex Hormones / Q000008:administration & dosage / Q000627:therapeutic use*; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage; D001323:Autoantibodies / Q000032:analysis; D001327:Autoimmune Diseases / Q000175:diagnosis / Q000188:drug therapy* / Q000276:immunology; D001483:Base Sequence; D004796:Clinical Enzyme Tests; D017931:DNA Primers; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage; D016174:Hepacivirus / Q000235:genetics* / Q000276:immunology; D006505:Hepatitis / Q000175:diagnosis / Q000188:drug therapy* / Q000276:immunology; D006526:Hepatitis C / Q000175:diagnosis / Q000188:drug therapy*; D018937:Hepatitis C Antibodies / Q000032:analysis*; D006521:Hepatitis, Chronic / Q000175:diagnosis / Q000188:drug therapy*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D011239:Prednisolone / Q000008:administration & dosage; D011241:Prednisone / Q000008:administration & dosage; D012367:RNA, Viral / Q000032:analysis*; D019105:Random Amplified Polymorphic DNA Technique; D012189:Retrospective Studies; D013997:Time Factors
D000305:Adrenal Cortex Hormones; D000893:Anti-Inflammatory Agents; D001323:Autoantibodies; D017931:DNA Primers; D005938:Glucocorticoids; D018937:Hepatitis C Antibodies; D012367:RNA, Viral; D011239:Prednisolone; D011241:Prednisone