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Silent Celiac Disease in Chronic Hepatitis C

Impact of Interferon Treatment on the Disease Onset and Clinical Outcome

Durante-Mangoni, Emanuele, MD*; Iardino, Patrizia, PhD; Resse, Marianna, MD; Cesaro, Giuseppe, MD*; Sica, Antonello, MD*; Farzati, Bartolomeo, MD; Ruggiero, Giuseppe, MD*; Adinolfi, Luigi E., MD*

Journal of Clinical Gastroenterology: November-December 2004 - Volume 38 - Issue 10 - p 901-905
Liver, Pancreas and Biliary Tract: Clinical Research
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Goals: To assess the impact of interferon treatment on celiac disease onset in hepatitis C patients and to clarify its clinical relevance and outcome.

Background: Hepatitis C is associated with autoimmunity, which can be exacerbated by interferon treatment. Cases of celiac disease activation during interferon treatment have been reported.

Study: Retrospective evaluation of 534 hepatitis C patients with or without symptoms compatible with celiac disease onset during interferon treatment and 225 controls. Anti-transglutaminase antibodies were assayed. HLA-DQA1 and -B1 loci were typed. Upper gastrointestinal endoscopy was applied to confirm the diagnosis in antibody-positive patients.

Results: Anti-transglutaminase antibodies were detected before treatment in 1.3% of hepatitis C patients and in 0.4% of controls (not significant). Eighty-six percent of patients with anti-transglutaminase antibodies showed activation of celiac disease while on interferon. Symptoms ranged from mild to severe, and interferon had to be discontinued in 2 of 7 (29%) patients. Symptoms disappeared in 6 of 7 patients after interferon withdrawal. Onset of symptoms compatible with celiac disease during interferon therapy was significantly associated with the presence of anti-transglutaminase antibodies (OR 53).

Conclusions: In hepatitis C patients, the activation of silent celiac disease during interferon treatment is almost universal and should be suspected, but it uncommonly requires interferon treatment discontinuation. Symptoms subside after interferon withdrawal.

From the Divisions of *Internal Medicine and Hepatology, †Laboratory Medicine, and ‡Immuno-Hematology, Second University of Naples Medical School, Napoli, Italy.

Received for publication February 17, 2004; accepted April 13, 2004.

Supported by research grants from MIUR and Regione Campania, Italy.

Reprints: Luigi E. Adinolfi, MD, Division of Internal Medicine and Hepatology, Second University of Naples, Ospedale Gesù e Maria, Via Cotugno 1, 80135 Napoli, Italy (e-mail: luigielio.adinolfi@unina2.it).

© 2004 Lippincott Williams & Wilkins, Inc.