Silent celiac disease in chronic hepatitis C: impact of interferon treatment on the disease onset and clinical outcome.
OBJECTIVE
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.


METHODS
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.
Durante-Mangoni
Emanuele
E
Divisions of Internal Medicine and Hepatology, Second University of Naples Medical School, Napoli, Italy.
Iardino
Patrizia
P
Resse
Marianna
M
Cesaro
Giuseppe
G
Sica
Antonello
A
Farzati
Bartolomeo
B
Ruggiero
Giuseppe
G
Adinolfi
Luigi E
LE
D000328:Adult; D017668:Age of Onset; D000368:Aged; D000998:Antiviral Agents / Q000009:adverse effects*; D001323:Autoantibodies / Q000032:analysis; D002446:Celiac Disease / Q000139:chemically induced* / Q000235:genetics / Q000276:immunology; D005260:Female; D005838:Genotype; D019698:Hepatitis C, Chronic / Q000188:drug therapy*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000009:adverse effects*; D008297:Male; D008875:Middle Aged; D011994:Recombinant Proteins; D012189:Retrospective Studies; D011503:Transglutaminases / Q000097:blood; D016896:Treatment Outcome
D000998:Antiviral Agents; D001323:Autoantibodies; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D011503:Transglutaminases