TY - JOUR
T1 - Insulin-dependent diabetes mellitus during alpha-interferon therapy for chronic viral hepatitis
AU - Fabris, Paolo
AU - Betterle, Corrado
AU - Greggio, Nella A.
AU - Zanchetta, Renato
AU - Bosi, Emanuele
AU - Biasin, Maria Raffaella
AU - De Lalla, Fausto
PY - 1998/3
Y1 - 1998/3
N2 - A 29-year-old man was observed to develop insulin-dependent diabetes mellitus following a 5-month treatment with recombinant α-2b-interferon for chronic hepatitis C. After the onset of the disease, serum samples that had, respectively, been collected before therapy commencement, at month 3, and at the onset of insulin-dependent diabetes mellitus were tested for islet-cell (ICA-IgG), glutamic acid decarboxylase (GAD-Abs), IA2 (IA2-Abs) and insulin (IA-Abs) autoantibodies. The following results were obtained: ICA-IgG, 5, >80, and >80 JDF-U, respectively; GAD-Abs: >100 U/ml in all three measurements; IA2-Abs and IA-Abs: negative. During treatment, thyroid microsomal autoantibodies increased markedly (from 1:100 to 25 600 titer); thyroid-stimulating hormone was persistently normal. HLA class II typing revealed a genetic predisposition to insulin-dependent diabetes mellitus as demonstrated by the presence of DRB1* 04/08, DQ A1 52 Arg+/Arg+, and DQB1 57 N-Asp/Asp alleles. One year after the onset of insulin-dependent diabetes mellitus, the patient is still receiving 30 IU insulin daily; the liver function tests are normal and HCV-RNA is negative. These data support the hypothesis that, in predisposed patients, α-interferon therapy can enhance an ongoing autoimmune process against pancreatic β-cells and induce overt insulin-dependent diabetes mellitus. We therefore suggest that, in patients with a documented predisposition to insulin-dependent diabetes mellitus, α- IFN therapy should be administered with caution.
AB - A 29-year-old man was observed to develop insulin-dependent diabetes mellitus following a 5-month treatment with recombinant α-2b-interferon for chronic hepatitis C. After the onset of the disease, serum samples that had, respectively, been collected before therapy commencement, at month 3, and at the onset of insulin-dependent diabetes mellitus were tested for islet-cell (ICA-IgG), glutamic acid decarboxylase (GAD-Abs), IA2 (IA2-Abs) and insulin (IA-Abs) autoantibodies. The following results were obtained: ICA-IgG, 5, >80, and >80 JDF-U, respectively; GAD-Abs: >100 U/ml in all three measurements; IA2-Abs and IA-Abs: negative. During treatment, thyroid microsomal autoantibodies increased markedly (from 1:100 to 25 600 titer); thyroid-stimulating hormone was persistently normal. HLA class II typing revealed a genetic predisposition to insulin-dependent diabetes mellitus as demonstrated by the presence of DRB1* 04/08, DQ A1 52 Arg+/Arg+, and DQB1 57 N-Asp/Asp alleles. One year after the onset of insulin-dependent diabetes mellitus, the patient is still receiving 30 IU insulin daily; the liver function tests are normal and HCV-RNA is negative. These data support the hypothesis that, in predisposed patients, α-interferon therapy can enhance an ongoing autoimmune process against pancreatic β-cells and induce overt insulin-dependent diabetes mellitus. We therefore suggest that, in patients with a documented predisposition to insulin-dependent diabetes mellitus, α- IFN therapy should be administered with caution.
KW - α-IFN therapy
KW - Autoimmunity
KW - HCV
KW - Insulin-dependent diabetes mellitus
KW - Side effects
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U2 - 10.1016/S0168-8278(98)80328-0
DO - 10.1016/S0168-8278(98)80328-0
M3 - Article
C2 - 9551692
AN - SCOPUS:0032030743
VL - 28
SP - 514
EP - 517
JO - Journal of Hepatology
JF - Journal of Hepatology
SN - 0168-8278
IS - 3
ER -