Onset of diabetes with high titer anti-GAD antibody after IFN therapy for chronic hepatitis

Shiba, Teruo; Morino, Yoshihiro; Tagawa, Kunio; Fujino, Hitoshi; Unuma, Tadao

doi:10.1016/0168-8227(95)01188-9

Cited by 35 publications

(13 citation statements)

References 14 publications

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“…7 In one study in man, increased serum IFN-␥ was seen more frequently in patients with autoimmune diabetes than in non-diabetic controls. 5,6 In contrast, in the present case, IFN-␥ appeared to aggravate insulin resistance and cause hyperglycaemia with insulin resistance rather than by ␤-cell injury. 5,6 In contrast, in the present case, IFN-␥ appeared to aggravate insulin resistance and cause hyperglycaemia with insulin resistance rather than by ␤-cell injury.…”

Section: Discussioncontrasting

confidence: 78%

Hyperglycaemia due to insulin resistance caused by interferon-γ

Shiba¹,

Higashi²,

Nishimura³

1998

Diabet. Med.

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Marked hyperglycaemia (30.9 mmol l −1 ) during interferon-␥ (IFN-␥) therapy for asymptomatic recurrent renal cancer as multiple lung metastases in a 52-year-old man is described. Although the involvement of IFN-␥ has been reported in the development of autoimmune diabetes, in this case, antibodies against pancreatic ␤-cells including anti-islet cell antibody (ICA) and anti-glutamic acid decarboxylase (GAD) antibody were negative. Moreover, serum level of immunoreactive insulin (IRI) (11 U ml −1 at fasting) and urinary excretion of C-peptide (108 g day −1 , reference range: 20-130) suggested insulin resistance, supported by results of insulin tolerance tests. With insulin therapy and cessation of IFN-␥, fasting blood glucose concentration returned to 6.2 mmol l −1 , and insulin therapy was discontinued. The injection of IFN-␥ may cause hyperglycaemia because of insulin resistance, rather than ␤-cell injury.

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Section: Discussioncontrasting

confidence: 78%

Hyperglycaemia due to insulin resistance caused by interferon-γ

Shiba¹,

Higashi²,

Nishimura³

1998

Diabet. Med.

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“…Twenty-eight cases of type 1 diabetes mellitus diagnosed after the start of IFN+RBV therapy have thus far been reported in the English language literature 3,8–25. We reviewed the data for each of these cases, focusing on the length of time from the start of IFN+RBV therapy to the onset of type 1 diabetes mellitus, continuation/ discontinuation of IFN therapy after the onset of type 1 diabetes, weaning/nonweaning from insulin therapy after discontinuation of IFN+RBV, presence/absence of pancreas-associated autoantibodies before and after IFN+RBV therapy, and the HLA haplotype of the patients (Table 1).…”

Section: Discussionmentioning

confidence: 99%

“…While in most cases IFN+RBV therapy had been discontinued immediately after the diagnosis of type 1 diabetes,3,8–16,18,20–24 the treatment had been continued in two cases, including the present case 25. Insulin therapy could be discontinued later in only two of the 19 cases in which IFN+RBV therapy had been stopped immediately after the diagnosis of type 1 diabetes 8,23. Weaning from insulin therapy appears to be difficult in cases of type 1 diabetes mellitus developing after the start of IFN+RBV therapy, and it has been reported that weaning was impossible in 75% of such cases 1.…”

Section: Discussionmentioning

confidence: 99%

Type 1 Diabetes Mellitus Associated with Pegylated Interferon-α Plus Ribavirin Treatment for Chronic Hepatitis C: Case Report and Literature Review

Oka

Hiroi

Shigemitsu

et al. 2011

Clin Med Insights Endocrinol Diabetes

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Combined pegylated interferon (PEG-IFN)+ribavirin (RBV) therapy has been used as a primary treatment for chronic hepatitis C. However, IFN-induced autoimmune disease, including type 1 diabetes mellitus, has been highlighted as one of the problems with this therapy. Here we report the case of a patient who developed type 1 diabetes mellitus during combined PEG-IFN+RBV therapy for hepatitis C but who showed no exacerbation of diabetes despite continued use of IFN. A 63-year-old man with chronic hepatitis C and a nonresponder to previous IFNα treatments, was admitted to our hospital because of excessive thirst, polydipsia, and polyuria 24 weeks after the start of PEG-IFNα+RBV therapy. High levels of blood glucose and glycosylated hemoglobin and low levels of C-peptide and immunoreactive insulin were observed. The serum antiglutamic acid decarboxylase antibody titer was 27,700 U/mL. We diagnosed IFN-induced type 1 diabetes mellitus; however PEG-IFNα+RBV therapy was continued for 48 weeks. Serum HCV remains negative five years after this treatment. Intensive insulin therapy was started immediately after the diagnosis of type 1 diabetes. Although the patient initially required 22 U/day of insulin, the dosage could be gradually reduced after completion of PEG-IFNα+RBV therapy and blood glucose remained well controlled. Prediction of onset of type 1 diabetes mellitus on the basis of baseline measurement of pancreas-associated autoantibodies is difficult. Therefore, it would be advisable to consider the possibility of onset of type 1 diabetes mellitus in all patients receiving IFN+RBV therapy.

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“…Examples include nicotinic acid and glucocorticoids (77,78). Patients receiving ␣-interferon have been reported to develop diabetes associated with islet cell antibodies and, in certain instances, severe insulin deficiency (83,84). The list shown in Table 1 is not all-inclusive, but reflects the more commonly recognized drug-, hormone-, or toxin-induced forms of diabetes.…”

Section: Drug-or Chemical-induced Diabetesmentioning

confidence: 99%