c-peptide and Transfusion-Reaction

Hepatitis C virus (HCV) has been associated with Type 2 diabetes mellitus, and many other viral infections have been associated with Type 1 diabetes mellitus (Type 1 DM). An association between HCV and Type 1 DM, however, has never been reported. We report the case of a 66-year-old man who developed Type 1 DM 1 year after a blood transfusion-related HCV infection. Testing of serum specimens obtained in the weeks following blood transfusion demonstrated evidence of both acute HCV infection and development of Type 1 DM-related autoantibodies.. A 66-year-old Taiwanese male received blood transfusions during coronary artery bypass surgery in 1987. Serum specimens, obtained as part of a study on post-transfusion hepatitis, demonstrated that the patient had no evidence of hepatitis C prior to transfusion, but developed acute HCV infection after transfusion. One year later, the patient, who had no personal or family history of diabetes, presented with diabetic ketoacidosis, and tests for C-peptide confirmed that he had Type 1 DM. Testing of pre- and post-operative serum specimens demonstrated that the patient developed positive tests for islet cell and glutamic acid decarboxylase antibodies 4 weeks after transfusion, concurrent with the development of acute HCV infection.. The simultaneous development of HCV infection and diabetes-related autoantibodies suggest a relationship between HCV and Type 1 DM.

Topics: Acute Disease; Aged; Autoantibodies; C-Peptide; Diabetes Mellitus, Type 1; Glutamate Decarboxylase; Hepacivirus; Hepatitis C; Humans; Islets of Langerhans; Male; Taiwan; Transfusion Reaction

We report a case of chronic hepatitis C presenting insulin-dependent diabetes mellitus (IDDM) associated with various autoantibodies including possible anti-insulin receptor antibody (AIRA) during interferon (IFN) therapy. A 57-year-old man having chronic hepatitis C virus (HCV) infection with chronic thyroiditis received IFN therapy. The thyroid function was well-controlled by administration of thyroid hormone, although thyroid autoantibodies were positive. At 15 weeks after starting IFN (reaching 530 million units of total dose), marked thirst happened, with increased fasting plasma glucose level (488 mg/dl) and decreased daily urinary C peptide immunoreactivity level (less than 4.2 microg/day). IDDM occurred with anti-nuclear antibody (ANA), anti-DNA antibody and possible AIRA, and thyroid autoantibodies titers increased, but without pancreatic islet cell antibody and anti-glutamic acid decarboxylase antibody. Administration of IFN was stopped and insulin treatment was started, but plasma glucose level was not controlled well. AIRA became negative 2 months later, however, insulin antibody (IA) was positive when tested after 18 months. Serum HCV RNA has been negative, and a normal level of serum transaminase has been observed since IFN therapy. It is likely that IFN therapy induced the immunological disturbance and resulted in occurrence of various autoantibodies and IDDM in the patient.

Topics: Antibodies, Antinuclear; Antiviral Agents; Autoantibodies; Blood Glucose; C-Peptide; Diabetes Mellitus, Type 1; Glutamate Decarboxylase; Glycated Hemoglobin; Hepatitis C, Chronic; Humans; Hypothyroidism; Insulin; Insulin Antibodies; Interferon alpha-2; Interferon-alpha; Male; Middle Aged; Receptor, Insulin; Recombinant Proteins; Thyroid Hormones; Transfusion Reaction