CONTEXT: Type B insulin resistance syndrome is a rare condition characterized by the presence of autoantibodies directed against the insulin receptor. It has been reported in association with autoimmune diseases such as systemic lupus erythematosus. OBJECTIVE: We report a case of type B insulin resistance syndrome in a patient with HIV infection on highly active antiretroviral therapy (HAART). PATIENT AND METHODS: A 27-yr-old African woman with ketosis-prone diabetes and HIV infection developed severe insulin resistance after the initiation of HAART. Standard oral glucose tolerance tests using 75 g of glucose performed 1, 2, and 3 months after the initiation of HAART showed severe hyperinsulinemia and hypoglycemia. Six months later, she developed symptomatic hyperglycemia resistant to high-dose insulin therapy. To determine the cause of insulin resistance, we assayed the titer of insulin receptor autoantibodies in the serum of the patient. RESULTS: Plasma insulin receptor autoantibodies were present at the time of marked hyperglycemia and insulin resistance, confirming the diagnosis of type B insulin resistance syndrome. Simultaneously the diagnosis of immune reconstitution inflammatory syndrome was established according to increased CD4 T cell count, decreased plasma HIV1-RNA level, and tuberculosis reactivation, shortly after institution of HAART. Corticosteroid therapy improved insulin resistance and hyperglycemia. CONCLUSION: We report the first case of type B insulin resistance syndrome associated with immune reconstitution inflammatory syndrome in an HIV-infected patient.
CONTEXT: Type B insulin resistance syndrome is a rare condition characterized by the presence of autoantibodies directed against the insulin receptor. It has been reported in association with autoimmune diseases such as systemic lupus erythematosus. OBJECTIVE: We report a case of type B insulin resistance syndrome in a patient with HIV infection on highly active antiretroviral therapy (HAART). PATIENT AND METHODS: A 27-yr-old African woman with ketosis-prone diabetes and HIV infection developed severe insulin resistance after the initiation of HAART. Standard oral glucose tolerance tests using 75 g of glucose performed 1, 2, and 3 months after the initiation of HAART showed severe hyperinsulinemia and hypoglycemia. Six months later, she developed symptomatic hyperglycemia resistant to high-dose insulin therapy. To determine the cause of insulin resistance, we assayed the titer of insulin receptor autoantibodies in the serum of the patient. RESULTS: Plasma insulin receptor autoantibodies were present at the time of marked hyperglycemia and insulin resistance, confirming the diagnosis of type B insulin resistance syndrome. Simultaneously the diagnosis of immune reconstitution inflammatory syndrome was established according to increased CD4 T cell count, decreased plasma HIV1-RNA level, and tuberculosis reactivation, shortly after institution of HAART. Corticosteroid therapy improved insulin resistance and hyperglycemia. CONCLUSION: We report the first case of type B insulin resistance syndrome associated with immune reconstitution inflammatory syndrome in an HIV-infectedpatient.