Insulin receptor autoantibodies in sepsis.

This study was undertaken to investigate possible factors contributing to altered glucose homeostasis in a patient with a history of total pancreatectomy and intermittent sepsis. Blood was drawn when the patient had received no exogenous insulin for the previous 24 hours, had a serum insulin level of 0.3 microU/mL, and gave an inappropriately low glucose response to large amounts of infused glucose. The IgG fraction prepared from this serum stimulated glucose oxidation in vitro and inhibited binding of insulin labeled with I 125 to isolated rat adipocytes, thus fulfilling some of the criteria for autoantibodies to the insulin receptor. The results are compatible with the hypothesis that insulin-receptor autoantibodies may have developed as a result of perturbation of this patient's immune status promoted by intermittent septic episodes and that, preterminally, as these antibodies converted in vivo to their in vitro-type behavior, they may have been partially responsible for the severe disturbances of glucose homeostasis.