This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by KAWANISHI, K. Articles by FLIER, J. S. Search for Related Content PubMed PubMed Citation Articles by KAWANISHI, K. Articles by FLIER, J. S.

Successful Immunosuppressive Therapy in Insulin Resistant Diabetes Caused by Anti-Insulin Receptor Autoantibodies

Third Department of Internal Medicine, Okayama University Medical School Okayama 700, Japan
^* Diabetes Branch, National Institutes of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health Bethesda, Maryland 20014

A 45-year-old, non-obese female patient ith no previous history of insulin administration was found to have extreme insulin resistance and abnormally high plasma immunoreactive insulin in the absence of anti-insulin antibodies in the serum. Clinically, there was no ketonuria. The patient also had evidence of Sj¶gren's syndrome with several immunologic features including hypergammaglobulinemia, positive antinuclear antibodies, accelerated erythrocyte sedimentation rate and leukopenia. Plasma pancreatic glucagon and C-peptide were elevated, but other endocrinologic abnormalities were not present. In this patient the insulin resistance appeared to be due to anti-insulin receptor antibodies which could be detected even in 1:500 dilution of serum.

Immunosuppressive therapy with prednisolone and cyclophosphamide resulted in a decreased level of serum gamma globulin and a concomitant decrease of blood glucose level. After immunosuppressive therapy for eight months, the diabetic syndrome disappeared completely and anti-receptor antibodies in the serum were no longer detectable. Furthermore, insulin sensitivity returned to normal. However, the patient's glucose tolerance deteriorated after the temporary termination of cyclophosphamide treatment and the lowering of prednisolone dosage.

Received April 28, 1976.

This article has been cited by other articles:

				S. SELINGER, J. TSAI, M. PULINI, A. SAPERSTEIN, and S. TAYLOR Autoimmune Thrombocytopenia and Primary Biliary Cirrhosis with Hypoglycemia and Insulin Receptor Autoantibodies: A Case Report Ann Intern Med, November 1, 1987; 107(5): 686 - 688. [Abstract] [PDF]

				G. C. TSOKOS, P. GORDEN, T. ANTONOVYCH, C. B. WILSON, and J. E. BALOW Lupus Nephritis and Other Autoimmune Features in Patients with Diabetes Mellitus Due to Autoantibody to Insulin Receptors Ann Intern Med, February 1, 1985; 102(2): 176 - 181. [Abstract] [PDF]

				R. J. POLLET and G. S. LEVEY Principles of Membrane Receptor Physiology and Their Application to Clinical Medicine Ann Intern Med, May 1, 1980; 92(5): 663 - 680. [Abstract] [PDF]