title: Clinical efficacy of insulin-like growth factor-1 in a patient with autoantibodies to insulin receptors: a case report.
abstract: The type B insulin-resistance syndrome is characterized by the presence of anti-insulin receptor antibodies that cause severe insulin resistance. Treatments including steroids, cyclophosphamide, plasmapheresis, or insulin-like growth factor-1 (IGF-1) are chosen according to severity of insulin resistance. We describe a patient with type B insulin resistance syndrome who was treated successfully with human recombinant (hr) IGF-1, although this treatment provoked a severe allergic reaction. An elderly man with impaired glucose tolerance and unpredictable hypoglycemic episodes which were gradually worsening increased in hemoglobin (Hb)A1c concentration from 6.5 to 13.4%. His fasting and postprandial hyperglycemia were associated with severe hyperinsulinemia. The patient was diagnosed with type B insulin-resistance syndrome by the presence of anti-insulin receptor antibodies. Double-filtration plasmapheresis, plasma exchange, and immunosuppressive therapy with cyclophosphamide and cyclosporin all failed to suppress anti-insulin receptor antibodies more than transiently. When we attempted the treatment by daily administration of hrIGF-1, fasting and postprandial plasma glucose concentrations became normal and HbA1c levels decreased to 7.1% over 2 months, until on one occasion administration resulted in anaphylaxis. After the patient became stable, desensitization therapy was performed successfully, and hrIGF-1 could be administered again with the plasma glucose returning. We concluded that IGF-1 therapy was an effective treatment choice for type B insulin-resistance syndrome in cases whose plasma exchange and immunosuppressive therapy have failed.
authors.affiliation: Department of Internal Medicine, Osaka City General Hospital, 2-13-22, Miyakojima-hondori, Miyakojima-ku, Osaka, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yamamoto
authors.forename: T
authors.initials: T
authors.lastname: Sato
authors.forename: T
authors.initials: T
authors.lastname: Mori
authors.forename: T
authors.initials: T
authors.lastname: Yamakita
authors.forename: T
authors.initials: T
authors.lastname: Hasegawa
authors.forename: M
authors.initials: M
authors.lastname: Miyamoto
authors.forename: M
authors.initials: M
authors.lastname: Hosoi
authors.forename: T
authors.initials: T
authors.lastname: Ishii
authors.forename: K
authors.initials: K
authors.lastname: Yoshioka
authors.forename: S
authors.initials: S
authors.lastname: Tanaka
authors.forename: S
authors.initials: S
authors.lastname: Fujii
mesh_terms: D000368:Aged; D001323:Autoantibodies / Q000276:immunology*; D001786:Blood Glucose / Q000032:analysis; D002096:C-Peptide / Q000097:blood; D003520:Cyclophosphamide / Q000627:therapeutic use; D016572:Cyclosporine / Q000627:therapeutic use; D003888:Desensitization, Immunologic; D005951:Glucose Tolerance Test; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D006943:Hyperglycemia / Q000188:drug therapy; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007333:Insulin Resistance / Q000276:immunology*; D007334:Insulin-Like Growth Factor I / Q000276:immunology / Q000592:standards / Q000627:therapeutic use*; D008297:Male; D010951:Plasma Exchange; D010956:Plasmapheresis; D011972:Receptor, Insulin / Q000276:immunology*; D013575:Syncope / Q000276:immunology
chemical_list: D001323:Autoantibodies; D001786:Blood Glucose; D002096:C-Peptide; D003520:Cyclophosphamide; D016572:Cyclosporine; D006442:Glycated Hemoglobin; D007166:Immunosuppressive Agents; D007334:Insulin-Like Growth Factor I; D011972:Receptor, Insulin