title: Type B Insulin Resistance Masquerading as Ovarian Hyperthecosis.
abstract: Hyperinsulinemia can lead to pathologic ovarian growth and androgen production.
  
  
  
  A 29-year-old woman developed an autoantibody to the insulin receptor (type B insulin resistance), causing extreme insulin resistance and hyperinsulinemia. Testosterone levels were elevated to the adult male range. Treatment with gonadotropin-releasing hormone (GnRH) analog led to normalization of testosterone, despite persistent extreme insulin resistance.
  
  
  
  This case demonstrates that gonadotropins are necessary for insulin to cause pathologic ovarian androgen production. Suppression of gonadotropins with GnRH analogs may be a useful therapeutic option in patients with severe hyperandrogenism or ovarian enlargement because of hyperinsulinemia.
authors.affiliation: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
authors.forename: Rebecca J
authors.initials: RJ
authors.lastname: Brown
authors.affiliation: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
authors.forename: Jalaja
authors.initials: J
authors.lastname: Joseph
authors.affiliation: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
authors.forename: Elaine
authors.initials: E
authors.lastname: Cochran
authors.affiliation: The University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge CB2 OQQ, United Kingdom.|The National Institute for Health Research Cambridge Biomedical Research Centre, Cambridge CB2 OQQ, United Kingdom.
authors.forename: Cornelia
authors.initials: C
authors.lastname: Gewert
authors.affiliation: The University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge CB2 OQQ, United Kingdom.|The National Institute for Health Research Cambridge Biomedical Research Centre, Cambridge CB2 OQQ, United Kingdom.
authors.forename: Robert
authors.initials: R
authors.lastname: Semple
authors.affiliation: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
authors.forename: Phillip
authors.initials: P
authors.lastname: Gorden
mesh_terms: D000328:Adult; D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use; D001323:Autoantibodies / Q000276:immunology; D003520:Cyclophosphamide / Q000627:therapeutic use; D003907:Dexamethasone / Q000627:therapeutic use; D003937:Diagnosis, Differential; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives; D006801:Humans; D017588:Hyperandrogenism / Q000097:blood / Q000175:diagnosis* / Q000188:drug therapy; D006946:Hyperinsulinism / Q000097:blood / Q000175:diagnosis*; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007333:Insulin Resistance / Q000276:immunology*; D016729:Leuprolide / Q000627:therapeutic use; D010049:Ovarian Diseases / Q000097:blood / Q000175:diagnosis* / Q000188:drug therapy; D011972:Receptor, Insulin / Q000276:immunology*; D000069283:Rituximab / Q000627:therapeutic use; D013739:Testosterone / Q000097:blood
chemical_list: D018931:Antineoplastic Agents, Hormonal; D001323:Autoantibodies; D007166:Immunosuppressive Agents; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D000069283:Rituximab; D003907:Dexamethasone; D003520:Cyclophosphamide; D011972:Receptor, Insulin; D016729:Leuprolide