Identification of the source of androgen excess in hyperandrogenic type 1 diabetic patients.

W e recently reported that the prevalence of hyperandrogenic disorders is markedly increased in women with type 1 diabetes (1). The polycystic ovary syndrome (PCOS) defined by endocrine criteria was found in 18.8% of the type 1 diabetic women who followed-up in our hospital (1), as compared with the 6.5% prevalence in nondi-abetic women from similar ethnic and genetic backgrounds (2). The prevalence of hirsutism in type 1 diabetic women was 30.6% (1), which is markedly higher than the 7.1% prevalence of hirsutism found in nondiabetic women (2). In the present study, we evaluated the adrenal and ovarian steroidogenic profiles of hyperandrogenic and nonhy-perandrogenic type 1 diabetic women and compared them with those of nondi-abetic hyperandrogenic women and healthy control subjects. A total of 24 women with type 1 diabetes were recruited for the study (1). Fourteen diabetic patients (age [mean Ϯ SD] 20.6 Ϯ 4.0 years, BMI 24.8 Ϯ 2.9 kg/m 2) were considered to have hyperan-drogenism. The other 10 women with type 1 diabetes (age 19.0 Ϯ 3.0 years, BMI 23.3 Ϯ 2.6 kg/m 2) had no evidence of clinical or biochemical hyperandro-genism and had regular menstrual cycles. Both groups of type 1 diabetic patients had similar HbA 1c levels (7.4 Ϯ 1.2 vs 7.8 Ϯ 1.2% in nonhyperandrogenic and hyperandrogenic diabetic patients, respectively , F ϭ 0.591, P ϭ 0.450), and there were no differences in the mean daily insulin dose used for their treatment (0.82 Ϯ 0.27 vs. 0.66 Ϯ 0.28 U ⅐ kg Ϫ1 body wt ⅐ day Ϫ1 in nonhyperandrogenic and hyperandrogenic diabetic patients, F ϭ 1.875, P ϭ 0.185). A total of 86 nondiabetic women were included as control subjects. Nondiabetic women were matched for BMI and age with the diabetic patients to avoid any influence of age and obesity on the results. Thirteen regularly menstruating women (age 23.2 Ϯ 3.2 years, BMI 24.6 Ϯ 5.1 kg/m 2) without signs or symptoms of hy-perandrogenism served as healthy control subjects; 73 untreated nondiabetic hyper-androgenic patients (age 20.6 Ϯ 3.8 years, BMI 23.7 Ϯ 3.2 kg/m 2) were included as hyperandrogenic control subjects. Basal and adrenocorticotropic hormone (ACTH)-stimulated samples were obtained and assayed as previously described (1,3). The study was conducted according to the principles expressed in the Declaration of Helsinki. The group of hyperandrogenic type 1 diabetic patients comprised seven women with PCOS and seven women with hirsut-ism and regular menstrual cycles. The percentage …