No abstract

To evaluate the effects of Diane-35 on androgenized oligomenorrheic women with polycystic ovarian syndrome, 32 women with PCOS were recruited to an open study of one-year duration. The effects of Diane-35 on signs of androgenization and on morphological and hormonal parameters were assessed in the pre- and posttreatment cycles and in the 3rd, 6th, 9th, and 12th treatment cycles. Twenty-two women completed the 12-month study period, five withdrew due to adverse events, two were lost to follow-up, and three stopped early because of a lack of efficacy. Ultrasound demonstrated significant reductions in ovarian volume, stromal density, and follicle number and size. Serum concentrations of LH, FSH, testosterone, androstenedione, and dehydroepiandrosterone sulfate decreased, and serum SHBG increased significantly. Mean Ferriman-Gallwey hirsutism scores declined from 14.3 before treatment to 5.7 at completion of therapy. Severe facial hirsutism, present in 23 (71.9%) of 32 women, disappeared in 6 women and improved in 6 women--a healing/improvement rate of 54.6% of 22 women who completed the study. Cycle control was good, amenorrhea occurred in 5 (1.6%) of 322 treatment cycles, while 94.8% of withdrawal bleeds were normal or scanty. Intermenstrual spotting occurred in 7.1% and break-through bleeding in 4.4% of all treatment cycles. The incidence of adverse events was similar to that of other gestagen-estrogen combinations. The results of the study demonstrate that Diane-35 provides an effective therapy for androgenized oligomenorrheic women with PCOS wishing simultaneous contraceptive protection.

Twenty-seven women with polycystic ovary syndrome (PCO) and 17 control women had a 75 g oral glucose tolerance test (oGTT) performed. Although glucose tolerance was impaired in the obese (body mass index greater than 25 kg/m2) women with PCO, glycosylated hemoglobin (HbA1) concentrations did not exceed the normal upper limit (7.2%). In all 44 women, there was no correlation between HbA1 and fasting glucose (r = 0.082, p = 0.63) but there was a significant correlation between HbA1 and summed glucose levels through the oGTT (r = 0.389, p = 0.02). HbA1 measurement does not predict the presence of impaired glucose tolerance in women with PCO.

To investigate the effects of medical treatment of endometriosis on concentrations of insulin and glucagon in comparison with those of androgens, 12 nonobese women with minimal endometriosis were randomly allocated to receive treatment with either danazol or the gonadotropin-releasing hormone analogue, goserelin. In subjects treated with danazol, mean (sd) summed serum insulin (1.08 (0.22) nmol/l pretreatment; 3.00 (1.50) nmol/l after treatment, p<0.05) and summed plasma glucagon (94 (21) pmol/l pretreatment; 238 (113) pmol/l after treatment, p<0.05) responses to oral glucose administration increased significantly, but remained unchanged in subjects treated with goserelin. In the danazol-treated group, the mean free testosterone index increased from 3.3 (1.6) to 13.3 (4.2) (p<0.01), but there was no correlation between either glucagon or insulin and free testosterone index. In the goserelin-treated subjects, however, there was no change in mean free testosterone indices (pretreatment 3.6 (1.0), post-treatment 3.9 (1.8). Thus, the increase in free testosterone index induced by danazol treatment is not responsible for the concomitant development of hyperinsulinaemia and hyperglucagonaemia.

SUMMARY To investigate the glucagon status of women with polycystic ovary syndrome (PCO) and to relate this to serum concentrations of insulin, androgens and SHBG, 44 women with PCO and 23 control subjects underwent a 75‐g oral glucose tolerance test. Although obese (body mass index > 30kg/m2) women with PCO had higher concentrations of glucose and insulin than overweight (BMI 25‐30kg/m2) and non‐obese (BMI <25kg/m2) women with PCO and control subjects, fasting and summed values of glucagon in response to oral glucose were similar in all groups. The fasting and summed concentrations of glucagon were inversely related to those of testosterone and androstenedione in obese women with PCO, but no other relationships were demonstrated between hormone values and those of glucagon in the other groups. We conclude that glucagon is not implicated in peripheral insulin resistance in women with PCO.