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Biomedical subjects

A Parra

Publications and source records attributed to A Parra.

147 records · Page 9Linked to original sources

Serum insulin in clomiphene responders and nonresponders with polycystic ovarian disease.

OBJECTIVE: To investigate insulin levels in women with polycystic ovarian disease (PCOD) who are responders or nonresponders to clomiphene citrate (CC). DESIGN: Open and prospective study. SETTING: Outpatient infertility clinic of a third level medical institution. PATIENTS: Ten healthy women (group 1) and 35 PCOD women classified as responders (group 2 n = 10) or nonresponders (group 3 n = 25) on the basis of serum progesterone > or = 19 nmol/L in response to CC repeatedly administered in doses up to 250 mg/day for five days; they were further subdivided if body mass index (BMI) was below (N) or above (H) mean + 3 SD of group 1. INTERVENTIONS: Blood samples were obtained in a 100-g, 2-hours oral glucose tolerance test (OGTT). MAIN OUTCOME MEASURES: Serum glucose, insulin, free testosterone (free-T), dehydroepiandrosterone sulphate (DHEA-S), and androstenedione (A) were determined in the samples OGTT and the areas under the curve (AUC) were calculated. RESULTS: Group 3 had higher BMI, basal LH, and insulin and AUC insulin than groups 1 and 2; free-T was higher in groups 2 and 3 than in group 1, and basal PRL was higher in group 2 compared to groups 1 and 3. When BMI < or = 25.4 kg/m2 (mean + 1 SD of group 1) 77% of the PCOD cases responded (10 out of 13) whereas none with BMI > 25.4 responded to CC (n = 22) irrespectively of basal insulin concentration or AUC insulin. CONCLUSION: Moderate to excessive overweight seems more frequently and closely associated to a negative CC response in women with PCOD than hyperinsulinemia.

Adult↗

[Androgen response in women with polycystic ovary syndrome and hyperinsulinemia during stimulation with corticotrophin and inhibition with dexamethasone].

The adrenal response to adrenocorticotropic hormone (ACTH) stimulation and dexamethasone (DEX) inhibition tests in six healthy ovulatory control women (31.6 +/- SD 0.6 years old) with a body mass index (BMI) of 24.8 +/- 1.3 kg/m2 (Group 1) were compared against seven women (28.1 +/- 0.8 years old, BMI 30.9 +/- 2.1 kg/m2) with polycystic ovary syndrome (PCOS) and hyperinsulinism (Group 2). In both groups the following tests were performed: a) a 100-g 2-h oral glucose tolerance test (OGTT) with serum glucose and insulin measurements; b) an ACTH stimulation test (2-h 0.25 mg iv bolus); and c) a 1 mg oral midnight DEX inhibition test. Assays of serum cortisol. 17-hydroxyprogesterone, dehydroepiandrosterone sulfate (DHEA-S), free testosterone (FT), and androstenedione during the ACTH and DEX tests were performed. Contrary to Group 1, Group 2 showed: a) higher basal luteinizing hormone follicle-stimulating hormone ratio, FT, and insulin, and hyperinsulinism during the OGTT; b) FT significantly higher after ACTH; and c) FT and DHEAS did not show a significant inhibition with DEX. Our results suggest a certain degree of adrenal participation in the pathogenesis of the hyperandrogenism in these women, which may be the final expression of a synergistic stimulation of the adrenals by hyperinsulinism, relatively high LH, and chronic hyperestrogenism, all of which are present virtually in all women with PCOS.

17-alpha-Hydroxyprogesterone↗