OBJECTIVE: To determine the prevalence of adrenal enzyme dysfunction in women presenting with oligomenorrhoea and hirsutism, two clinical features of polycystic ovary syndrome (PCOS). DESIGN: A prospective study of women attending outpatient clinics with these complaints. Androstenedione, dehydroepiandrosterone (DHEA), 17-hydroxyprogesterone (17-OHP), 11-deoxycortisol and cortisol were measured before and after overnight dexamethasone suppression and at 60 minutes after adrenal stimulation by ACTH injection. SUBJECTS: Fifty women with clinical features of PCOS and 37 control women with regular cycles and normal hair distribution from the catchment area of the Royal Victoria Infirmary which includes Newcastle upon Tyne, Co. Durham, Cleveland, Cumbria and Northumberland. MEASUREMENTS: Number of women with steroid responses to ACTH beyond the normal range, as defined by the responses of the control group and in previous studies. RESULTS: Nineteen women (38%) were found to have some abnormality. One woman (2%) was identified with 21-hydroxylase (21-OHase) deficiency and a second (2%) had an increase in 17-OHP compatible with the heterozygote state for 21-OHase deficiency. Four women (8%) had isolated elevations in the DHEA response consistent with minimal 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) deficiency. Thirteen women (26%) showed increases in both androstenedione and DHEA, or androstenedione alone, compatible with enhanced 17-20 lyase activity. CONCLUSIONS: Twelve per cent of the group showed evidence consistent with an adrenal enzyme deficiency; 26% had results in keeping with increased adrenal androgen production without an enzyme deficiency. These findings may be of relevance both in the pathogenesis of the features of PCOS and in determining appropriate treatment for individual patients.
OBJECTIVE: To determine the prevalence of adrenal enzyme dysfunction in women presenting with oligomenorrhoea and hirsutism, two clinical features of polycystic ovary syndrome (PCOS). DESIGN: A prospective study of women attending outpatient clinics with these complaints. Androstenedione, dehydroepiandrosterone (DHEA), 17-hydroxyprogesterone (17-OHP), 11-deoxycortisol and cortisol were measured before and after overnight dexamethasone suppression and at 60 minutes after adrenal stimulation by ACTH injection. SUBJECTS: Fifty women with clinical features of PCOS and 37 control women with regular cycles and normal hair distribution from the catchment area of the Royal Victoria Infirmary which includes Newcastle upon Tyne, Co. Durham, Cleveland, Cumbria and Northumberland. MEASUREMENTS: Number of women with steroid responses to ACTH beyond the normal range, as defined by the responses of the control group and in previous studies. RESULTS: Nineteen women (38%) were found to have some abnormality. One woman (2%) was identified with 21-hydroxylase (21-OHase) deficiency and a second (2%) had an increase in 17-OHP compatible with the heterozygote state for 21-OHase deficiency. Four women (8%) had isolated elevations in the DHEA response consistent with minimal 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) deficiency. Thirteen women (26%) showed increases in both androstenedione and DHEA, or androstenedione alone, compatible with enhanced 17-20 lyase activity. CONCLUSIONS: Twelve per cent of the group showed evidence consistent with an adrenal enzyme deficiency; 26% had results in keeping with increased adrenal androgen production without an enzyme deficiency. These findings may be of relevance both in the pathogenesis of the features of PCOS and in determining appropriate treatment for individual patients.