ECE2006 Poster Presentations Reproduction (80 abstracts)
1Department of Diabetes & Endocrinology,Ysbyty Gwynedd, Bangor, United Kingdom; 2Department of Clinical Biochemistry,Ysbyty Gwynedd, Bangor, United Kingdom; 3School of Human & Life Sciences, Roehampton University, London, United Kingdom.
Hyperandrogenism of adrenal origin evidenced by elevated dehydroepiandrosterone sulphate (DHEAS) levels has been reported in 20% to 30% of patients with polycystic ovary syndrome.
We studied 50 patients with PCOS (defined by the Rotterdam Consensus Workshop group criteria, 2003). Adrenal hyperandrogenaemia was defined as a DHEAS level> 10.5 micromoles/litre was found in 10 patients (20%). Clinical features studied were body mass index (BMI) and hirsutism by means of Ferriman and Gallwey (F&G) scores. Biochemical parameters included fasting glucose, insulin, total testosterone, FSH, LH, SHBG, DHEAS, androstenedione, basal and ACTH stimulated 17 hydroxyprogesterone levels. Free and bioavailable testosterone levels were calculated using a software programme available from
Significant differences were found between patients with adrenal hyperandrogenaemia (AH) and normal adrenal androgens (NA). BMI 30.80+7.12/35.60+9.15 kg/m2 (P 0.078), androstenedione 19.76+4.55/14.18+4.61 nmol/l (P 0.001), insulin 65.60+64.47/129.55+129.63 pmol/l (P 0.048),insulinresistance1.2+1.16/2.26+0.9 (P=0.046) and insulin sensitivity 131.82+77.97/84.93+71.81% (P 0.047) for AH/NA respectively. All data expressed as mean+standard deviation. No significant differences were found in F&G score, fasting glucose, total testosterone, FSH, LH, SHBG and 17 hydroxyprogesterone levels. Negative correlations were found between DHEAS and fasting insulin levels (r=−0.04, P<0.05) and DHEAS and BMI (r=−0.33, P<0.05).
These results suggest the existence of a unique subpopulation of patients with PCOS identified by low BMI, absence of insulin resistance and adrenal hyperandrogenaemia. The similar basal and stimulated 17-hydroxyprogesterone levels indicate a difference in downstream adrenal androgen generation.