Endocrine Abstracts (2006) 11 P702

A unique subgroup of patients with polycystic ovary syndrome identified by clinical and biochemical features

TME Abdalla1, A Wilton1, D Wilton1, K Griffiths2, A Wayte2 & J Huber3

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 www.issam.ch/freetesto.htm. Insulin sensitivity% and insulin resistance were determined using the homeostatic model assessment (HOMA 2) software programme available from www.dtu.ox.ac.uk.

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.

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