Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SAT 532-553-Hyperandrogenic Disorders
Saturday, June 15, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SAT-538
Daniela Romualdi*, Antonio Mancini, Sebastiano Raimondo, Donatella Gagliano, Valentina Immediata, Cristina Tartaglia, Angela Zumpano, Antonio Lanzone and Alfredo Pontecorvi
Catholic University of the Sacred Heart, Rome, Italy
It is known that thyroid hormones (TH) influence ovarian activity, via direct and indirect mechanisms; they are among main regulators of SHBG. Moreover, hypothyroidism is frequently characterized by insulin resistance (IR), which is also a metabolic feature of polycystic ovary syndrome (PCOS). However few data do exist about the relationships among TH, androgen secretion, nutritional status and IR in PCOS.  Therefore, we studied 112 consecutive women affected by PCOS, attending our divisional outpatient services; 44 were overweight or obese (BMI >27 kg/m2, subgroup A) and 68 normal weight (subgroup B). We enrolled  PCOS women (age range 18-35 years), diagnosed according to Rotterdam criteria. Anthropometric parameters, hormonal assays, oral glucose tolerance test (OGTT) and euglycaemic-hyperinsulinaemic clamp were evaluated in all  patients. TSH values resulted to be directly correlated with waist to hip ratio (WHR) (r: 0.22; p=0.03) and inversely correlated with M-clamp, a reliable measure of peripheral total body glucose utilization (r: -0.24; p=0.03). Neither basal nor after-load glycemia were correlated with TSH. No correlations were found between TSH levels and gonadotropins, plasma androgens (testosterone, androstenedione, DHEAS, 17OH progesterone), AMH, sex hormone-binding-globulin. Similarly, the hirsutism score and the menstrual pattern seemed not to be influenced by thyroid function. After dividing patients on the basis of BMI, we did not observed significant difference in TSH values (subgroup A TSH: 1.98 ± 0.80 μUI/ml; subgroup B TSH: 1.90 ± 0.76 μUI/ml) and in free-thyroxine levels (subgroup A FT4: 11.46 ± 1.24 pg/ml; subgroup B FT4: 11.75 ± 1.33 pg/ml). TSH levels resulted positively correlated with both stimulated insulin secretion (r: 0.40; p=0.009) and peripheral insulin resistance (r: 0.35; p=0.04) in subgroup A but not in the subgroup B. In conclusion, thyroid function seems to be linked to insulin metabolism in this syndrome. It remains to be determined if the relative TSH elevation may be a cause, presumably via systemic oxidative stress, or a consequence of insulin resistance, as suggested by previous reports on TSH normalization after insulin-sensitizers administration.

Nothing to Disclose: DR, AM, SR, DG, VI, CT, AZ, AL, AP

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