Endocrine Abstracts (2011) 26 P573

Low sex hormone binding globulin - strong association with metabolic syndrome in patients with acute coronary syndrome

J P Payer, A B Banarova, T K Koller & P J Jackuliak


5th Department of Internal Medicine, Medical Faculty of Comenius University, Bratislava, Slovakia.


Objective: Despite of conflicting data, reduced levels of endogenous sex hormones and especially sex hormone binding globulin (SHBG) seem to be associated with metabolic syndrome (MS). In this study we determined relationship between endogenous sex hormone levels and SHBG and components of metabolic syndrome in both sexes.

Methods: In 39 men (median age 70.2) with total testosterone level in the lowest quartile of normal range (median 12.8 nmol/l) and 29 postmenopausal women (median age 74.5, median estradiol 78.6 pmol/l) without hormone replacement therapy who were admitted with acute coronary syndrome we determined concentrations of endogenous sex hormones: total testosterone (TT), calculated free androgen index (FAI), estradiol (E) and SHBG. Using correlation analyze we determined their relationship to components of MS: waist circumference, serum concentration of triacylglycerides (TAG) and high density lipoproteins (HDL), diabetes mellitus, arterial hypertension and body mass index (BMI).

Results: In men low TT was associated with higher BMI (P=0.0009) and waist circumference (P=0.017), low SHBG was associated with higher BMI (P=0.0014), waist circumference (P=0.0073) and level of TAG (P=0.03). FAI did not have relationship to MS. In women low estradiol was associated with higher level of TAG (P=0.02). Lower TT was associated with higher BMI (P=0.02) and waist circumference (P=0.03) and low SHBG was associated with higher BMI (P=0.05), arterial hypertension (P=0.006) and TAG (P=0.007). FAI in women correlated negatively with BMI (P=0.05), waist circumference (P=0.04) and diabetes mellitus (P=0.02).

Conclusions: We confirmed inverse association between metabolic syndrome and endogenous sex hormones but especially SHBG. This supports the theory of possible nongenomic action of sex steroids mediated by SHBG although the exact pathogenesis of this relationship is still not well understood.

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