Circulating endothelial cells as marker of endothelial damage in male hypogonadism

Testosterone (T) deficiency has become a frequently diagnosed condition in current society affected by epidemic obesity and is associated with cardiovascular risk. Recent studies have established the importance of altered vascular endothelium function to cardiovascular disease. The damage to the endothelium might also cause endothelial cell detachment, resulting in increased numbers of circulating endothelial cells (CECs) within the bloodstream. In order to evaluate if hypogonadism could modify CEC count in peripheral bloodstream, we investigated in peripheral blood CEC count by the CellSearch System, a semiauthomatic method to accurately and reliably enumerate CECs, which are sorted based on a CD146+, CD105+, DAPI+, CD45- phenotype, in a population of twenty hypogonadic patients. The control group comprised ten age- and gender-matched healthy subjects. CEC count/ml was significantly increased in hypogonadic patients vs control group. In the hypogonadic group an inverse exponential correlation was present between T levels and CEC count/ml. A direct linear correlation was present between waist circumference (WC) and CECs and between BMI and CECs. The regression analysis showed that T was the significant independent determinant of CECs. Our results underline that male hypogonadism is associated with endothelial dysfunction. The correlation between CEC and WC underlines that visceral obesity may be synergically implicated in this regulation. Future studies are required to unveil the mechanisms involved in the pathogenesis of testosterone-induced endothelial disfunction, which may provide novel therapeutic targets to be incorporated in the management of hypogonadism.