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Risk of Primary Hypogonadism in Patients with OSA Due to High Leptin Levels pp. 155-164 $100.00
Authors:  (Madalina Miniciu Macrea, Leon Zagrean, Salem Veterans Affairs Medical Center, Salem, Virginia, USA)
Obstructive sleep apnea (OSA) is a complex disease characterized by repetitive collapse of the pharyngeal airway during sleep, yielding hypoxia and hypercapnia. Apnea-induced hypoxia leads to arousal and termination of the obstructive events [1]. The myriad of adverse effects of OSA, including that of hyperleptinemia, become especially important for the young adult, as they may portend sub or even infertility. Leptin, a protein of 167-amino acids with a structure similar to that of cytokines, is secreted predominantly by the adipocyte cells. Recent evidence has surfaced concerning its multifaceted neuroendocrine role, including that on the pituitary-gonadal axis and sexual dysfunction. The mechanism of action by which hyperleptinemia is present in adults with OSA [2] is likely multifactorial. These patients develop central or peripheral (receptor and postreceptor) [3] leptin resistance with subsequent high circulating leptin levels, possibly related to the hypoxia-enhanced sympathetic drive [4, 5] or hypoventilation [8, 9], as leptin levels fall subsequent to initiation of continuous positive airway pressure (CPAP) therapy [6, 7]. Regardless of its exact mechanism of action, adults with OSA have higher than normal serum leptin levels that may directly inhibit the testicular and ovarian cell function [10]. Previous studies have agreed on OSA disease being associated with secondary hypogonadism; to our knowledge, our study is the first to attempt to demonstrate that OSA disease may be also associated with primary hypogonadism due to hyperleptinemia. 

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Risk of Primary Hypogonadism in Patients with OSA Due to High Leptin Levels pp. 155-164