Obstructive Sleep Apnea and Testosterone Replacement Therapy

Sandro La Vignera,Rossella Cannarella,Rosita A Condorelli,Antonio Aversa,Cristina Magagnini,Aldo E Calogero

doi:10.1089/andro.2020.0001

Abstract

The evidence on the role of obstructive sleep apnea (OSA) in the pathogenesis of hypogonadism and the impact of testosterone replacement therapy (TRT) in OSA patients are still contradictory. OSA is generally considered to be a relative contraindication as TRT is feared to worsen sleep apnea so that ventilatory capacity should be strictly investigated in advance and monitored thereafter. Few controlled studies have been released on the long-term effects of TRT in patients with OSA due to methodological limitations at study entry. Data from recent randomized placebo-controlled studies show a time-dependent influence on nocturnal hypoxia, and a positive impact after a longer time of exposure in selected patients. Since these results await further confirmation from larger studies, we suggest to use TRT cautiously in obese hypogonadal patients with hypoventilatory syndrome, especially if they are not on continuous positive airway pressure treatment.

Highlights

Sleep disorders are clinical conditions that worsen the quality of life and prognosis.[1]
obstructive sleep apnea (OSA) is generally considered to be a relative contraindication as testosterone replacement therapy (TRT) is feared to worsen sleep apnea so that ventilatory capacity should be strictly investigated in advance and monitored thereafter
In summary, this review summarizes the evidence on the mechanisms involved in the pathogenesis of hypogonadism in patients with OSA syndrome’’ (OSAS), such as abnormal circadian rhythm of gonadotrophin secretory patterns associated with obesity

Summary

Introduction

Sleep disorders are clinical conditions that worsen the quality of life and prognosis.[1]. One of the most common forms of sleep disorders is obstructive sleep apnea (OSA).[2] OSA is characterized by repetitive and intermittent, partial or complete collapse of the upper airway during sleeping, regardless of the presence of daytime symptoms This happens because upper airway dilator muscles fail to counter the negative pressure in the airways during inspiration. This condition is called ‘‘OSA syndrome’’ (OSAS) and the main presentations are sleep fragmentation with breathing interruptions, decreased sleep time, shorter REM time, loud snoring, and daytime sleepiness This leads to oxygen (O2) desaturation with hypoxemia and hypercapnia.[3] Over 50 years, *1–2% of women and 2–4% of men have OSA.[4] OSA severity is classified by measuring the ‘‘apnea– hypopnea index’’ (AHI). Etiopathogenesis of OSAS implies several factors, the main being obesity due to fatty deposits in the upper airways

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Conclusion