Male Obesity-related Secondary Hypogonadism - Pathophysiology, Clinical Implications and Management.

Autor:	Fernandez CJ; Department of Endocrinology & Metabolism, Pilgrim Hospital, United Lincolnshire Hospitals NHS Trust, Boston, UK., Chacko EC; Department of Endocrinology, Jersey General Hospital, St Helier, Jersey., Pappachan JM; Department of Endocrinology & Metabolism, Lancashire Teaching Hospitals NHS Foundation Trust, Preston, UK.
Jazyk:	angličtina
Zdroj:	European endocrinology [Eur Endocrinol] 2019 Aug; Vol. 15 (2), pp. 83-90. Date of Electronic Publication: 2019 Aug 16.
DOI:	10.17925/EE.2019.15.2.83
Abstrakt:	The single most significant risk factor for testosterone deficiency in men is obesity. The pathophysiological mechanisms involved in male obesity-related secondary hypogonadism are highly complex. Obesity-induced increase in levels of leptin, insulin, proinflammatory cytokines and oestrogen can cause a functional hypogonadotrophic hypogonadism with the defect present at the level of the hypothalamic gonadotrophin-releasing hormone (GnRH) neurons. The resulting hypogonadism by itself can worsen obesity, creating a self-perpetuating cycle. Obesity-induced hypogonadism is reversible with substantial weight loss. Lifestyle-measures form the cornerstone of management as they can potentially improve androgen deficiency symptoms irrespective of their effect on testosterone levels. In selected patients, bariatric surgery can reverse the obesity-induced hypogonadism. If these measures fail to relieve symptoms and to normalise testosterone levels, in appropriately selected men, testosterone replacement therapy could be started. Aromatase inhibitors and selective oestrogen receptor modulators are not recommended due to lack of consistent clinical trial-based evidence. Competing Interests: Disclosure: Cornelius J Fernandez, Elias C Chacko and Joseph M Pappachan have nothing to declare in relation to this article. (© The Author(s) 2019.)
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu