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Endocrine Frailty in the Elderly
Endocrine Frailty in the Elderly
Diabetes mellitus and infertility: different pathophysiological effects in type 1 and type 2 on sperm funcion...
Sandro La Vignera and Roberto Vita
Thyroid hormones act on testis in multiple ways and exert their effect on different cell types, including Leydig and Sertoli cells, and germ cells. An excess or deficit of thyroid hormones results in alterations of testis function, including semen abnormalities. More frequently, hyperthyroidism has been associated with reduced semen volume and reduced sperm density, motility, and morphology, whereas hypothyroidism is associated with reduced sperm morphology. Therefore, thyroid function tests should be part of the diagnostic workup of the infertile man. This article is aimed at (1) elucidating how hyperthyroidism and hypothyroidism lead to a reduction in semen quality, briefly reviewing the current literature on murine models and humans, and (2) pinpointing the limitations of the studies carried out so far and identifying new perspectives for future research.
Giorgio I. Russo, Aldo E. Calogero, Rosita A. Condorelli, Guido Scalia, Giuseppe Morgia & Sandro La Vignera (2018)
Human papillomavirus and risk of prostate cancer: a systematic review and meta-analysis, The Aging Male DOI: 10.1080/13685538.2018.1455178
Reproductive function in male patients with type 1 diabetes mellitus
1S. La Vignera, 1R. A.Condorelli, 1M. Di Mauro, 2D. Lo Presti, 1L. M. Mongio ı, 3G. Russo and 1A. E. Calogero 1Department of Clinical and Experimental Medicine, 2Unit of Pediatrics, Teaching Hospital “Policlinico - Vittorio Emanuele”, and 3Department of Urology, University of Catania, Catania, Italy
SUMMARY This study was undertaken to evaluate conventional and some of the main bio-functional spermatozoa parameters, serum gonadal hormones and didymo-epididymal ultrasound features in patients with type 1 diabetes mellitus (DM1). DM1 affects an increasing number of men of reproductive age. Diabetes may affect male reproduction by acting on the hypothalamic–pituitary–testicular axis, causing sexual dysfunction or disrupting male accessory gland function. However, data on spermatozoa parameters and other aspects of the reproductive function in these patients are scanty. Thirty-two patients with DM1 [27.0 (25.0–30.0 years)] and 20 age-matched fertile healthy men [28.0 (27.25–30.75 years)] were enrolled. Patients with diabetic neuropathy, other endocrine disorders or conditions known to alter spermatozoa parameters were excluded. Each subject underwent semen analysis, blood withdrawal for fasting and post-prandial glycaemia, hormonal analysis and didymo-epididymal ultrasound evaluation before and after ejaculation. Patients with DM1 had a lower percentage of spermatozoa with progressive motility [10.0 (7.0–12.75) vs. 45.0 (42.0–47.75) %; p < 0.01] and a higher percentage of spermatozoa with abnormal mitochondrial function than controls [47.0 (43.0–55.0) vs. 2.0 (1.0–5.0) %; p < 0.01]. Patients also had greater post-ejaculatory diameters of cephalic [11.5 (10.2–13.6) vs. 6.0 (4.0–7.0) mm; p < 0.01] and caudal epididymis [5.5 (4.00–7.55) vs. 3.0 (2.0–4.0) mm; p < 0.01] compared to controls, suggesting a lack of the physiological post-ejaculation epididymal shrinkage. Correlation analysis suggested that progressive motility was associated with fasting glucose (r = 0.68; p < 0.01). The other parameters did not show any signiﬁcant difference. Patients with DM1 had a lower percentage of spermatozoa with progressive motility, impaired mitochondrial function and epididymal post-ejaculatory dysfunction. These ﬁndings may explain why patients with DM1 experience fertility disturbance. Larger multi-centric studies are necessary to conﬁrm these results...