Thyroid dysfunction and semen quality

Sandro La Vignera and Roberto Vita

Abstract

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.

IJIP 2018.pdf

Funzione riproduttiva maschile in corso di Diabete Mellito Tipo 1

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...

Reproductive function of type 1 diabetes.pdf

Controllo endocrino della iperplasia prostatica benigna

Endocrine control of benign prostatic hyperplasia

1S. La Vignera, 1R. A. Condorelli, 2G. I. Russo, 2G. Morgia and 1A. E. Calogero 1Department of Clinical and Experimental Medicine, University of Catania, and 2Department of Urology, University of Catania, Catania, Italy

SUMMARY - Benign prostatic hyperplasia (BPH) is the most common benign proliferative disease among aging men. Androgens play a key role in the development and growth of the male genital tract favoring differentiation and proliferation of stromal and epithelial cells of the prostate gland. It is known that growth factors play a crucial role in the cross-talk between stromal cells and epithelial cells. These factors, mainly secreted by stromal cells, act in an autocrine/paracrine manner to maintain prostate cellular homeostasis. A number of experimental studies support the interdependence between growth factors (IGF, FGF, TGF) and the steroid hormone milieu of the prostate. Alterations of these interactions may alter the balance between proliferation and cell death leading to the development of BPH. The onset of BPH is closely related to an inflammatory microenvironment. Chronic inflammation, which generally follows the acute inflammation because of infectious agents, is favored by hormonal or metabolic abnormalities. However, a close correlation between these mechanisms and metabolic or sexual hormones (androgen/estrogen ratio) alteration has been shown suggesting a key role of hypogonadism in the development of prostate inflammation. This review clear shows that the BPH pathogenesis and the subsequent onset of the lower urinary tract symptoms (LUTS) depends from different etio-pathogenetic factors whose mechanism of action remains to be evaluated…

Endocrine control of Benign Prostatic Hyperplasia.pdf