ISSN 1470-3947 (print)
ISSN 1479-6848 (online)

Searchable abstracts of presentations at key conferences in endocrinology

Published by BioScientifica
Endocrine Abstracts (2010) 22 P526 
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Effects of atorvastatin on male fertility

Hanae Pons-Rejraji1,2, Benoit Sion1, Florence Brugnon1,2, Christine Artonne1, Gérald Gouby3, Geneviève Grizard1,2, Laurent Janny1,2 & Igor Tauveron4

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Introduction: Dyslipidemia and impaired fertility are highly related. In animals, statin intake reduces sperm parameters deterioration associated with hypercholesterolemia. However, statin effects on human fertility are controversial. Their intake by hypercholesterolemic patients could reduce circulating testosterone concentration and sperm quality. While recommendations for cardiovascular prevention advocate lowering total cholesterol and LDL-C, atorvastatin, the most prescribed statin in France, is the subject of questions over its impact on male fertility.

Objective: This study aims to analyze the consequences on sperm parameters of atorvastatine intake by normocholesterolemic subjects achieving lipids concentrations recommended in secondary cardiovascular prevention.

Materials and methods: Atorvastatin (10 mg/day) has been administrated per se to 17 men (24.4±0.9 years) with normal blood lipid and spermatozoa parameters during 5 months. Blood lipids and hormones concentrations, conventional semen parameters (WHO, 1999), functional markers of the genital tract, sterols levels in spermatozoa and seminal fluid, sperm capacitation ability and acrosome membrane integrity have been assayed before taking the treatment, after 5 months of treatment, and 3 months after its withdrawal.

Results: Atorvastatin significantly decreased circulating LDL-C and cholesterol concentrations (respectively −40 and −23%, P<0.0001), without affecting HDL-C and triglycerides, reaching the targets for secondary prevention. The concentrations of gonadotropins and testosterone were not affected. Overall sperm quality (concentration, mobility, sterols levels in spermatozoa and seminal fluid, capacitation ability) was not affected. However, live spermatozoa percentage was reduced by atorvastatin (−8%, P<0.05). The seminal fluid concentrations of α-glucosidase was significantly decreased 3 months after ending the treatment (P<0.01), as well as the proportion of spermatozoa having spontaneously lost their acrosome (P<0.05).

Conclusion: The intake of atorvastatine, in secondary prevention conditions, significantly affects epididymal functional marker and live spermatozoa proportion. However, the low significance of differences measured is consistent with an absence of clinically significant deleterious effects.

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