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Stéroides sexuels et ostéoporose chez l'homme
Sex steroids and osteoporosis in men
Andrologie volume 12, pages 24–31 (2002)
Résumé
Les études épidemiologiques récentes ont confirmé que l'ostéoporose était fréquente chez l'homme. Après 50 ans, 18% des hommes seront victimes d'au moins une fracture ostéoporotique et 6 à 8% auront une fracture de l'extrémité supérieure du fémur. Dans 60% des cas environ la perte osseuse est secondaire à des facteurs étiologiques intriqués: corticothérapie prolongée, hypogonadisme franc, intoxication tabagique ou alcoolique, maladie digestive ou hépatique chronique. L'ostéoporose masculine primitive ou idiopathique, qui représente environ 40% des patients, touche souvent des hommes jeunes, entre 40 et 60 ans, indemnes de toute autre pathologie. Plusieurs voies pathogéniques sont actuellement explorés pour comprendre les raisons de cette perte osseuse chez ces patients: les facteurs génétiques, un éventuel déficit cellulaire de la formation osseuse mais surtout le rôle des stéroides sexuels biodisponibles. La carence en androgènes s'accompagne d'une accélération du remodelage osseux au profit de la résorption et d'une perte osseuse franche, prédominant dans le secteur trabéculaire. En fait l'action des androgènes sur le tissu osseux est double: directe, en raison d'un rôle stimulant de la testostérone sur la formation osseuse mais surtout indirecte par l'intermédiaire de l'estradiol, produit par aromatisation de la testostérone, qui régule le remodelage osseux et freine la résortpion osseuse. Finallement la densité osseuse et le risque de fracture sont mieux corrélés avec les taux sériques d'estradiol biodisponible et de Sex Hormone Binding Globulin (SHBG) qu'avec le taux plasmatique de testostérone, chez les hommes âgés de plus de 60 ans.
Abstract
Several epidemiological studies have shown that about 25 per cent of hip fractures and 20 per cent of symptomatic vertebral fractures occur in men. The lifetime risk of hip fracture was estimated to be about 6 to 8 per cent and the risk of any osteoporotic fracture was estimated to be about 18 per cent in 50-year-old white men. In about 60% of cases in men, bone loss is secondary to several pathological conditions, such as long-term steroid therapy, severe hypogonadism, smoking or alcohol abuse or gastrointestinal disorders. In 40% of cases, osteoporosis is primary or idiopathic in men between the ages of 40 and 60 years. Genetic factors, a defect of boneforming cells or abnormal serum levels of bioavailable sex steroids could explain bone loss and fragility fractures in these men. It has been shown that hypogonadism is associated with a marked increase in bone remodelling and particularly in bone resorption with a dramatic loss in trabecular bone. It is now known that testosterone is partly transformed into estradiol by aromatase. Testosterone may therefore act on bone in two ways: it directly stimulates bone formation and estradiol regulates bone remodelling and inhibits bone resorption. Finally, in men over the age of 60 without hypogonadism, it has been shown that bone mineral density and fracture risk were better correlated with serum levels of bioavailable estradiol and Sex Hormone Binding Globulin than with serum testosterone levels.
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Legrand, E., Simon, V. & Audran, M. Stéroides sexuels et ostéoporose chez l'homme. Androl. 12, 24–31 (2002). https://doi.org/10.1007/BF03034945
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DOI: https://doi.org/10.1007/BF03034945