Ebeling P R
Department of Diabetes and Endocrinology, Royal Melbourne Hospital, Victoria, Australia.
Drugs Aging. 1998 Dec;13(6):421-34. doi: 10.2165/00002512-199813060-00002.
Osteoporosis is increasingly recognised in men. Low bone mass, risk factors for falling and factors causing fractures in women are likely to cause fractures in men. Bone mass is largely genetically determined, but environmental factors also contribute. Greater muscle strength and physical activity are associated with higher bone mass, while radial bone loss is greater in cigarette smokers or those with a moderate alcohol intake. Sex hormones have important effects on bone physiology. In men, there is no abrupt cessation of testicular function or 'andropause' comparable with the menopause in women; however, both total and free testosterone levels decline with age. A common secondary cause of osteoporosis in men is hypogonadism. There is increasing evidence that estrogens are important in skeletal maintenance in men as well as women. Peripheral aromatisation of androgens to estrogens occurs and osteoblast-like cells can aromatise androgens into estrogens. Human models exist for the effects of estrogens on the male skeleton. In men aged > 65 years, there is a positive association between bone mineral density (BMD) and greater serum estradiol levels at all skeletal sites and a negative association between BMD and testosterone at some sites. It is crucial to exclude pathological causes of osteoporosis, because 30 to 60% of men with vertebral fractures have another illness contributing to bone disease. Glucocorticoid excess (predominantly exogenous) is common. Gastrointestinal disease predisposes patients to bone disease as a result of intestinal malabsorption of calcium and colecalciferol (vitamin D). Hypercalciuria and nephrolithiasis, anticonvulsant drug use, thyrotoxicosis, immobilisation, liver and renal disease, multiple myeloma and systemic mastocytosis have all been associated with osteoporosis in men. It is possible that low-dose estrogen therapy or specific estrogen receptor-modulating drugs might increase BMD in men as well as in women. In the future, parathyroid hormone peptides may be an effective treatment for osteoporosis, particularly in patients in whom other treatments, such as bisphosphonates, have failed. Men with idiopathic osteoporosis have low circulating insulin-like growth factor-1 (IGF-1; somatomedin-1) concentrations, and IGF-1 administration to these men increases bone formation markers more than resorption markers. Studies of changes in BMD with IGF-1 treatment in osteoporotic men and women are underway. Osteoporosis in men will become an increasing worldwide public health problem over the next 20 years, so it is vital that safe and effective therapies for this disabling condition become available. Effective public health measures also need to be established and targeted to men at risk of developing the disease.
男性骨质疏松症越来越受到关注。女性中出现的低骨量、跌倒风险因素和导致骨折的因素同样可能致使男性发生骨折。骨量在很大程度上由基因决定,但环境因素也有影响。更强的肌肉力量和体育活动与更高的骨量相关,而吸烟者或适度饮酒者的桡骨骨质流失更为严重。性激素对骨骼生理有重要影响。在男性中,不存在与女性绝经类似的睾丸功能突然停止或“男性更年期”;然而,总睾酮和游离睾酮水平都会随年龄下降。男性骨质疏松症常见的一个继发性病因是性腺功能减退。越来越多的证据表明,雌激素在男性和女性的骨骼维持中都很重要。雄激素可在外周芳香化为雌激素,而成骨细胞样细胞也能将雄激素芳香化为雌激素。有人类模型可用于研究雌激素对男性骨骼的影响。在65岁以上的男性中,所有骨骼部位的骨密度(BMD)与更高的血清雌二醇水平呈正相关,而在某些部位,BMD与睾酮呈负相关。排除骨质疏松症的病理原因至关重要,因为30%至60%的椎体骨折男性还有其他导致骨病的疾病。糖皮质激素过量(主要是外源性的)很常见。胃肠道疾病会因肠道对钙和骨化二醇(维生素D)吸收不良而使患者易患骨病。高钙尿症和肾结石、抗惊厥药物的使用、甲状腺毒症、制动、肝脏和肾脏疾病、多发性骨髓瘤和系统性肥大细胞增多症都与男性骨质疏松症有关。低剂量雌激素疗法或特定的雌激素受体调节药物有可能增加男性和女性的骨密度。未来,甲状旁腺激素肽可能成为治疗骨质疏松症的有效方法,特别是对于双膦酸盐等其他治疗方法无效的患者。特发性骨质疏松症男性的循环胰岛素样生长因子-1(IGF-1;生长调节素-1)浓度较低,对这些男性给予IGF-1后,骨形成标志物的增加幅度大于骨吸收标志物。目前正在对骨质疏松症男性和女性接受IGF-1治疗时骨密度的变化进行研究。在未来20年里,男性骨质疏松症将成为一个日益严重的全球公共卫生问题;因此,为这种致残性疾病提供安全有效的治疗方法至关重要。还需要制定有效的公共卫生措施,并针对有患该病风险的男性。