Scane A C, Sutcliffe A M, Francis R M
University of Newcastle upon Tyne, Newcastle General Hospital, UK.
Baillieres Clin Rheumatol. 1993 Oct;7(3):589-601. doi: 10.1016/s0950-3579(05)80081-0.
Bone is lost with advancing age in men as in women, leading to an increased incidence of osteoporotic fractures of the fore-arm, vertebral body and femoral neck. By the ninth decade of life, 4% of men will have sustained a fore-arm fracture, 7% a vertebral fracture and 5% a femoral neck fracture. The absolute number of osteoporotic fractures is rising in men, because of the ageing population and an increase in the age-specific incidence of fractures. Even if the age-specific incidence of fractures stabilizes, demographic trends suggest that a further increase in the number of men with osteoporotic fractures is inevitable. Peak bone mass in men is influenced by race, hereditary, hormonal factors, physical activity and calcium intake during childhood and adolescence. Bone loss in men starts at about the age of 35 years and is regulated by genetic, endocrine, mechanical and nutritional factors. Secondary causes of osteoporosis may be detected in about 55% of men with vertebral crush fractures. The major causes are steroid therapy, hypogonadism, skeletal metastases, multiple myeloma, gastric surgery and anticonvulsant treatment. Hypogonadism is found in up to 20% of men with vertebral crush fractures, although the clinical features of testosterone deficiency may not always be present. Hypogonadal osteoporosis is associated with increased bone resorption and decreased mineralization, which is reversed by treatment with testosterone, leading to an increase in bone density. There is little published information on the treatment of primary osteoporosis in men. Although calcitonin, bisphosphonates and testosterone may be effective in the management of osteoporosis in men, confirmation is required in formal clinical trials.
与女性一样，男性的骨质也会随着年龄的增长而流失，从而导致前臂、椎体和股骨颈骨质疏松性骨折的发生率增加。到90岁时，4%的男性会发生前臂骨折，7%会发生椎体骨折，5%会发生股骨颈骨折。由于人口老龄化以及特定年龄段骨折发病率的上升，男性骨质疏松性骨折的绝对数量正在增加。即使特定年龄段的骨折发病率稳定下来，人口趋势表明，男性骨质疏松性骨折患者的数量进一步增加也是不可避免的。男性的骨峰值受种族、遗传、激素因素、体力活动以及儿童期和青春期钙摄入量的影响。男性的骨质流失大约从35岁开始，并受遗传、内分泌、机械和营养因素的调节。在约55%的椎体压缩性骨折男性患者中可检测到骨质疏松的继发性病因。主要病因包括类固醇治疗、性腺功能减退、骨转移、多发性骨髓瘤、胃部手术和抗惊厥治疗。在高达20%的椎体压缩性骨折男性患者中可发现性腺功能减退，尽管睾酮缺乏的临床特征可能并不总是存在。性腺功能减退性骨质疏松与骨吸收增加和矿化减少有关，睾酮治疗可逆转这种情况，从而增加骨密度。关于男性原发性骨质疏松症治疗的公开信息很少。尽管降钙素、双膦酸盐和睾酮可能对男性骨质疏松症的治疗有效，但需要正式的临床试验加以证实。
