男性骨质疏松症临床研究最新进展

男性骨质疏松症常被忽视,但男性骨质疏松性骨折的死亡率比女性高,且男性诊断骨质疏松症的T值和BMD范围等还存在不同意见。我们综述近几年来男性骨质疏松症临床研究最新进展,包括：男性骨质疏松性骨折的流行病学、男性骨质疏松症的病因、诊断、预防和治疗以及近年来的骨质疏松临床指南。并提出我们的建议,以期提高临床医师的重视。     

老年男性骨质疏松症药物治疗的现状调查

目的通过调查老年男性骨质疏松症(OP)患者的药物治疗现状,来寻找提高老年男性OP患者药物治疗率的方法。方法对478例老年(≥70岁)男性进行问卷调查和骨密度检测,并调查OP患者的用药情况,然后进行统计分析。结果老年男性OP发病率高达25.31%,但OP患者的药物治疗率仅为18.48%。医患双方OP防治知识欠缺,老年男性OP患者用药依从性低、治疗药物匮乏。结论老年男性OP患者药物治疗率很低,而加强OP防治知识的宣教,提高OP患者的用药依从性,不断丰富抗OP的药物种类,可能是目前提高老年男性OP患者药物治疗率的主要方法。     

男性骨质疏松症与睾酮关系的研究进展

随着老龄人口的增加,男性骨质疏松症和睾酮缺乏越来越常见。近年来研究表明,睾酮水平与男性骨质疏松症的发生密切相关,睾酮缺乏的患者发生骨质疏松症及骨折的风险增加。睾酮可通过雄激素受体和雌激素受体调节骨代谢,且睾酮替代治疗可以有效增加男性骨密度,降低发生骨质疏松症的风险。本文回顾最近的文献,就睾酮与骨质疏松症的关系做一综述。     

性激素与男性骨质疏松症

随着人口平均寿命的延长，男性骨质疏松症（male osteoporosis，MOP）发病率呈明显升高的趋势，逐渐受到人们的关注，其发生机制目前尚未完全明了。酒精的滥用、长期的糖皮质激素的使用、性功能低下被认为是男性骨质疏松症发生的三个主要因素，尤其是性功能低下是男性骨质疏松症发生的重要原因之一。     

雄激素与男性骨质疏松症

男性也有更年期，年龄大约在40～55岁。男性更年期的发生虽然也源于雄激素下降，但与女性有所不同。男性雄激素的分泌始终没有完全停止，只是随着增龄，分泌下降而已。因而，确切的说，男性更年期应称为“部分雄激素缺乏综合征”（PADAM）。     

雄激素与男性骨质疏松症

男性体内雄激素水平随年龄的增长而下降。研究证实男性骨质疏松组雄激素明显低于非骨质疏松组。雄激素替代治疗可以增加骨形成、减少骨吸收，同时也带来一些存在争议的副作用。     

雄激素与男性骨质疏松症

男性体内雄激素水平随年龄的增长而下降。研究证实男性骨质疏松组雄激素明显低于非骨质疏松组。雄激素替代治疗可以增加骨形成、减少骨吸收，同时也带来一些存在争议的副作用。     

阿仑膦酸钠治疗男性骨质疏松症的临床研究

目的 观察阿仑膦酸钠治疗男性骨质疏松症的疗效和安全性。方法 ３７例男性骨质疏松症患者,选用阿仑膦酸钠治疗６个月。比较治疗前后患者疼痛、骨密度、血生化指标和副反应的变化。结果 经６个月治疗后,患者疼痛明显改善,腰椎、股骨颈和髋部骨密度增加,尿钙与尿肌酐比值（Ｃａ／Ｃｒ）及尿羟脯氨酸与尿肌酐比值（Ｈｏｐ／Ｃｒ）降低,副反应轻微且耐受性好。结论 阿仑膦酸钠治疗男性骨质疏松症疗效显著、安全性好。     

男性骨质疏松症诊治现状与进展

骨质疏松症（osteoporos is,OP）是一种以骨量减少、质量改变、骨强度降低、脆性增加及易致骨折为主要特征的全身性的代谢性骨病。随着社会人口结构的老龄化,骨质疏松症的诊治问题已成为当前国内外医学界研究的热门课题。以往骨质疏松症被视为女性疾病,一般都认为男性骨质疏松的发病率低于绝经后女性,故对男性骨质疏松的重视程度不及女性患者,大量男性骨质疏松症患者未得到及时诊断和治疗。近年来研究证实,尽管男性在青年时期比女性有更高的峰值量,骨量丢失开始的时间也比女性迟,但其危害性和死亡率却高于女性[1]。虽然近年来针对男性骨质疏松症的研究逐渐增多,但其发病机制、诊断和治疗标准尚无定论。     

男性骨质疏松症:诊断和治疗

一、诊断方法及其诊断意义凡符合下述3条之一者作骨密度检查:①轻微外伤后骨折,查体发现脊椎骨折。②骨Ｘ线片的骨质丢失征象。③相关于骨质疏松的各种危险因子。骨密度(ＢＭＤ)正常者应定期随访复查ＢＭＤ。ＢＭＤ降低值>10ＳＤ者,仍缺乏合理诊断的,称为“特发性骨质疏松”,可以考虑骨活检,也可考虑作经验性治疗。Ｔ值(Ｔｓｃｏｒｅ)是男或女性骨峰值的标准差(ＳＤ)。各国均借用ＷＨＯ关于女性骨质疏松的定义,男性骨密度减少量≤10ＳＤ者为正常;>10ＳＤ为骨量减少;≥25ＳＤ为骨质疏松症,伴1个以上部位骨折为严重骨质疏松。1病史、查体、常…     

利塞膦酸钠不同给药方式治疗男性骨质疏松症疗效分析

【摘要】〓目的〓观察利塞膦酸钠不同给药方式在男性骨质疏松症治疗中的疗效和耐受性。方法〓共纳入72例男性骨质疏松症患者,其中38例为口服利塞膦酸钠每日5 mg;34例为每周35 mg口服,随访1年。分别测定两组患者治疗前后L1~L4椎体骨密度值和骨转化指标,并观察两组骨质疏松性骨折的发生率及服药后的不良反应。结果〓口服利塞膦酸钠治疗后,患者L1~L4椎体和股骨颈的骨密度值较治疗前上升显著,每日口服组和每周口服组间比较无统计学差异(P>0.05);两组间的骨转化指标和骨折发生率亦无统计学差异。结论〓观察口服利塞膦酸钠治疗后1年,每周口服35 mg与每日口服5 mg比较,均能有效地提高骨质量。     

Two cases of male hypogonadal osteoporosis

Two males with bone abnormalities associated with hypogonadotropic hypogonadism are reported. Case 1, 28 years old male, developed growth disturbance at the age of eight years, after suffering from tuberculous meningitis. No secondary sex characteristics appeared and fractures occurred at five times. Case 2, 29 years old male, also suffered from growth disturbance from around the age of 6 years, without appearance of secondary sex characteristics even after puberty. Bone X-ray studies and bone biopsy revealed marked osteoporosis in Case 1, while in Case 2, slipped capital femoral epiphysis was also noted with mild osteoporosis. In these two cases, osteoporosis is associated with eunuchoidism, in agreement of the concept of so-called “male hypogonadal osteoporosis”. Both patients showed insufficient secretion of somatomedin C, testosterone and growth hormone (GH) with insulin tolerance test and arginine tolerance test. The insufficient secretion of LH and FSH with LH-RH tolerance test was also revealed in both cases. The decrease of GH and somatomedin C was quite pronounced in Case 1, whereas the fall of testosterone was more conspicuous in Case 2. The imbalance between these hormone deficiencies might lead to different expression of bone abnormalities.     

Dried plum prevents bone loss in a male osteoporosis model via IGF-I and the RANK pathway

Previously, dietary supplementation with dried plums, a rich source of polyphenolic compounds with antioxidant and anti-inflammatory properties, has been shown to improve bone density, microstructure and biomechanics in female animal models of osteopenia. We designed this study to determine the extent to which dried plum prevents skeletal deterioration in gonadal hormone deficient male animals and to begin to understand its mechanism of action. Sixty 6-month-old male Sprague–Dawley rats were either sham-operated (Sham = 1 group) or orchidectomized (ORX = 4 groups) and randomly assigned to dietary treatments: standard semi-purified diet (Control) with either LD = 5%, MD = 15%, or HD = 25% (w/w) dried plum for 90 days. At the end of the treatment period, both the MD and HD dried plum completely prevented the ORX-induced decrease in whole body, femur, and lumbar vertebra bone mineral density (BMD). Biomechanical testing indicated that the MD and HD of dried plum prevented the ORX-induced decrease in ultimate load of the cortical bone as well as the compressive force and stiffness of trabecular bone within the vertebrae. Analyses of trabecular microarchitecture of the distal femur metaphysis and vertebral body revealed that HD dried plum protected against the decrease in trabecular bone volume (BV/TV) induced by ORX. In the distal femur, all doses of dried plum improved trabecular number (TbN) and separation (TbSp) compared to the ORX-control group, while MD and HD dried plum prevented the ORX-induced changes in vertebral TbN and TbSp. At the end of the 90-day treatment, no remarkable changes in serum osteocalcin or alkaline phosphatase in any of the treatment groups were observed, while serum insulin-like growth factor (IGF)-I was increased by dried plum. The ORX-induced increase in urinary deoxypyridinoline (DPD) excretion was completely prevented by all doses of dried plum coinciding with down-regulation of gene expression for receptor activator of NFκ-B ligand (RANKL) and osteoprotegerin (OPG) in the bone. We conclude that dried plum prevents osteopenia in androgen deficient male rats, and these beneficial effects may be attributed in part to a decrease in osteoclastogenesis via down-regulation of RANKL and stimulation of bone formation mediated by IGF-I.     

绝经后骨质疏松症的临床中药治疗进展

绝经后骨质疏松症(postmenopausal osteoporosis, PMOP)是绝经后妇女的常见病及多发病, 主要因绝经后妇女的卵巢功能减退、雌激素水平下降,导致骨生成和骨吸收的代谢失衡。其特征是全身骨量减少和骨组织的微细结构破坏,临床主要表现为骨痛和骨折风险增加。大量研究表明,中医药可以提高绝经后骨质疏松症患者的骨密度,改善其疼痛症状,在防治绝经后骨质疏松症方面有其独特的优势。目前对绝经后骨质疏松症的研究主要分为单味中药的实验研究和复方中药的临床研究。通过对近5年国内外对绝经后骨质疏松症的中药治疗进行相关回顾,在单味中药方面,根据绝经后骨质疏松症的病机特点和用药频次,主要从骨测量指标、细胞因子变化、基因水平等方面综述了淫羊藿、杜仲、骨碎补3种常用中药的实验研究进展;在复方中药方面,普遍认为肾虚是绝经后骨质疏松的主要病机,此外与肝脾不足、血瘀痰浊等密切相关,主要论述了补肾法在临床上治疗绝经后骨质疏松中的应用,并探讨未来治疗绝经后骨质疏松症可能的研究方向。     

原发性骨质疏松症慢性疼痛的康复治疗进展

原发性骨质疏松症(primary osteoporosis,POP)是以低骨量及骨组织微结构退化为特征的一种全身性骨病,伴有骨脆性增加,且容易发生骨折,是绝经后女性及老年人的常见病、多发病。疼痛是本病最典型的临床表现和首要就诊原因,其中70%～80%的患者表现为腰背痛,对老年人的生活质量产生了严重影响。目前很多学者从中西医康复治疗的角度进行了临床报道,虽各具特色,但疗效不一。本文就其康复治疗的最新进展进行综述。     

儿童骨质疏松的诊疗进展

骨质疏松症属代谢性骨病范畴,常见于老年人,儿童骨质疏松相对少见但更值得关注。在病因学上同样分为原发性和继发性,原发性主要见于潜在遗传性疾病的儿童,而继发性主要起因于慢性病及其相关治疗。既往骨折史以及后背痛常提示骨质疏松的存在,而在影像学上骨皮质变薄或低骨密度同样预示着骨折的风险。儿童骨质疏松的诊断工具优选双能X线骨密度仪,对于那些处于继发性骨质疏松风险的儿童,要保持高度警惕,而对于那些已经罹患骨质疏松的儿童,应尽量避免或减少可能进一步损伤骨骼的因素,以及尽早给予充足的钙及维生素D。治疗重点应侧重于改善功能结局,同时也应认识到生长发育期本身椎体重塑或症状自发缓解的可能性,因此应尽量避免不必要的治疗。双膦酸盐目前为治疗首选,但在儿童骨质疏松中证据有限,长期应用的时间及剂量仍有争议。尽管目前抗骨吸收的药物有很多种,但仍缺乏促进骨形成药物的研究,希望未来有更多适合儿童骨质疏松治疗的证据来填补这个空缺。     

Sex hormone-binding globulin, estradiol, and bone turnover markers in male osteoporosis

The role of estrogen deficiency in male osteoporosis is still under discussion. One hundred five subjects, 65 of them suffering from osteoporosis (mean age, 53.9 years) and 40 age-matched controls were studied. Osteoporosis was defined by a T score < −2.5 in the lumbar spine or at the femoral neck. Forty-one (63.1%) of the subjects had a history of low-energy fractures, involving vertebrae in 33 cases (50.8%). Osteoporosis was considered to be idiopathic in 33 subjects (50.8%) for whom no etiology could be found. We measured levels of total estradiol (pg/ml, with a detection threshold of 4 pg/ml), total testosterone (ng/ml), and their carrier protein, that is, sex hormone-binding globulin (SHBG, pmol/ml). Various markers of bone remodeling were also measured. Two of them provide an estimate of bone formation—osteocalcin (OC) and bone alkaline phosphatase (BAP). Two others evaluate bone resorption—procollagen type I C-terminal telopeptide (ICTP) and serum C-telopeptide of type I collagen (sCTX).

There was no significant difference in estradiol levels between controls and osteroporosis patients. We did not find any significant correlation between estradiol levels and spinal bone mineral density (BMD) (r = 0.15, P > 0.05), and the relationship between estradiol levels and BMD at the femoral neck was weak (r = 0.25, P < 0.05). On the other hand, SHBG was significantly higher in the osteoporotic patients than in controls (P < 0.01). This difference persisted after adjustment for body mass index (BMI) and after exclusion of patients with a condition known to increase SHBG levels. Moreover, this carrier protein was negatively correlated with BMD at the femoral neck (r = −0.37, P < 0.01) and at the lumbar spine (r = −0.27, P < 0.05). SHBG also correlates strongly with sCTX (r = 0.37, P < 0.01). Finally, logistic regression analysis showed that serum SHBG concentration was significantly associated with the presence of fractures; the odds ratio of having a fracture was 2.04 [95% confidence interval (CI) 1.2–3.4, P < 0.01] for each increase of 1 standard deviation (SD) in the patient's SHBG level. The stronger relationship was nearly the same for the whole group and for patients with idiopathic osteoporosis.

This study therefore suggests that SHBG may play a key role in male patients with idiopathic or secondary osteoporosis. It shows that serum SHBG concentration is increased in middle-aged men with osteoporosis and is correlated with hip, spine BMD, and sCTX levels. Finally, our findings are in agreement with previous studies which suggest that serum SHBG is a new biological marker of fracture risk in men.     

男性老年性骨质疏松与血清TGF-β1、性激素水平的相关性

目的探讨转化生长因子β1(TGFβ1)、性激素与男性老年性骨质疏松的相关性。方法用ELISA法测定男性老年性骨质疏松组20例,与年龄相匹配的骨量减少组26例,非骨质疏松组26例的血清TGFβ1水平,同时用IRMA法测定其睾酮(T)、雌二醇(E2)水平。用双能X线骨密度仪测定腰椎及股骨的骨密度及骨矿含量。结果男性老年性骨质疏松组及骨量减少组TGFβ1含量明显低于老年男性非骨质疏松组(含量分别为9.68±7.77ngmL、8.82±6.55ngmL、16.76±8.15ngmL,P<0.05)。男性老年性骨质疏松组及骨量减少组血清E2明显低于老年男性非骨质疏松组(含量分别为26.16±13.14pmolL、26.14±11.2pmolL、40.69±13.87pmolL,P<0.05)。男性老年性骨质疏松组与骨量减少组TGFβ1、E2含量比较,差别无显著意义。3组之间两两比较T的含量差别均无显著意义。骨质疏松组、骨量减少组及非骨质疏松组腰椎、股骨各个测量部位的骨密度及骨矿含量与血清TGFβ1、E2均呈正相关,而与T不相关。TGFβ1与E2呈正相关。结论男性老年性骨质疏松与雌激素缺乏、TGFβ1降低有关。雌激素可能通过TGFβ1影响骨代谢。