Abstract: Objective　To investigate the relationship between alcoholic osteoporosis and alcoholic liver disease and the pathogenesis. Methods　One hundred and twenty-two patients who had been drinking for over 5 years and who were treated at First Hospital and Second Hospital of Baotao Medical College, Inner Mongolia University of Science and Technology were retrospectively studied, and they were (40.0±14.6) years old. There were 82 males, who drank alcohol ≥ 40 g/d, and 40 females, who drank alcohol ≥ 20 g/d. The bone mineral density (BMD), liver function, osteocalcin, 25-hydroxyvitamin D [25(OH)D3], tumor necrosis factor α (TNF-α) were detected and liver color ultrasound examination was performed in all the patients. According to the BMD, liver function, and abdominal color ultrasound results, the patients were divided into an alcoholic osteoporosis group (35 cases), an alcoholic liver disease group (45 cases), and an alcoholic osteoporosis complicated with alcoholic liver disease group (42 cases). Forty-five healthy examinees of an age during the same period were selected as a healthy control group. SPSS 24.0 was used to analyze the data. t test was used for the measurement data. Results　The levels of osteocalcin in the alcoholic osteoporosis group, the alcoholic liver disease group, and the alcoholic osteoporosis complicated with alcoholic liver disease group were (24.73±3.66) μg/L, (27.34±2.94) μg/L, and (17.44±3.09) μg/L, and the levels of 25(OH)D3 were (22.47±2.82) μg/L, (25.63±3.84) μg/L, and (16.87±4.33) μg/L, which were lower than those in the healthy control group [(32.65±3.27) μg/L and (30.21±4.22) μg/L], and the levels of osteocalcin and 25(OH)D3 in the alcoholic osteoporosis complicated with alcoholic liver disease group were lower than those in the alcoholic osteoporosis group and the alcoholic liver disease group, with statistical differences (all P<0.05). The levels of osteocalcin and 25(OH)D3 in the alcoholic osteoporosis group were lower than those in the alcoholic liver disease group, but with no statistical differences (both P>0.05). The levels of TNF-α in the alcoholic osteoporosis group, the alcoholic liver disease group, and the alcoholic osteoporosis complicated with alcoholic liver disease group were (10.33±3.41) pg/ml, (13.23±4.02) pg/ml, and (16.94±3.92) pg/ml, which were higher than that in the healthy control group [(5.54±2.39) pg/ml], and the level in the alcoholic osteoporosis complicated with alcoholic liver disease group was higher than those in the alcoholic osteoporosis group and the alcoholic liver disease group, and the level in the alcoholic osteoporosis group was higher than that in the alcoholic liver disease group, with statistical differences (all P<0.05). Conclusions　We consider that alcoholic liver disease and alcoholic osteoporosis play a complementary role in the pathogenesis. Osteocalcin, 25(OH)D3, and TNF-α may be the common pathogenesis, which is not only the initial factor of the disease, but also the results.

Key words: Alcoholic osteoporosis, Alcoholic liver disease, Osteocalcin, 25-hydroxyvitamin D, Tumor necrosis factor α

摘要： 目的　探讨酒精性骨质疏松和酒精性肝病的关系及其发病机制。方法　回顾性研究2016年3月至2020年12月内蒙古科技大学包头医学院第二附属医院及第一附属医院收治的122例饮酒超过5年，折合乙醇量男性≥40 g/d，女性≥20 g/d的患者为研究对象，男82例，女40例，年龄（40.0±14.6）岁。所有患者测量骨密度，检测肝功能、骨钙素、25-羟基维生素D［25（OH）D3］、肿瘤坏死因子α（TNF-α）及肝脏彩超检查。根据骨密度检查结果、肝功能检测结果及腹部彩超分为3组，酒精性骨质疏松症组35例、酒精性肝病组45例、酒精性肝病合并骨质疏松症组42例。选择同期性别及年龄相匹配的体检健康者45例纳入健康对照组。采用SPSS 24.0进行数据分析，计量资料行t检验。结果　酒精性骨质疏松组、酒精性肝病组、酒精性肝病伴骨质疏松组的骨钙素分别为（24.73±3.66）μg/L、（27.34±2.94）μg/L、（17.44±3.09）μg/L，25（OH）D3分别为（22.47±2.82）μg/L、（25.63±3.84）μg/L、（16.87±4.33）μg/L，均不同程度地低于健康对照组［分别为（32.65±3.27）μg/L、（30.21±4.22）μg/L］，酒精性肝病伴骨质疏松组骨钙素、25（OH）D3均低于酒精性骨质疏松组和酒精性肝病组，差异均有统计学意义（均P<0.05），酒精性骨质疏松组骨钙素、25（OH）D3低于酒精性肝病组，但是差异均无统计学意义（均P>0.05）。酒精性骨质疏松组、酒精性肝病组、酒精性肝病伴骨质疏松组TNF-α分别为（10.33±3.41）pg/ml、（13.23±4.02）pg/ml、（16.94±3.92）pg/ml，均不同程度地高于健康对照组［（5.54±2.39）pg/ml］，酒精性肝病伴骨质疏松组高于酒精性骨质疏松组和酒精性肝病组，酒精性骨质疏松组低于酒精性肝病组，差异均统计学意义（均P<0.05）。结论　我们考虑酒精性肝病、酒精性骨质疏松在发病过程中呈相辅相成作用。骨钙素、25（OH）D3、TNF-α可能为其共同的发病机理，其既是发病的始动因素，又是其导致的结果。

关键词: 酒精性骨质疏松, 酒精性肝病, 骨钙素, 25-羟基维生素D, 肿瘤坏死因子α