Gonzalez-Calvín J L, Garcia-Sanchez A, Bellot V, Muñoz-Torres M, Raya-Alvarez E, Salvatierra-Rios D
Department of Internal Medicine, University of Granada Hospital, Spain.
Alcohol Alcohol. 1993 Sep;28(5):571-9.
The role of ethanol as a risk factor for osteopenia was studied in alcoholic subjects without liver cirrhosis. The study was carried out in 58 male subjects classified into three groups: (1) 26 heavy drinkers, alcohol intake more than 100 g ethanol/day for more than 10 years; (2) 13 moderate drinkers, 60-100 g ethanol/day; (3) 19 healthy non-drinkers who served as control subjects. None of the drinkers had liver cirrhosis (normal clinical and biochemical data and/or liver biopsy). Mineral metabolism and serum bone Gla-protein (BGP) were studied while they were active drinkers and after they had abstained from ethanol for 7 days. Bone mineral density (BMD) was determined at the beginning of the study. Osteopenia was observed in 23% of the heavy drinkers. We found a significant inverse correlation between BMD and an index of cumulative alcohol intake. Heavy and moderate drinkers had significantly lower mean BGP values (1.6 +/- 0.4 and 1.9 +/- 0.3 ng/ml) (P < 0.01 for both) than controls (3.5 +/- 0.4 ng/ml); these values increased significantly (2.9 +/- 0.4 ng/ml; P < 0.01) after 7 days of abstinence. The data show that chronic ethanol ingestion can induce osteopenia regardless of the absence of liver cirrhosis, and that some relationship can be expected between the amount and duration of ethanol consumption and the degree of bone loss. The low serum BGP levels in drinkers are reversible upon withdrawal of ethanol, suggesting that reduction of osteoblastic activity is probably the main factor responsible for alcohol-associated bone disease.
在无肝硬化的酗酒者中研究了乙醇作为骨质减少危险因素的作用。该研究对58名男性受试者进行，分为三组：（1）26名重度饮酒者，乙醇摄入量超过100克/天，持续超过10年；（2）13名中度饮酒者，乙醇摄入量为60 - 100克/天；（3）19名健康非饮酒者作为对照。所有饮酒者均无肝硬化（临床和生化数据正常及/或肝活检正常）。在他们饮酒期间及戒酒7天后研究了矿物质代谢和血清骨钙素（BGP）。在研究开始时测定骨密度（BMD）。在23%的重度饮酒者中观察到骨质减少。我们发现BMD与累积酒精摄入量指数之间存在显著负相关。重度和中度饮酒者的平均BGP值（分别为1.6±0.4和1.9±0.3纳克/毫升）（两者P均<0.01）显著低于对照组（3.5±0.4纳克/毫升）；戒酒7天后这些值显著升高（2.9±0.4纳克/毫升；P<0.01）。数据表明，无论有无肝硬化，慢性乙醇摄入均可诱发骨质减少，并且乙醇摄入量和持续时间与骨质流失程度之间可能存在某种关系。饮酒者血清BGP水平低在戒酒时是可逆的，提示成骨细胞活性降低可能是酒精相关骨病的主要原因。
