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MINERAL METABOLISM, OSTEOBLASTIC FUNCTION AND BONE MASS IN CHRONIC ALCOHOLISM

JORGE L. GONZALEZ-CALVIN, ANTONIO GARCIA-SANCHEZ, VICENTE BELLOT, MANUEL MUNOZ-TORRES, ENRIQUE RAYA-ALVAREZ, DOMINGO SALVATIERRA-RIOS
DOI: http://dx.doi.org/ 571-579 First published online: 1 September 1993

Abstract

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.