Alcohol‐induced bone disease in the absence of severe chronic liver damage

Adolfo Díez, Jordi Puig, Sergi Serrano, Maria‐Lluisa ‐L Marin̄oso, Jaume Bosch, Jaume Marrugat, Leonardo Mellibovsky, Xavier Nogués, Hernando Knobel, Jaume Aubía

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Abstract

To define and identify metabolic bone disease and mineral alterations induced by chronic heavy alcoholism in patients without severe liver damage, we studied a prospective series of unselected patients admitted to a 300‐bed general hospital in Barcelona (Spain). A total of 26 chronic heavy drinkers of more than 150 g/day for at least 3 years were included. A general analytic and hormonal study, including liver biopsy in cases with any abnormality in liver function tests, and plasma and urine biochemistry with calcium regulating hormones and osteocalcin levels were determined. A transiliac bone biopsy after double‐tetracycline labeling, with histomorphometric study of undecalcified bone, was performed. Statistical analysis was adjusted by age and sex by means of logistic regression. A total of 26 (20 men and 6 women) chronic alcohol abusers were studied. After adjustment for age and sex, alcoholic patients showed slight but significantly increased concentrations of plasma calcium (9.56 ± 0.56; OR = 17.93; 95% CI 3.17–101.48) and decreased cPTH (0.36 ± 0.11; OR = 0.097;95% CI 0.018–0.528) compared with controls. Osteocalcin values were low (1.49 ± 0.89, normal range 1.8–6.6). There was a significant decrease in bone volume, BV/TV (12.56 ± 5.29; OR = 0.06; 95% CI 0.01–0.34), with increased resorption surfaces, ES/BS (4.28 ± 2.43; OR = 9.86; 95% CI 2.16–45.07), and increased osteoclast number, N.Oc/TA (0.21 ± 0.37; OR = 6.41; 95% CI 1.27–32.25). Dynamic parameters were abnormal (Fisher's exact test), as follows: decreased BFR/BS (0.023 ± 0.028 versus 0.049 ± 0.020; p = 0.013), MAR (0.309 ± 0.269 versus 0.771 ± 0.529; p = 0.029), MS/BS (3.743 ± 4.433 versus 5.890 ± 2.882; p = 0.008, and OMR (2.402 ± 2.833 versus 3.057 ± 0.083; p = 0.011) and increased MLT (175.80 ± 405.49 versus 34.53 ± 8.117; p = 0.008). We conclude that chronic alcohol consumption induces osteopenia with low turnover and increased osteoclast number and resorption surfaces. The increase in plasma calcium levels and decreased PTH suggests a primary effect of alcohol on bone, resulting in bone loss and calcium infusion from bone into plasma. These effects were observed in the absence of significant liver damage. Copyright © 1994 ASBMR
Original languageEnglish
Pages (from-to)825-831
JournalJournal of Bone and Mineral Research
Volume9
Issue number6
DOIs
Publication statusPublished - 1 Jan 1994

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