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Bone Disease in Alcohol Abuse

DANIEL D. BIKLE, M.D., Ph.D.; HARRY K. GENANT, M.D.; CHRISTOPHER CANN, Ph.D.; ROBERT R. RECKER, M.D.; BERNARD P. HALLORAN, Ph.D.; and GORDON J. STREWLER, M.D.
[+] Article and Author Information

Grant support: in part by a grant from the Veterans Administration, and grant AM 28116 from the National Institutes of Health.

▸Requests for reprints should be addressed to Daniel D. Bikle, M.D., Ph.D.; Veterans Administration Medical Center (111N), 4150 Clement Street; San Francisco, CA 94121.


San Francisco, California; and Omaha, Nebraska


© 1985 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1985;103(1):42-48. doi:10.7326/0003-4819-103-1-42
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We evaluated bone disease in eight white men between the ages of 49 and 61 years who had been abusing alcohol for at least 10 years. The mean density of vertebral cancellous bone was 58% of normal, whereas the mean density of appendicular cortical bone was 90% of normal. Marked reduction in active bone resorption and bone formation was seen without evidence of osteomalacia. Serum levels of calcium and magnesium were in the lower range of normal; serum levels of phosphorus, calcifediol, and calcitriol were normal; and serum levels of parathyroid hormone and nephrogenous cyclic adenosine monophosphate were in the higher range of normal. These data suggest that bone disease in these subjects is not due to inhibition of parathyroid hormone secretion or function, or abnormal vitamin D metabolism, but to an inhibition of bone remodeling by a mechanism independent of the calciotropic hormones.

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