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Alcohol‐Induced Bone Disease: Relationship to Age and Parathyroid Hormone Levels
Author(s) -
Bikle Daniel D.,
Stesin A.,
Halloran B.,
Steinbach L.,
Recker R.
Publication year - 1993
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1993.tb00821.x
Subject(s) - osteomalacia , parathyroid hormone , medicine , bone resorption , endocrinology , bone mineral , bone remodeling , resorption , bone density , vitamin d and neurology , osteoporosis , metabolic bone disease , osteopenia , calcium
Alcohol abuse leads to osteopenia and fractures. Epidemiological evidence suggests that older alcoholics are at substantially greater risk of fractures than younger alcoholics. To examine the interaction of age and alcohol abuse on bone mineral homeostasis, we studied 27 subjects with a history of 10 or more years of alcohol abuse ranging in age from 26–68 years. They were evaluated for disordered bone mineral homeostasis by assessing bone density (by quantitative computed tomography of the lumbar spine), histomorphometry of a transcortical biopsy from the iliac crest, serum levels of vitamin D metabolites and parathyroid hormone, and serum and urine levels of bone minerals. Seventeen of the subjects were found to have spinal compression fractures by routine radiologic procedures. The older the subject the more likely the subject was to have such a fracture. Bone densitometry indicated a marked reduction in spinal bone density with 15 subjects below 2 SD of normal aged‐matched controls. Bone density fell sharply with the age of the subject. Histomorphometry of iliac crest bone biopsies revealed no evidence of osteomalacia, but total resorption surfaces were increased. Consistent with the lack of osteomalacia were the normal levels of the vitamin D metabolites. The increased total resorption surfaces were correlated with high normal or elevated levels of parathyroid hormone as indicated both by radioimmunoassay and by urinary cAMP levels. Bone formation and active bone resorption (resorption surfaces containing osteoclasts) did not correlate with parathyroid hormone levels, however, but correlated negatively with age. Younger alcoholics tended to have increased bone remodeling, whereas older alcoholics tended to have suppressed bone remodeling out of proportion to the normal decline with age. We conclude that parathyroid hormone may play a role in stimulating bone resorption in younger alcoholics. With time the cumulative effects of alcohol abuse result in reduced bone resorption, as well as reduced bone formation, regardless of the levels of parathyroid hormone, ultimately leading to osteoporosis.

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