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Alcohol‐induced bone disease in the absence of severe chronic liver damage
Author(s) -
Díez Adolfo,
Puig Jordi,
Serrano Sergi,
Marin̄oso MariaLluisa,
Bosch Jaume,
Marrugat Jaume,
Mellibovsky Leonardo,
Nogués Xavier,
Knobel Hernando,
Aubía Jaume
Publication year - 1994
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650090608
Subject(s) - medicine , osteocalcin , endocrinology , gastroenterology , chronic liver disease , bone resorption , bone disease , prospective cohort study , bone remodeling , calcium , cirrhosis , osteoporosis , chemistry , alkaline phosphatase , biochemistry , enzyme
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.