Kalevi Laitinen , Riitta Tähtelä , Kimmo Luomanmäki , Matti J. Välimäki
{"title":"Mechanisms of hypocalcemia and markers of bone turnover in alcohol-intoxicated drinkers","authors":"Kalevi Laitinen , Riitta Tähtelä , Kimmo Luomanmäki , Matti J. Välimäki","doi":"10.1016/S0169-6009(08)80134-1","DOIUrl":null,"url":null,"abstract":"<div><p>Studies of hypocalcemia and osteoporosis frequently encountered in heavy users of alcohol have previously been performed on alcoholic people who have already recovered from alcohol intoxication. Bone and mineral metabolism during and after the intoxication may be different. We measured serum parameters of bone and mineral metabolism in 26 alcohol-intoxicated men and in 19 healthy control men. Although serum ionized calcium was 12% (<em>P</em> < 0.0001) lower in the patients than in the controls, serum intact parathyroid hormone was similar in the study groups. As reflected by decreased serum levels of osteocalcin (−43%; <em>P</em> < 0.001), bone formation was depressed in the patients. Serum cross-linked carboxyterminal telopeptide of human type I collagen (ICTP), a novel parameter of bone matrix degradation, was 9% higher in the patients (<em>P</em> = 0.03) than controls. The positive correlation between serum osteocalcin and ICTP in the controls (<em>r</em> = 0.59, <em>P</em> < 0.01) was absent in the patients (<em>r</em> = 0.05, <em>P</em> = 0.8). We conclude that in alcohol-intoxicated alcohol users, the parathyroid glands do not respond normally to a hypocalcemic stimulus, and that depressed bone formation is uncoupled from accelerated bone resorption.</p></div>","PeriodicalId":77047,"journal":{"name":"Bone and mineral","volume":"24 3","pages":"Pages 171-179"},"PeriodicalIF":0.0000,"publicationDate":"1994-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0169-6009(08)80134-1","citationCount":"36","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bone and mineral","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0169600908801341","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 36
Abstract
Studies of hypocalcemia and osteoporosis frequently encountered in heavy users of alcohol have previously been performed on alcoholic people who have already recovered from alcohol intoxication. Bone and mineral metabolism during and after the intoxication may be different. We measured serum parameters of bone and mineral metabolism in 26 alcohol-intoxicated men and in 19 healthy control men. Although serum ionized calcium was 12% (P < 0.0001) lower in the patients than in the controls, serum intact parathyroid hormone was similar in the study groups. As reflected by decreased serum levels of osteocalcin (−43%; P < 0.001), bone formation was depressed in the patients. Serum cross-linked carboxyterminal telopeptide of human type I collagen (ICTP), a novel parameter of bone matrix degradation, was 9% higher in the patients (P = 0.03) than controls. The positive correlation between serum osteocalcin and ICTP in the controls (r = 0.59, P < 0.01) was absent in the patients (r = 0.05, P = 0.8). We conclude that in alcohol-intoxicated alcohol users, the parathyroid glands do not respond normally to a hypocalcemic stimulus, and that depressed bone formation is uncoupled from accelerated bone resorption.