Laitinen K, Lamberg-Allardt C, Tunninen R, Karonen S L, Tähtelä R, Ylikahri R, Välimäki M
Research Unit of Alcohol Diseases, University of Helsinki, Finland.
N Engl J Med. 1991 Mar 14;324(11):721-7. doi: 10.1056/NEJM199103143241103.
Persons with chronic alcoholism frequently have hypocalcemia, hypomagnesemia, and osteoporosis. The short-term effects of alcohol ingestion on calcium and magnesium metabolism are poorly understood, however.
We measured serum calcium, magnesium, and phosphate concentrations in 17 normal men and 7 normal women before and at intervals up to 16 hours after the ingestion of 1.2 to 1.5 g of alcohol per kilogram of body weight over a 3-hour period (doses sufficient to cause acute intoxication). Urinary excretion of calcium, magnesium, and phosphate and serum calciotropic hormone levels were measured in 16 of these subjects. As a control, the same measurements were made after the ingestion of fruit juice instead of alcohol.
The mean (+/- SE) peak blood alcohol level in the men was 37.5 +/- 1.6 mmol per liter, and in the women it was 38.0 +/- 3.2 mmol per liter. In the men the mean serum parathyroid hormone concentration decreased from 16.1 +/- 2.1 to 6.8 +/- 0.9 ng per liter at the end of the three-hour drinking period. The value at this time was 30 percent of that at the end of the three-hour session during which the men drank fruit juice (P = 0.004). The serum concentration of ionized calcium reached a nadir eight hours after the beginning of alcohol administration (decreasing from 1.18 +/- 0.01 to 1.15 +/- 0.01 mmol per liter; P less than 0.001 as compared with values during the fruit-juice study), and urinary excretion of calcium increased from 0.34 +/- 0.08 to 0.36 +/- 0.08 mmol per hour (P less than 0.01 as compared with values during the fruit-juice study). Serum parathyroid hormone levels exceeded base-line values during the last 4 hours of the 16-hour study period; this increase was accompanied by a decrease in the urinary excretion of calcium. Both serum levels of magnesium (in the first 6 hours) and urinary levels (in the first 12 hours) increased after the ingestion of alcohol. In the women, serum parathyroid hormone levels decreased from 29.2 +/- 2.8 to 17.3 +/- 2.6 ng per liter two hours after the administration of alcohol was begun (P less than 0.001) and increased above base-line values during the last four hours of the study period. The serum concentration of ionized calcium decreased from 1.20 +/- 0.01 to 1.16 +/- 0.01 mmol per liter, reaching a nadir 8 to 12 hours after alcohol administration was begun (P less than 0.001).
Short-term alcohol administration causes transitory hypoparathyroidism. This decline in the secretion of parathyroid hormone accounts at least in part for the transient hypocalcemia, hypercalciuria, and hypermagnesuria that follow alcohol ingestion.
慢性酒精中毒患者常伴有低钙血症、低镁血症和骨质疏松症。然而,酒精摄入对钙和镁代谢的短期影响尚不清楚。
我们测量了17名正常男性和7名正常女性在3小时内每公斤体重摄入1.2至1.5克酒精(足以引起急性中毒的剂量)之前及之后长达16小时的血清钙、镁和磷酸盐浓度。对其中16名受试者测量了尿钙、尿镁、尿磷酸盐排泄量及血清钙调节激素水平。作为对照,在摄入果汁而非酒精后进行同样的测量。
男性的平均(±标准误)血酒精峰值水平为每升37.5±1.6毫摩尔,女性为每升38.0±3.2毫摩尔。在男性中,3小时饮酒期结束时,血清甲状旁腺激素平均浓度从16.1±2.1降至6.8±0.9纳克/升。此时的值是男性饮用果汁的3小时时段结束时的30%(P = 0.004)。酒精摄入开始8小时后,离子钙血清浓度降至最低点(从1.18±0.01降至1.15±0.01毫摩尔/升;与果汁研究期间的值相比,P<0.001),尿钙排泄量从0.34±0.08增加至0.36±0.08毫摩尔/小时(与果汁研究期间的值相比,P<0.01)。在16小时研究期的最后4小时,血清甲状旁腺激素水平超过基线值;这种升高伴随着尿钙排泄量的减少。酒精摄入后,血清镁水平(在前6小时)和尿镁水平(在前12小时)均升高。在女性中,酒精摄入开始2小时后,血清甲状旁腺激素水平从29.2±2.8降至17.3±2.6纳克/升(P<0.001),并在研究期的最后4小时升至基线值以上。离子钙血清浓度从1.20±0.01降至1.16±0.01毫摩尔/升,在酒精摄入开始8至12小时达到最低点(P<0.001)。
短期饮酒导致暂时性甲状旁腺功能减退。甲状旁腺激素分泌的这种下降至少部分解释了饮酒后随之出现的短暂性低钙血症、高钙尿症和高镁尿症。