Original Article
Transient Hypoparathyroidism during Acute Alcohol Intoxication
N Engl J Med 1991; 324:721-727March 14, 1991
- Abstract
- Abstract
Background.
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.
Methods.
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.
Results.
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<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<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<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<0.001 ).
Conclusions.
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. (N Engl J Med 1991; 324:721–7.)
Media in This Article
Figure 1
Mean (±SE) Serum Concentrations of Parathyroid Hormone during the Alcohol and Control Studies in Nine Normal Men.Figure 2
Mean (±SE) Serum Concentrations of Ionized Calcium (9 Subjects) and Total Calcium (17 Subjects) and Urinary Excretion of Calcium (9 Subjects) during the Alcohol and Control Studies in Normal Men.Article Activity
- Article
HYPOCALCEMIA and hypomagnesemia are frequently encountered in heavy users of alcohol.1 2 3 4 5 These changes have been ascribed to concomitant hypoalbuminemia,3 poor nutrition, and increased urinary and intestinal loss of calcium and magnesium.6 , 7 Hypocalcemia in alcoholics also has been ascribed to impaired intestinal calcium absorption8 9 10 due to hypovitaminosis D,2 , 11 12 13 hypoparathyroidism, and parathyroid hormone resistance resulting from severe magnesium deficiency.14 , 15
Despite the frequent occurrence of hypocalcemia and hypomagnesemia in persons with chronic alcoholism, the role of alcohol itself in their development has remained obscure. The few controlled studies of the effects of short-term alcohol ingestion on calcium and magnesium metabolism in healthy subjects6 , 7 , 16 17 18 19 20 have consistently shown that alcohol increases urinary excretion of calcium and magnesium,6 , 7 but there is no consensus about the changes in serum calcium and magnesium concentrations.6 , 16 17 18 19 In particular, the role of parathyroid hormone in the changes observed in serum and urinary calcium and magnesium levels after the short-term administration of alcohol is poorly understood. Detailed knowledge of the short-term effects of alcohol on the metabolism of calcium, magnesium, and parathyroid hormone could be of particular importance in elucidating the mechanisms underlying the bone disease associated with alcohol abuse.21 22 23 24 We therefore performed a controlled study in normal men and women to determine the short-term effects of alcohol on calcium and magnesium metabolism and on the levels of parathyroid hormone, vitamin D, and calcitonin. Our results suggest that short-term alcohol administration causes transitory hypoparathyroidism, thereby leading to hypocalcemia, hypercalciuria, and hypermagnesuria.
Methods
Subjects and Study Design
We studied 17 normal men (age range, 21 to 35 years; mean, 25) and 7 normal women (age range, 20 to 42 years; mean, 27) with a daily alcohol consumption of one to two drinks. The subjects were asked to abstain from alcohol for one week before the study. None were taking any drugs at the time of the study. All the subjects took part in two study sessions, one involving the ingestion of alcohol and the other the ingestion of fruit juice, in random order. The interval between these sessions was at least two weeks for the men. The women were studied during the early follicular phase of two successive menstrual cycles; the interval between the alcohol and control sessions was four weeks. The study protocol was approved by the university ethics committee, and each subject gave informed consent.
On each study day, the participants had lunch between 2 and 3 p.m. Before both studies the women were served meals in the metabolic ward that contained identical amounts of carbohydrate, protein, calcium, and magnesium. The men did not eat in the metabolic ward but were asked to eat the same meal before both studies. All studies were begun at 6 p.m. During each session participants drank either alcohol (1.5 g per kilogram of body weight for men and 1.2 or 1.4 g per kilogram for women) as a 15 percent (vol/vol) solution in fruit juice or an equal volume (10 ml per kilogram) of fruit juice containing no alcohol. The drinks were consumed at regular intervals during a three-hour period from 6 to 9 p.m. The doses of alcohol were equivalent to four to nine "standard" drinks (15 g) and sufficient to cause acute intoxication. The fruit-juice solution contained 0.70 mmol of calcium per liter (28 mg per liter) and 0.58 mmol of magnesium per liter (14 mg per liter). At 10 p.m. a test dose of strontium (see below) was given to eight of the men with a standard meal containing 50 mg of calcium and 44 mg of magnesium. The women were given the standard meal but no strontium. At midnight the subjects drank 250 ml of orange juice containing 0.5 mmol (20 mg) of calcium and 1.2 mmol (30 mg) of magnesium. No other meals were served. The subjects were allowed to sleep or move about in the hospital ward.
Blood samples were collected twice at base line (before the ingestion of alcohol or juice), every hour from 7 p.m. to 10 p.m., and then at midnight, 2 a.m., 6 a.m., and 10 a.m. In the samples from nine of the men and all seven women, alcohol concentrations and serum concentrations of total and ionized calcium, magnesium, phosphate, parathyroid hormone, and osteocalcin were measured. Samples were also collected from these nine men for the measurement of serum calcitonin, 25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, and insulin-like growth factor I. In the other eight men, only serum levels of total calcium, magnesium, and phosphate were measured in the samples collected at these times. The results were similar in both groups of men, and therefore the values for the two groups were combined. Intravenous cannulas and evacuated blood-collecting tubes (Terumo Europe N.V., Leuven, Belgium) were used for the blood sampling. Urine was collected from nine men and all seven women from 4 to 6 p.m., 6 to 9 p.m., 9 p.m. to midnight, midnight to 7 a.m., and 7 to 10 a.m. for the determination of the urinary excretion of calcium, magnesium, phosphate, and creatinine.
Laboratory Analysis
Serum and urinary calcium, magnesium, and phosphate, as well as urinary creatinine, were measured by methods routinely used in clinical laboratories. Blood alcohol concentrations were measured by head-space gas chromatography as described by Eriksson et al.25 For the determinations of serum levels of ionized calcium, the blood samples were centrifuged immediately after they were drawn and the serum was analyzed with an ion-selective analyzer (Microlyte, Kone, Helsinki, Finland) within a half-hour of blood collection (intraassay coefficient of variation, 1.6 percent). The samples were handled anaerobically to avoid alterations in the partial pressure of carbon dioxide. In the men, intact parathyroid hormone in the serum was measured with an immunoradiometric-assay26 kit from Incstar (Stillwater, Minn.); in the women it was measured with kits obtained from the Nichols Institute (San Juan Capistrano, Calif.). The addition of alcohol in a concentration of 44 mmol per liter to five serum samples did not alter the parathyroid hormone concentration in either assay. Serum 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol were measured as described previously,27 and serum osteocalcin, calcitonin, and insulin-like growth factor I were measured with radioimmunoassay kits obtained from Compagnie Oris Industrie (Cedex, France), the Nichols Institute, and Incstar, respectively. All samples from an individual subject were analyzed in duplicate at the same time in each assay. The intraassay and interassay coefficients of variation for these assays ranged from 3 to 14 percent and from 6 to 15 percent, respectively.
The intestinal absorption of strontium reflects that of calcium,28 even though the renal and skeletal disposal of the two elements differs. The absorption of strontium was measured according to the method of Milsom et al.28: 2.5 mmol of stable strontium chloride was administered to eight of the men in 200 ml of distilled water, and blood was sampled four hours later. The strontium concentration was measured in a single assay with an atomic absorption spectrophotometer (Perkin-Elmer 603, Norwalk, Conn.) at 460.7 nm; a lanthanum chloride—hydrochloric acid diluent was used to prevent interference from phosphate. The intraassay coefficient of variation was 1.8 percent (at a level of 20 μmol per liter). The Spearman rank-correlation coefficient for the intestinal absorption of strontium and of carbon-47 was found to be 0.86 (P = 0.0006) in a group of 10 additional normal men (age, 21 to 33 years) given 10 μCi of carbon-47, with 20 mg of calcium chloride as a carrier, together with the dose of strontium. The reproducibility of the strontium-absorption test was studied by repeating the test in the same subjects five weeks later. The Spearman rank-correlation coefficient for the results of two tests was also 0.86 (P = 0.0006).
Statistical Analysis
The data are expressed as means ±SE. The mean of the first two blood samples was used as the base-line value for each subject. To study each variable, the two test periods (alcohol ingestion and fruit-juice ingestion) were first compared by analysis of variance with repeated measures. If a statistically significant difference (P<0.05) was found, Student's paired t-test (normal distribution) or the Wilcoxon matched-pairs test (non-normal distribution) was used to study the significance of the differences in the same variable at each time point. Spearman rank correlations were used to analyze the degree of dependence between variables. These analyses were performed with BMDP statistical programs and a VAX/VMS minicomputer.29
Results
The mean blood alcohol concentration reached a peak of 37.5±1.6 mmol per liter in the men and 38.0±3.2 mmol per liter in the women (Table 1Table 1
Mean Blood Alcohol Concentrations in Normal Men and Women before, during, and after the Ingestion of Alcohol.*) four hours after the administration of alcohol was begun. As shown for men in Figures 1Figure 1Mean (±SE) Serum Concentrations of Parathyroid Hormone during the Alcohol and Control Studies in Nine Normal Men. 2Figure 2Mean (±SE) Serum Concentrations of Ionized Calcium (9 Subjects) and Total Calcium (17 Subjects) and Urinary Excretion of Calcium (9 Subjects) during the Alcohol and Control Studies in Normal Men. 3Figure 3
Mean (±SE) Serum Concentrations of Magnesium (17 Subjects) and Urinary Excretion of Magnesium (9 Subjects) during the Alcohol and Control Studies in Normal Men. 4Figure 4
Mean (±SE) Serum Concentrations of Phosphate (17 Subjects) and Urinary Excretion of Phosphate (9 Subjects) during the Alcohol and Control Studies in Normal Men. and for women in Tables 2Table 2
Mean Serum Concentrations of Parathyroid Hormone, Ionized Calcium, Magnesium, and Phosphate during the Control and Alcohol Studies in Seven Normal Women.* and 3Table 3
Mean Urinary Excretion of Calcium, Magnesium, and Phosphate in Seven Normal Women during the Control and Alcohol Studies.*, the basal levels of all variables measured in serum and urine were similar during both sessions. In addition, the urinary excretion of creatinine was similar at all times during both studies (data not shown).Studies in Men
During the alcohol-ingestion phase of the study, the mean serum parathyroid hormone concentration decreased from 16.1±2.1 to 6.8±0.9 ng per liter, reaching a nadir in three hours. The value at that time was 30 percent of that during the control session (P<0.004) (Fig. 1). It then increased above the baseline level and was 34 and 52 percent higher (P<0.05) than the corresponding control values 12 and 16 hours, respectively, after alcohol ingestion began (Fig. 1).
The decrease in the serum concentrations of ionized calcium (from 1.18±0.01 to 1.15±0.01 mmol per liter) after alcohol ingestion occurred after the serum parathyroid hormone concentration had decreased, and the levels were lower than the values after fruit-juice ingestion from six hours onward (Fig. 2). The change in serum total calcium concentrations followed a similar pattern, although the levels were significantly lower than in the control study only at 8 and 12 hours (Fig. 2). The urinary excretion of calcium was two-fold higher during the ingestion of alcohol than during the ingestion of fruit juice (P<0.01), and it remained so for three hours after the administration of juice or alcohol had stopped (P<0.05) (Fig. 2). At the time of the rebound increase in serum parathyroid hormone concentration, the urinary excretion of calcium was lower than during the control study (P<0.01) (Fig. 2). The intestinal absorption of calcium, as measured by the stable-strontium assay, was similar after alcohol ingestion or fruit-juice ingestion.
After alcohol ingestion, the mean serum magnesium concentration increased, reaching a maximum at four hours, when it was 7.9 percent higher than during the control study (P<0.05) (Fig. 3). It then declined gradually (Fig. 3). The changes in the urinary excretion of magnesium were similar to those in the urinary excretion of calcium. As compared with the values during the control study, magnesium excretion was two to three times higher during and three hours after the ingestion of alcohol (P<0.01), but at the end of the study the situation was reversed (P<0.05) (Fig. 3).
During alcohol ingestion the serum phosphate levels were 90 to 91 percent of those in the control study (P<0.05 to <0.01), a difference that quickly disappeared after the administration of alcohol was stopped (Fig. 4). The only statistically significant difference in the urinary excretion of phosphate occurred from 13 to 16 hours after the beginning of the study: phosphate excretion was 46 percent higher after alcohol ingestion than after fruit-juice ingestion (Fig. 4).
The administration of alcohol had no effect on the serum levels of 25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, calcitonin, or insulin-like growth factor I. However, it seemed to abolish the normal nocturnal increase in osteocalcin. The mean serum osteocalcin concentrations were 5.2±0.5 and 5.7±1.2 μg per liter at the start of the control and alcohol studies, respectively. The respective values at six hours were 9.2±0.6 and 6.2±1.1 μg per liter (P<0.05). The values at 8 and 16 hours were also slightly higher in the control study than in the alcohol study.
Studies in Women
The changes in the serum concentrations of parathyroid hormone, ionized calcium, and magnesium (Table 2) and in the urinary excretion of calcium, magnesium, and phosphate (Table 3) were similar in the women. The mean serum parathyroid hormone concentration reached a nadir of 17.3±2.6 ng per liter 2 hours after the administration of alcohol was begun and then gradually increased to a high of 57.9±4.8 ng per liter at 12 hours. The decrease in serum ionized calcium concentrations during and after alcohol ingestion in these women was similar in magnitude to that in the men, although the values were less often significantly different from those during the control study. The women's serum phosphate and osteocalcin concentrations were similar during the two studies.
Discussion
These results demonstrate that acute ethanol intoxication can cause transitory hypoparathyroidism, hypocalcemia, hypermagnesemia, hypercalciuria, and hypermagnesuria. The study was conducted among subjects whose dietary intake of calcium and magnesium was restricted: a 70-kg subject was allowed 90 mg of calcium and 84 mg of magnesium during the 16-hour experimental period. As a manifestation of this restriction, the urinary excretion of both elements declined during both studies, especially the control study. The base-line urinary excretion of calcium and magnesium as well as the serum levels of these substances was similar at the start of the experiments, indicating identical dietary intakes of the elements before each study period. Moreover, each study period was begun three hours after the subjects ate lunch, so that most intestinal absorption of calcium30 , 31 and magnesium32 , 33 had already occurred. The intake of protein and carbohydrate was also similar during both study periods. Therefore, the changes that occurred were associated with the alcohol intake itself.
The most remarkable finding was the decrease in serum parathyroid hormone concentrations during the period of alcohol ingestion and intoxication, and its rebound increase, surpassing base-line levels, during recovery. In a manner consistent with the developing hypoparathyroidism, the serum levels of ionized and total calcium decreased and the urinary excretion of calcium increased. The later increase in serum parathyroid hormone levels was best reflected by the lower urinary excretion of calcium and higher excretion of phosphate (as compared with values for the control study) during the last three hours of the alcohol study.
There have been only two previous studies of serum parathyroid hormone levels during acute alcohol ingestion. 19 , 20 In both studies a dose of 0.8 g of alcohol per kilogram was used; this amount of alcohol caused an elevation of parathyroid hormone levels in one study20 but no change in the other.19 In addition to using lower doses of alcohol, the earlier studies used methods to measure serum parathyroid hormone concentrations that detected short-term changes poorly, because they do not discriminate well between parathyroid hormone and its biologically inert carboxyterminal fragments. In another study the urinary excretion of cyclic AMP diminished after acute ethanol intoxication,34 a finding compatible with the decreased secretion of parathyroid hormone. Furthermore, studies in animals support the concept that alcohol induces hypoparathyroidism.35
Reduced serum concentrations of parathyroid hormone may result from either decreased secretion or increased clearance of the hormone. Although we are not able to distinguish between these two alternatives, the former seems more likely. If that is the case, what might cause the reduced secretion of parathyroid hormone? One possibility is a direct effect of alcohol. The fact that serum calcium concentrations had not increased before the parathyroid hormone levels decreased makes increased intestinal absorption of calcium an improbable mediator of transitory hypoparathyroidism, a conclusion supported by the results of the strontium-absorption studies and by the fact that the studies were conducted while dietary intake of calcium was restricted. It is also noteworthy that the serum concentrations of 1,25-dihydroxycholecalciferol did not change throughout the study. Alcohol may augment the early insulin response to a glucose load,36 and hyperinsulinemia may further increase the urinary excretion of divalent cations,37 but hyperinsulinemia is not known to alter the secretion of parathyroid hormone.
The increase in serum magnesium concentrations coincided with the decline in serum parathyroid hormone concentrations. Hypermagnesemia is known to inhibit the secretion of parathyroid hormone,32 but it is not known whether increments in serum magnesium within the normal range as small as those that occurred in these subjects have such an action. On the other hand, it is unlikely that alcohol induced sufficient intracellular loss of magnesium to impair the secretion of parathyroid hormone.15
Under circumstances in which dietary intake of magnesium is restricted and its urinary excretion is increased, liberation of magnesium from bone or its redistribution between the extracellular and intracellular compartments is the most likely explanation for alcohol-induced hypermagnesemia,38 even though intracellular magnesium has been considered to be only slowly exchangeable.32 Alcohol-induced hypermagnesuria has been ascribed to a direct renal effect of alcohol, but our results suggest that it could be due to hypermagnesemia and transitory hypoparathyroidism39 as well.
Might our findings explain the development of alcohol-associated bone disease? Decreased bone mineral density and osteoporosis are not characteristic of persistent hypoparathyroidism. Nevertheless, cycles of hypoparathyroidism and hyperparathyroidism, such as those observed in our subjects during and after alcohol intoxication, might be detrimental to bone tissue. Transitory hypoparathyroidism causes transient hypercalciuria, and rebound hyperparathyroidism leads to the mobilization of calcium from bone. On the other hand, alcohol abolished the normal nocturnal increase in the serum osteocalcin level, albeit only in the men, suggesting that even short-term alcohol intoxication suppresses the function of the osteoblasts; chronic alcohol abuse24 , 40 , 41 and even long-term social drinking (Laitinen K, et al.: unpublished data) may also inhibit the activity of osteoblasts. Of special importance is the fact that the possibly deleterious effects of alcohol on bone and mineral metabolism were also found in women, who are more prone to osteoporosis than men.
Supported by grants from the Yrjö Jahnsson Foundation and the Academy of Finland, Helsinki, Finland.
*Deceased.
We are indebted to Ms. Leena Lehikoinen, Terttu Kerman, and Terttu Lönnblad for their expert help in collecting and analyzing the blood and urine samples; to Ms. Arja Mikkelinen for preparing the figures; to Professor Risto Pelkonen for his valuable advice; to Assistant Professor Matti Härkönen for placing the facilities of his laboratory at our disposal; and to Kone, Inc., for placing the ionselective analyzer at our disposal.
Source Information
From the Research Unit of Alcohol Diseases (K.L., R.Y.), the Third Department of Medicine (M.V.), and the Department of Clinical Chemistry (R. Tunninen, S.-L.K.), University of Helsinki; the Minerva Foundation Institute for Medical Research (C.L.-A.); the Research Laboratories of the Finnish State Alcohol Company (Alko Ltd.) (R.Y.); and United Laboratories (R. Tunninen, S.-L.K., R. Tähtelä, M.V.); all in Helsinki, Finland. Address reprint requests to Dr. Välimäki at the Third Department of Medicine, Helsinki University Central Hospital, SF-00290 Helsinki, Finland.
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