Significance of Elevated Parathyroid Hormone After Parathyroidectomy

ObjectiveTo review the prevalence of parathyroid hormone elevation after parathyroidectomy for primary hyperparathyroidism and to discuss possible mechanisms.MethodsA Medline search of the English-language literature published between 1990 and 2009 was performed using the search terms “elevated PTH after parathyroidectomy.” All of the identified articles reported either prospective or retrospective studies without control groups. Studies that included patients with secondary or tertiary hyperparathyroidism were not reviewed.ResultsWithin 1 week to 5 years after parathyroidectomy, 9% to 62% of patients with a normal serum calcium concentration are reported to have an elevated parathyroid hormone concentration. No evidence suggests that postoperative normocalcemic parathyroid hormone elevation is an indication of surgical failure and recurrent hypercalcemia. Preoperative findings in patients with postoperative parathyroid hormone elevation include lower vitamin D concentration, higher concentrations of bone turnover markers, and higher parathyroid hormone concentration. Potential mechanisms for parathyroid hormone elevation in the setting of normocalcemia include vitamin D deficiency, hungry bone syndrome, and parathyroid hormone resistance. Study findings suggest a possible benefit of postoperative calcium and vitamin D supplementation, but no randomized trials have been done.ConclusionElevation of parathyroid hormone commonly occurs after parathyroidectomy for primary hyperparathyroidism, although the underlying mechanism remains unclear. (Endocr Pract. 2010;16:112-117)     

A bout of resistance exercise increases urinary calcium independently of osteoclastic activation in men

Ashizawa, Noriko, Rei Fujimura, Kumpei Tokuyama, andMasashige Suzuki. A bout of resistance exercise increases urinary calcium independently of osteoclastic activation in men.J. Appl. Physiol. 83(4):1159-1163, 1997.Metabolic acidosis increases urinary calciumexcretion in humans as a result of administration of ammonium chloride,an increase in dietary protein intake, and fasting-inducedketoacidosis. An intense bout of exercise, exceeding aerobic capacity, also causes significant decrease in blood pH as aresult of increase in blood lactate concentration. In this study weinvestigated changes in renal calcium handling, plasma parathyroidhormone concentration, and osteoclastic bone resorption after a singlebout of resistance exercise. Ten male subjects completed about of resistance exercise with an intensity of 60% of one repetitionmaximum for the first set and 80% of one repetition maximum for thesecond and third sets. After exercise, blood and urine pH shiftedtoward acidity and urinary calcium excretion increased.Hypercalciuria was observed in the presence of an increased fractionalcalcium excretion and an unchanged filtered load of calcium. Therefore,the observed increase in urinary calcium excretion was due primarily todecrease in renal tubular reabsorption of calcium. Likely causes of theincrease in renal excretion of calcium are metabolic acidosis itselfand decreased parathyroid hormone. When urinary calcium excretionincreased, urinary deoxypyridinoline, a marker of osteoclastic boneresorption, decreased. These results suggest that1) strenuous resistance exerciseincreased urinary calcium excretion by decreasing renal tubular calciumreabsorption, 2) urinary calciumexcretion increased independently of osteoclast activation, and3) the mechanism resulting inpostexercise hypercalciuria might involve non-cell-mediatedphysicochemical bone dissolution.

     

Carboxyterminal telopeptide of type I collagen,ICTP, as a marker of matrix degradation in neonatal mouse calvarial bones,in vitro

Bone resorption,in vitro, is often measured as the release of prelabelled⁴⁵Ca from neonatal mouse calvarial bones, or from fetal rat long bones. In this report we describe a technique to measure the breakdown of bone-matrix,in vitro. We also describe a new way to dissect neonatal mouse calvarial bones, in order to obtain large amounts of bone samples.Twelve bone fragments were dissected out from each mouse calvaria and were thereafter cultured in CMRL 1066 culture medium in serum-free conditions in 0.5 cm² multiwell culture dishes. Matrix degradation after treatment with parathyroid hormone was assessed by measuring the amount of carboxyterminal telopeptide of type I collagen (ICTP) by RIA. The data on matrix degradation was compared to the release of prelabelled⁴⁵Ca from neonatal mouse calvarial bones. We found that the dose-responses for parathyroid hormone-induced release of prelabelled⁴⁵Ca and ICTP were identical.In conclusion: RIA-analysis of the ICTP-release is an easy and accurate method to measure degradation of bone-matrix,in vitro. Furthermore, the new dissection technique, described in this report, makes it easy to obtain large amounts of bone samples and thus to perform extensive experiments, e.g. dose-responses for agents that enhance bone resorption.     

Hypoplasia of the bone marrow in rats following removal of the parathyroid glands

Removal of the parathyroid glands caused a marked and permanent lowering of the mitotic activity in rat bone marrow, which was followed by a pronounced decline (ca. 40%) in the size of the marrow's nucleated cell population. These changes occurred only when the hypocalcemia induced by the lack of parathyroid hormone (PTH) was maintained by feeding the animals a calcium deficient diet. Since the overall marrow hypoplasia was almost entirely due to strikingly large reductions (ca. 70%) in the size of the erythroid and lymphoid subpopulations, it is concluded that PTH and calcium are major physiological regulators of the proliferation of erythroid and lymphoid cells.     

Regulation of the receptor-mediated cyclic AMP response of kidney to parathyroid hormone in the vitamin D-deficient rat

Rats fed a diet deficient in vitamin D were found to exhibit a refractory cyclic AMP response of kidney slices to parathyroid hormone and a marked decrease in membrane parathyroid hormone-dependent adenylate cyclase activity. Both the characteristic calcium deficiency (hypocalcemia) and secondary elevation of circulating parathyroid hormone appeared before the first noticeable decrease in hormone-dependent enzyme activity. After repletion of D-deficient rats with vitamin D₂, we found that serum calcium and parathyroid hormone were both restored to normal levels before the depressed enzyme response to the hormone was reversed. Moreover, infusion of parathyroid hormone into vitamin D-replete rats led to a marked reduction in parathyroid hormone-dependent adenylate cyclase activity, which was partly restored to control level 3 hours after discontinuing the hormone infusion. Taken as a whole, this study suggests that the elevated endogenous parathyroid hormone in the vitamin D-deficient rat is involved in the “down-regulation” of renal cyclic AMP responsiveness to the hormone. However, these experiments do not rule out the possibility that calcium deficiency and/or vitamin D per se participate in the regulation of the renal cyclic AMP response to parathyroid hormone.     

The morphology and function of rat C-cells. 4. Determination of calcium, inorganic phosphorus and total nitrogen in the femora of untreated parathyroidectomized or thyreoparathyroidectomized and hormonally substituted female rats]

Female Wistar rats of a live weight of about 160 g and fed with a standard laboratory diet, were parathyroidectomized, or thyroparathyroidectomized and treated with thyroxine, parathyroid hormone, calcitonin. thyroxine and parathyroid hormone, or thyroxine and calcitonin. On the 15th day post operationem, and after twelve days of hormone treatment, the concentrations of calcium, inorganic phosphorus and total nitrogen were determined in the femur bone. Parathyroidectomy resulted in a decrease of phosphorus concentration in bone. After thyroparathyroidectomy (Tx), the concentrations of inorganic phosporus and nitrogen diminished during some days, whereas the calcium content decreased continuously. Thyroxine application normalized the concentration of inorganic phosphorus. The osteolytic and nitrogen-anabolic effect of parathyroid hormone took place only in simultaneous treatment with thyroxine. The injection of calcitonin had a nitrogen-anabolic effect on bone; the simultaneous treatment with thyroxine induced a loss of calcium out of bone, and a deposition of calcium phosphate in renal tissue. Calcitonin did not inhibit a significant decrease of calcium concentration in the femur bone; the hypophosphatemic effect was always present. The metabolism of bone tissue, influenced by hormonal actions, probably determined the localization of the deposition of inorganic phosphorus, deserting the serum under the influence of calcitonin.     

Bone density parathyroid hormone and 25-hydroxyvitamin D concentrations in middle aged women.

OBJECTIVE--To examine the relation between bone density and indices of calcium metabolism including parathyroid hormone and 25-hydroxyvitamin D concentrations in middle aged women. DESIGN--A cross sectional study. SETTING AND SUBJECTS--138 women volunteers aged 45-65 with no known osteoporosis and unselected for disease status recruited for a dietary assessment study from the community using general practice registers. Volunteer rate was 20%. MAIN OUTCOME MEASURE--Bone mineral density measured with dual energy x ray absorptiometry. RESULTS--Bone density at the lumbar spine and neck and trochanteric regions of the femur was inversely related to serum intact parathyroid hormone concentrations and positively related to serum 25-hydroxyvitamin D concentrations. These associations were independent of possible confounding factors, including age, body mass index, cigarette smoking habit, menopausal status, and use of diuretics and postmenopausal hormone replacement therapy. These associations were apparent throughout the whole distribution of bone density and 25-hydroxyvitamin D and parathyroid hormone concentrations within the normal range, suggesting a physiological relation. CONCLUSIONS--The findings are consistent with the hypothesis that parathyroid hormone and 25-hydroxyvitamin D concentrations influence bone density in middle aged women. Findings from this study together with other work suggest that the role of vitamin D in osteoporosis should not be neglected. The associations with parathyroid hormone also indicate plausible biological mechanisms. The roughly 5-10% difference in bone density between top and bottom tertiles of serum 25-hydroxyvitamin D concentrations, though not large in magnitude, may have considerable public health implications in terms of prevention of osteoporosis and its sequelae, fractures.     

Research on Intra-Operative Indocyanine Green Angiography of the Parathyroid for Predicting Postoperative Hypoparathyroidism: A Noninferior Randomized Controlled Trial

Objective: A noninferiority randomized controlled trial was undertaken to clarify whether the postoperative measurements of serum calcium and parathyroid hormone and oral supplementation of calcium and calcitriol could be omitted if patients had at least one well-perfused parathyroid gland evaluated by intra-operative indocyanine green (ICG) angiography.Methods: Patients with at least one parathyroid gland well-perfused by ICG angiography (ICG score >2) were randomized to the control group or test group. For the control group, oral calcium and calcitriol were systematically supplemented. For the test group, no oral calcium or calcitriol was supplemented to the patients. Levels of serum calcium and parathyroid hormone of patients on the first and 30th postoperative day were compared between the two groups.Results: Among all 68 selected patients, 56 patients had at least one well-perfused parathyroid gland evaluated by intra-operative ICG angiography. The 56 patients were randomized to the control group or test group. There were no statistically significant differences in the levels of serum calcium and parathyroid hormone between test group and control group on the first or 30th postoperative day.Conclusion: The postoperative measurements of serum calcium and parathyroid hormone and oral supplementation of calcium and calcitriol were evaluated as redundant, if patients had at least one well-perfused parathyroid gland evaluated by intra-operative ICG angiography.Abbreviations: ICG = indocyanine green; NIR = near infrared; POD = postoperative day; PTH = parathyroid hormone; SBR = signal background ratio     

THE MODE OF ACTION OF VITAMIN D

1. The purpose of this review article is to re-evaluate and integrate many of the observations related to the physiological effects of vitamin D, using as a working hypothesis the concept that the vitamin may be acting analogously to a steroid hormone in terms of its ability to interact with genetic information and ultimately elicit a physiological response. Prior to this time the problem of the mechanism of action of vitamin D has primarily been approached from the point of view that the vitamin was acting as a cofactor for some specific enzymic reaction. 2. The physiological activities of vitamin D are integrated with those of parathyroid hormone to provide a homeostatic control for the regulation of primarily calcium and secondarily phosphate metabolism. It is proposed that the role of vitamin D in this homeostatic control mechanism is older and more fundamental than that of parathyroid hormone. The interaction of vitamin D on skeletal calcium metabolism may have evolved before the effects of the vitamin on intestinal calcium absorption. 3. There are several physiological defects of calcium metabolism—rickets, osteo-malacia, vitamin D-resistant rickets and idiopathic hypercalcaemia—all of which may be a consequence of an aberration in one or another of the interlocking steps of the vitamin D-dependent and calcium-dependent homeostatic control mechanism. 4. The most thoroughly established action of vitamin D in vivo is to promote or facilitate the intestinal absorption of calcium. Although the exact biochemical details of this process are not available, this may involve vitamin D-mediated synthesis of the appropriate enzyme systems or the alteration of membrane structure necessary for calcium absorption. It is not yet unequivocally established whether calcium absorption is an energy-dependent active transport process or is a passive carrier-mediated or simple diffusion process. 5. The exact action of vitamin D on bone metabolism is not as well established, but the primary effect of the vitamin is likely to mediate bone resorption. The vitamin D-dependent activities of the cell in both the intestine and bone are to absorb calcium and transfer it to the blood. 6. No direct effects of vitamin D on intestinal absorption of phosphate have been found. Furthermore the validity of a vitamin D-mediated renal reabsorption of phosphate is questioned, for the major effects of vitamin D are cation oriented. If the renal effects of vitamin D are true, it is postulated that the mechanism of action of the vitamin here on the anion, phosphate, is fundamentally different from its cation oriented mechanism. 7. There is a lag in the action of vitamin D on the vitamin mediated: (a) transport of calcium both in vivo in rats and chicks, and in vitro with everted intestinal slices; (b) the apparent increased permeability of intestinal mucosa; (c) increased levels of citric acid in serum or bone; (d) the increased incorporation of radioactive inorganic phosphorus into intestinal mucosa phospholipids. As shown by the use of radioactive vitamin D, this lag is not due to a lack of the vitamin in the target organs. 8. Whereas large, unphysiological doses of radioactive vitamin D localize in all tissues and all subcellular fractions, small physiological doses of radioactive vitamin D localize predominantly in the nucleus of the intestinal mucosa. The amount of vitamin D localized in the nucleus would appear to be too low for the vitamin to function as a cofactor, and is more indicative of an interaction on or with deoxy-ribonucleic acid. 9. Actinomycin D, an inhibitor of DNA-directed RNA synthesis, inhibits the action of vitamin D in mediating intestinal calcium absorption and bone resorption. Vitamin D also stimulates messenger-RNA synthesis in intestinal mucosa within 1/2 hr. of vitamin treatment. Vitamin D may play a crucial role, along with parathyroid hormone and calcium, in a DNA, gene-dependent, homeostatic control mechanism for cal, ium metabolism. In this system the vitamin D molecule has certain very specific structural requirements which are probably a reflection of the specificity of its receptor molecule, rather than structural requirements for a cofactor-enzyme relationship.     

Treatment of Paget's Disease of Bone with Mithramycin

We report data from three patients with severe Paget''s disease of bone who were treated with mithramycin.Mithramycin infusion resulted in a fall in plasma calcium, phosphate, alkaline phosphatase, and urinary hydroxyproline excretion. There was an improvement in calcium and phosphorus balance in two of the three subjects studied. A pronounced or complete relief of bone pain occurred in all three.We suggest that mithramycin exerts its beneficial effect in Paget''s disease of bone by stimulating parathyroid hormone release. The parathyroid hormone released has a predominantly anabolic action on bone since its catabolic action is blocked by mithramycin, which inhibits bone resorption.     

Marathon related death due to brainstem herniation in rehydration-related hyponatraemia: a case report

Introduction

The natural history of patients with spontaneous parathyroid necrosis is unknown. In this case report we describe the clinical course, laboratory, radiographic, bone densitometry tests, parathyroid ultrasonography and scintigraphy examinations of a patient performed over a period of eight years after she first presented with a sudden episode of spontaneous resolution of primary hyperparathyroidism (PHPT).

Case presentation

A 24-year-old woman with a clinical history and laboratory and radiographic tests compatible with PHPT suffered a sudden episode of cervical pain and presented with clinical evidence of hypocalcemia. Biopsy of a cervical nodule revealed necrotic material compatible with ischemia of the parathyroid. The follow-up of the patient presented four distinct phases: the first, which lasted two years, was compatible with a period of bone hunger during which it was necessary to introduce calcitriol and calcium carbonate. During this period, the patient showed bone mass gain. The second phase was characterized by normalization of calcium and parathyroid hormone levels and its end was difficult to define. During the third phase there was a recurrence of hypercalcemia associated with elevated parathyroid hormone (PTH) levels and loss of bone mass. The last phase corresponded to the interval after parathyroidectomy, which was characterized by normalization of serum levels of calcium and PTH, as well as bone mass gain.

Conclusion

This case report indicates that spontaneous resolution of PHPT by adenoma necrosis is potentially temporary. Thus, in cases in which a conservative approach is chosen, clinical and laboratory follow-up is indispensable. Bone mass measurement is a useful tool in the follow-up of these cases. However, this option exposes the patient to a potential roller-coaster ride of bone mass gain and loss, whose long term consequences are still unknown.     

Calcium,Parathyroid Hormone,and Vitamin D in Patients with Primary Hyperparathyroidism: Normograms Developed from 10000 Cases

ObjectiveTo better define the typical and atypical biochemical profiles of patients with surgically proven primary hyperparathyroidism.MethodsIn this single-center, prospectively conducted study of consecutive patients with surgically proven primary hyperparathyroidism over a 7-year period, we analyzed serum calcium, parathyroid hormone, and 25-hydroxyvitamin D concentrations.ResultsA total of 10 000 patients were included, and more than 210 000 calcium, parathyroid hormone, and 25-hydroxyvitamin D values were evaluated. Both calcium and parathyroid hormone levels demonstrated a Gaussian distribution with the average calcium concentration being 10.9 ± 0.6 mg/dL and the average parathyroid hormone concentration being 105.8 ± 48 pg/mL. The average highest calcium and parathyroid hormone concentrations were 11.4 ± 0.7 mg/dL and 115.3 ± 50 pg/mL, respectively. At least 1 calcium value of 11.0 mg/dL was seen in 87% of patients, but only 21% had 1 or more calcium value above 11.5 mg/dL. Only 7% had a single serum calcium level reaching 12.0 mg/dL. Normocalcemic hyperparathyroidism was seen in just under 3% of patients who had identical findings at surgery. An average parathyroid hormone concentration less than 65 pg/mL was seen in 16%, with 10% of patients who had no high parathyroid hormone values. The average 25-hydroxyvitamin D concentration was 22.4 ± 9 ng/mL, with levels decreasing as calcium levels increased (P < .001); 36% had 25-hydroxyvitamin D levels below 20 ng/mL.ConclusionsPatients with PHPT present with a number of distinct biochemical profiles, but as a group, they present with a near-normal Gaussian distribution of both calcium and parathyroid hormone levels. Either serum calcium or parathyroid hormone remained normal in 13% of patients, yet the findings at surgery are similar to those of patients with elevated calcium or parathyroid hormone. Low 25-hydroxyvitamin D is an expected finding in patients with PHPT, decreasing as serum calcium levels increase. (Endocr Pract. 2011;17:384-394)     

In vitro effect of KCA-098, a derivative of coumestrol,on bone resorption of fetal rat femurs

The effects of 3,9-bis(N,N-dimethylcarbamoyloxy)-5H-benzofuro[3,2-c]quinoline-6-one (KCA-098), a derivative of coumestrol, on bone resorption was studied in organ cultures of 20-day fetal rat femora. KCA-098 increased the length, dry weight, and calcium and phosphorus contents of parathyroid hormone (PTH)-treated fetal rat femur. As PTH significantly reduced the calcium and phosphorus contents of the femora, probably by stimulating bone resorption, KCA-098 seems to inhibit bone resorption. In fact, KCA-098 inhibited the PTH-induced release of ⁴⁵Ca from pre-labeled fetal rat femora into the medium in organ culture. Coumestrol also inhibited the release of ⁴⁵Ca from bone into the medium. However, KCA-098 did not increase the uterine weight of ovariectomized rats, whereas coumestrol did so. Thus KCA-098 is a unique, new inhibitor of bone resorption that has no estrogenic activity.     

A STUDY ON VARIETAL DIFFERENCE IN FLOWERING HABITS OF SOYBEAN PLANTS AS FOLLOWED BY GRAFTING EXPERIMENTS

The material basis of varietal differences in flowering habitwas investigated from the standpoint that flowering is determinedby the balance in amounts of flowering promotor and inhibitor.The grafting method was used throughout the experiments. Late variety of Glycine max L. seems to produce flowering inhibitor(or inhibitors) under the conditions under which midseason varietyproduces flower. Early variety seems to produce flowering hormonewhich overcomes the flower-inhibiting action in the late variety. The amounts of flowering hormone produced under short day conditionbymidseason and late varieties were compared. The results showthat, under the short day condition, the midseason variety producesequal or smaller amounts of flowering hormone as compared withthe late variety. On the basis of these results, the mechanismby which the flowering habits are determined in various varietiesof soybean plants was discussed. (Received June 18, 1962; )     

Regulation of vitamin D metabolism.

Vitamin D can be regarded as a prohormone and its most potent metabolite, 1, 25-dihydroxyvitamin D₃, a hormone which mobilizes calcium and phosphate from bone and intestine. In true hormonal fashion, the biosynthesis of 1, 25-dihydroxyvitamin D₃ by kidney mitochondria is feed-back regulated by serum calcium and serum phosphorus levels. The lack of calcium brings about a secretion of parathyroid hormone which stimulates 1, 25-dihydroxyvitamin D₃ synthesis while low blood phosphorus stimulates 1, 25-dihydroxyvitamin D₃ synthesis even in the absence of the parathyroid glands. For such regulation to occur, vitamin D must be present probably because 1, 25-dihydroxyvitamin D₃ itself is needed for the regulation. The molecular and cellular mechanisms whereby 1, 25-dihydroxyvitamin D₃ synthesis is regulated are unknown despite many recent reports. Likely the elucidation of these mechanisms must await a detailed investigation of the enzymology of the renal 25-hydroxyvitamin D₃-1α-hydroxylase. In addition to the regulation at the 25-hydroxyvitamin D₃-1α-hydroxylase step, vitamin D metabolism is regulated at the hepatic vitamin D-25-hydroxylase level. This regulation is a suppression of the hydroxylase by the hepatic level of 25-hydroxyvitamin D₃ itself by an unknown mechanism. Much remains to be learned concerning the regulation of this newly discovered endocrine system but already the findings are not only relevant to calcium homeostasis but also to an understanding of a variety of metabolic bone diseases.     

Three large, functioning cystic parathyroid adenomas

ObjectiveTo report a very rare case of 3 large, functioning cystic parathyroid adenomas causing primary hyperparathyroidism.MethodsWe present the history, clinical findings, laboratory test results, radiologic findings, endocrine workup results, intraoperative surgical challenges, and surgical pathology report of the study patient. We review the literature and discuss the importance of intraoperative parathyroid hormone (PTH) measurement in such cases.ResultsA 79-year-old woman presented with primary hyperparathyroidism and elevated levels of calcium and PTH. Localization studies confirmed the presence of a large right upper parathyroid adenoma. On exploration, a very large cystic parathyroid gland was identified at that location. Because intraoperative PTH levels remained elevated, further exploration was pursued, which revealed 2 more large cystic glands on the left side that were resected. This resulted in an adequate but slow PTH drop. The right lower gland appeared normal. On follow-up 4 days and 6 weeks after surgery, the calcium and PTH levels had normalized.ConclusionThis case highlights the aspects of intraoperative PTH use and underscores the need to exclude multigland disease even in the setting of a very large parathyroid cyst with concordant localization studies. (Endocr Pract. 2012;18:e14-e16)     

Adaptation of intestinal calcium absorption: parathyroid hormone and vitamin D metabolism.

It has already been demonstrated that the adaptation of intestinal calcium absorption of rats on a low calcium diet can be eliminated by thyroparathyroidectomy plus parathyroid hormone administration. This treatment elevates intestinal and plasma levels of 1,25-dihydroxyvitamin D₃ in rats on a high calcium diet while producing no change in rats on a low calcium diet. It therefore appears likely that the modulation of intestinal calcium absorption by dietary calcium is mediated by the parathyroid glands and the renal biogenesis of 1,25-dihydroxyvitamin D₃. Changes in the other unknown vitamin D metabolite levels as a result of dietary calcium are also modified by thyroparathyroidectomy and parathyroid hormone administration, but the effect of these metabolites on intestinal calcium transport is unknown.     

Intestinal calcium transport: parathyroid hormone and adaptation to dietary calcium.

Thyroparathyroidectomy prevents the elevation of intestinal calcium transport in response to low dietary levels of calcium. Removal of the thyroparathyroid glands reduces elevated intestinal calcium transport of rats on low calcium diets to the levels found in rats fed high calcium diets. This reduction took place 4 days after surgery. The chronic administration of a constant exogenous source of parathyroid hormone to thyroparathyroidectomized rats fed either a high or low calcium diet resulted in high rates of intestinal calcium transport independent of dietary calcium. Since 1,25-dihydroxyvitamin D₃ supplementation eliminates adaptation in a similar manner, these results strongly support the idea that parathyroid glands mediate intestinal adaptation to low dietary calcium presumably by the stimulation of 1,25-dihydroxyvitamin D₃ biosynthesis by secreted parathyroid hormone.     

Mechanisms of hypocalcemia and markers of bone turnover in alcohol-intoxicated drinkers

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.