Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parathyroid (PT) glands from 20-day-old embryonic chicks cultured in a chemically defined medium secreted a stimulator of in vitro bone resorption. This stimulator was presumed to be parathyroid hormone (PTH) because: 1) the in vitro dose response curve was parallel to that obtained with bovine PTH; 2) the activity was eluted on Sephadex G-1--chromatography at a postition similar to that for PTH; and 3) the material produced hypercalcemia in vivo in chicks. The amount of PTH-activity secreted was inversely proportional to the calcium concentration of the medium over the range of 0.75-2.25 mM. The chick PT glands also secreted an inhibitor of PTH-stimulated bone resorption in vitro. This inhibitor was presumed to be calcitonin (CT) because: 1) the in vitro dose-response curve was parallel to that obtained with synthetic salmon CT; 2) the activity was eluted on Sephadex G-50 chromatography at a position similar to that for salmon CT; and 3) the material produced hypocalcemia in vivo in rats. In contrast to what would be expected for CT secretion, the CT-activity was secreted by the PT glands in response to a low, not high calcium concentration. The data suggest that the secretion of avian PTH is similar to that of the mammalian hormone, and that the ultimobranchialectomized chick with an intact parathyroid gland may not be deficient in CT.
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PMID:The detection of transmissible gastroenteritis viral antigens by immunodiffusion. 23 83

A patient with primary hyperparathyroidism underwent cervical exploration and hemithyroidectomy. Only one normal parthyroid gland was found and was removed. Hypercalcemia persisted and subsequent arteriography localized a large mediastinal adenoma which was excised. Parathyroid autotransplantation of a small part of this tissue was performed and the patient was well for over a year. He again became markedly hypercalcemic and graft-dependent elevation of parathromone levels was demonstrated. Autograft resection resulted in normocalcemia. Nineteen months later hypercalcemia and elevated parathormone levels prompted re-exploration of the graft site and another enlarged implant was removed. This restored normocalcemia and normal parathromone levels. Parathyroid adenomatous tissue has the potential for autonomous hyperfunction, and caution must be exercised in its use in autotransplantation.
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PMID:Hyperparathyroidism following parathyroid autotransplantation. 49 61

Twenty patients being treated with thiazides were found among 95 subjects (21%) with hyercalcemia verified in repeated determinations in a health screening of 15,903 persons. There were 1,034 patients treated with thiazides in this total health screening. The prevalence of hypercalcemia in the patients treated with thiazides in this total health screening. The prevalence of hypercalcemia in the patients treated with thiazide (1.9%) was considerably higher than the prevalence of hypercalcemia found in the entire health-screened population (0.6%). The thiazide treatment was withdrawn in the 20 hypercalcemic subjects after an examination, and the patients were observed at intervals during a follow-up period of one year. The necks of 14 were explored during or after the follow-up period because of an initial serum calcium level greater than 3.0 mmole/liter or persistent hypercalcemia. Parathyroid adenomas were seen in all patients receiving surgery. Single adenomas predominated in surgical findings. The finding of the present high number of patients with primary hyperparathyroidism may be associated with elevated blood pressure resulting in thiazide treatment after detection.
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PMID:Hypercalcemia and primary hyperparathyroidism. Prevalence in patients receiving thiazides as detected in a health screen. 90 Oct 82

Three patients had primary hyperparathyroidism and monoclonal serum immunoglobulins. Although multiple myeloma was suspected in each case, subsequent evaluation was consistent with a "benign monoclonal gammopathy". Parathyroid adenomas were removed from two patients. The three patients are presented and compared to the four other cases that have been reported previously. The association between primary hyperparathyroidism and benign monoclonal gammopathy is discussed in terms of possible pathogenetic mechanisms. Primary hyperparathyroidism should be suspected in patients with hypercalcemia and benigh monoclonal gammopathy, as well as in other conditions, like multiple myeloma, that are known to be associated with hypercalcemia.
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PMID:Primary hyperparathyroidism and benign monoclonal gammopathy. 90 Oct 89

Parathyroid (PT) glands from 20-day-old embryonic chicks cultured in a chemically defined medium secreted a stimulator of in vitro bone resorption. This stimulator was presumed to be parathyroid hormone (PTH) because: 1) the in vitro dose response curve was parallel to that obtained with bovine PTH; 2) the activity was eluted on Sephadex G-1-- chromatography at a position similar to that for PTH; and 3) the material produced hypercalcemia in vivo in chicks. The amount of PTH-activity secreted was inversely proportional to the calcium concentration of the medium over the range of 0.75-2.25 mM. The chick PT glands also secreted an inhibitor of PTH-stimulated bone resorption in vitro. This inhibitor was presumed to be calcitonin (CT) because: 1) the in vitro dose-response curve was parallel to that obtained with synthetic salmon CT; 2) the activity was eluted on Sephadex G-50 chromatography at a position similar to that for salmon CT; and 3) the material produced hypocalcemia in vivo in rats. In contrast to what would be expected for CT secretion, the CT-activity was secreted by the PT glands in response to a low, not high calcium concentration. The data suggest that the secretion of avian PTH is similar to that of the mammalian hormone, and that the ultimobranchialectomized chick with an intact parathyroid gland may not be deficient in CT.
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PMID:Avian parathyroid glands in organ culture: secretion of parathyroid hormone and calcitonin. 116 99

Parathyroid-hormone-related protein (PTHrP) has been implicated as a humoral mediator of hypercalcaemia in malignant disease. We have investigated the contributions of PTHrP and parathyroid hormone (PTH) to the hypercalcaemia seen in routine clinical practice by means of highly sensitive immunoradiometric assays. PTHrP concentrations in plasma and PTH concentrations in serum were measured in 121 consecutive patients with hypercalcaemia (corrected serum calcium above 2.65 mmol/l) identified from routine biochemical profiles in a district general hospital. Hypercalcaemia was due to primary hyperparathyroidism in 63 (52%) patients and to malignant disease in 40 (49%). Plasma PTHrP was detectable in 35 (88%) of 40 patients with solid tumours and 3 of 9 patients with haematological malignant disease; it was undetectable in 92% of patients with primary hyperparathyroidism. 7 patients with malignant disease had PTH concentrations above 4.0 pmol/l, consistent with coexisting primary hyperparathyroidism. Measurement of both PTH and PTHrP in all patients led to a change in the diagnosis in 7% of patients. This study provides direct evidence for a humoral role of tumour-derived PTHrP in hypercalcaemia, and shows how PTHrP assays can be used appropriately, in conjunction with PTH assays, to investigate hypercalcaemia in routine clinical practice.
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PMID:Role of assays for parathyroid-hormone-related protein in investigation of hypercalcaemia. 134 90

Parathyroid storm in patients with primary hyperparathyroidism has previously been described as hyperparathyroid crisis, parathyroid intoxication or acute hyperparathyroidism. Whatever the nomenclature, all emphasize the severity and urgency of this disease entity. Although fewer than 200 cases have been described since the first report by Dawson in 1932, it is generally agreed that parathyroid storm is more prevalent than commonly appreciated. The symptoms and signs of the syndrome are not only due to the hypercalcemia, but also to the toxic effects of the parathyroid hormone (PTH). Its wide, but nonspecific clinical presentations make it easily confused with other cardiovascular or renal diseases. The mortality rate in untreated cases of parathyroid storm is essentially 100%. With combined medical-surgical treatment, it is still reported to be as high as 40%. Two patients with parathyroid storm were encountered at our institute recently, they both presented with severe hypercalcemia, consciousness disturbance and acute renal failure. The serum level of the intact form of PTH (iPTH) in both patients was greater than 1,000 pg/mL. Case 1, a 63-year-old female, presented with hypercalcemic crisis. Initially, good responsiveness to a saline infusion, steroids and furosemide administration was noted. Unfortunately, she became comatous after fine-needle aspiration of the parathyroid tumor. The recurrent storm was refractory to medical therapy, but was treated successfully by surgical removal of the single adenoma. This is a rare reported case regarding a hyperparathyroid storm after fine-needle aspiration of a parathyroid adenoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Parathyroid storm: report of two cases]. 136 14

Parathyroid activity, bone aluminum (Al) metabolism, bone histology, and clinical bone disease were studied in 55 successfully grafted kidney recipients at transplantation (Tx) and after 1 yr of immunosuppression with a low dose corticosteroid and a high dose cyclosporin-A regimen. Symptoms of Al-related bone disease disappeared after Tx. Serum Al and stainable bone Al decreased. The rate of Al removal from the bone surfaces was independent of graft function (creatinine range, 62-415 mumol/L) and bone turnover. Osteoblast activity and bone formation rate increased, while mineralization lag time normalized. Indices of bone resorption remained elevated, indicating persisting hyperparathyroidism. Eighteen percent of the recipients had posttransplant hypercalcemia, most likely caused by incomplete involution of hyperplastic parathyroid glands, while 53% had normocalcemic hyperparathyroidism related to impaired graft function. Cortical thickness decreased, while cancellous bone volume remained stable after Tx; both indices correlated significantly at follow-up with their respective values at Tx. None of 46 radiologically examined recipients had aseptic bone necrosis 1 yr after Tx.
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PMID:Aluminum metabolism and bone histology after kidney transplantation: a one-year follow-up study. 156 61

Historically, primary hyperparathyroidism during pregnancy was associated with significant risk of maternal morbidity and fetal death. Maternal hypercalcemia results in fetal hypercalcemia, leading to suppression of fetal parathyroid gland function. Neonatal hypocalcemia with tetany is a common occurrence after birth when maternal calcium flow is interrupted. From 1930 to 1990, 109 cases of women with primary hyperparathyroidism associated with pregnancy have been reported, 39 of whom were treated surgically before delivery. Although fetal mortality rates for medically treated women have improved, fetal morbidity continues to remain higher than in women who undergo surgical treatment of parathyroid disease during pregnancy. Of 850 patients treated surgically for primary hyperparathyroidism since 1960, 12 were pregnant. Four of the patients were treated medically during pregnancy and underwent surgery after delivery; all four infants had neonatal hypocalcemia and tetany. The remaining eight patients were treated surgically during pregnancy: six in the second trimester and two (one with associated pancreatitis and one with hypercalcemic crisis) during the first trimester. There was no fetal or maternal morbidity or death in the surgical group. Parathyroid adenomas were present in 10 of the patients, hyperplasia in one, and parathyroid carcinoma in one. The management of maternal primary hyperparathyroidism diagnosed during pregnancy should be based on the patient's symptoms and severity of disease. Hyperparathyroidism characterized by progressive symptoms should be treated surgically, preferably during the second trimester. Symptom-free patients and those with mild hypercalcemia diagnosed in the third trimester may be managed medically, postponing operation until after delivery.
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PMID:Primary hyperparathyroidism during pregnancy. 174 71

Secondary hyperparathyroidism is common in dialysis patients. Intravenous calcitriol has proven to be an effective therapy for the reduction of parathyroid hormone (PTH) levels. However, the effect of i.v. calcitriol on parathyroid function, defined as the sigmoidal PTH-calcium curve developed during hypocalcemia and hypercalcemia, has not been evaluated during the prolonged administration of i.v. calcitriol. Six hemodialysis patients with marked secondary hyperparathyroidism, PTH levels greater than 500 pg/mL (normal, 10 to 65 pg/mL), were treated for 42 wk with 2 micrograms of i.v. calcitriol after each hemodialysis. Parathyroid function was evaluated before and after 10 and 42 wk of calcitriol therapy. Between baseline and 42 wk, the basal PTH level decreased from 890 +/- 107 to 346 +/- 119 pg/mL (P less than 0.02) and the maximally stimulated PTH level decreased from 1293 +/- 188 to 600 +/- 140 pg/mL (P less than 0.01). In addition, calcitriol administration significantly decreased PTH levels throughout the hypocalcemic range of the PTH-calcium curve. Although the slope of the PTH-calcium curve (with maximal PTH as 100%) decreased between baseline and 42 wk (P less than 0.05), the set point of calcium did not change. Two patients with a decrease in both basal and maximally stimulated PTH levels after 10 wk of calcitriol, developed marked hyperphosphatemia between 10 and 42 wk; this resulted in an exacerbation of hyperparathyroidism despite continued calcitriol therapy. In conclusion, prolonged i.v. calcitriol administration is an effective treatment for secondary hyperparathyroidism in hemodialysis patients provided that reasonable control of the serum phosphate is achieved. In addition, the slope of the PTH-calcium curve may be a better indicator of parathyroid cell sensitivity than the set point of calcium.
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PMID:The effect of long-term intravenous calcitriol administration on parathyroid function in hemodialysis patients. 176 May 37


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