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)

The functional evolution of autogenous parathyroid grafts was monitored in six patients with primary parathyroid hyperplasia using a sensitive radioimmunoassay specific for the midregion of parathyroid hormone (PTH). After successful total parathyroidectomy and graft implantation in the forearm, basal immunoreactive PTH (iPTH) fell to undetectable levels for about 12 to 18 weeks, and then rose to normal. By 3 weeks after surgery, an iPTH increment appeared in venous blood from the arm bearing the graft. Graft function was demonstrated in all six cases. Graft-independent hypercalcemia occurred in two patients and appeared to inhibit PTH secretion by the graft. In one case, elevated levels of calcium and iPTH persisted after surgery but iPTH remained equal in both arms. At 5 months, a fifth hyperplastic gland was resected from the mediastinum, and the calcium level decreased to normal; the parathyroid implant was secreting iPTH vigorously 5 days later. Hypercalcemia had not prevented establishment of a viable implant. In the second case, hypercalcemia developed 80 weeks after operation, and the previously demonstrated iPTH gradient disappeared; presumably a fifth gland had become hyperplastic. In this patient, iPTH had remained in the upper portion of the normal range during the first postoperative week, probably indicating the potential for recurrence. Each of the other five patients remains normocalcemic 4 to 103 weeks after grafting.
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PMID:Generalized primary parathyroid hyperplasia: studies of the evolution of autogenous parathyroid graft function. 682 63

Four patients with milk-alkali syndrome (MAS) presented with many of the characteristics of primary hyperparathyroidism including hypercalcemia, low or normal serum phosphorus levels, normal or increased urinary calcium levels, and inappropriately high or elevated serum parathyroid hormone levels. These laboratory findings differ from those classically described in MAS, i.e., hypercalcemia without hypercalciuria and a normal or high plasma phosphate level. Because the serum calcium level failed to return to normal after two weeks of hydration and a low calcium diet, and because of the inability to distinguish this syndrome from primary hyperparathyroidism, two of the four patients underwent neck exploration. Four normal parathyroid glands were histologically proven in each, and at autopsy in a third patient, there was no evidence of parathyroid hyperplasia or adenoma. Hypercalcemia eventually resolved in all patients with a low-calcium diet for as long as six months. Of the several features of MAS, hypercalcemia, alkalosis in the presence of azotemia, a history of increased calcium and alkali intake, and a response to dietary calcium restriction are helpful in differentiating this syndrome from primary hyperparathyroidism. Laboratory tests in patients with MAS may be confusing and the return to normocalcemia in response to a calcium deficient diet may be delayed.
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PMID:Milk alkali syndrome. Does it exist and can it be differentiated from primary hyperparathyroidism? 683 Mar 49

Familial hypocalciuric hypercalcemia (FHH) is an autosomal dominant trait comprising hypercalcemia, hypophosphatemia, parathyroid hyperplasia, and unusually low renal clearance of calcium. We evaluated the role of parathyroid hormone in the relative hypocalciuria of FHH and characterized the renal transport of calcium in this disorder using three previously hypercalcemic FHH patients with surgical hypoparathyroidism and three controls with surgical hypoparathyroidism. Intravenous infusion of calcium chloride in two patients with FHH and in three controls increased serum calcium from a mean basal of 5.0 to a mean peak of 6.8 meq/liter in two FHH patients and from 4.2 to 5.7 in three control subjects. Urinary calcium in a third FHH patient was studied without calcium infusion during recovery from hypercalcemia of vitamin D intoxication. At all serum concentrations of calcium, calcium clearance was lower in FHH than in controls; at base-line serum calcium, the ratio of calcium clearance to inulin clearance (C(Ca)/C(IN)) in FHH subjects was 32% of that in controls and decreased to 19% during hypercalcemia. Calcium infusion increased the ratio of sodium clearance to inulin clearance in controls from a base line of 0.020 to 0.053 at peak concentrations of calcium in serum, but did not affect this parameter in FHH (0.017 at base-line serum calcium vs. 0.019 at peak). When calcium infusion studies were performed (in two patients with FHH and one control) during administration of acetazolamide, a drug whose principal renal action causes inhibition of proximal transport of solute, C(Ca)/C(IN) in the patients with FHH was 29 and 7% of that of the control at base-line and peak serum calcium, respectively. In contrast, ethacrynic acid, a diuretic that acts in the ascending limb of the loop of Henle, increased C(Ca)/C(IN) more in the FHH patients than in the control subject; C(Ca)/C(IN) was 65% at base-line and 47% at peak serum calcium, compared with that of the control subject. The greater calciuric response to ethacrynic acid than to acetazolamide or calcium infusion alone in FHH indicates that a major renal locus of abnormal calcium transport in this disorder may be the ascending limb of the loop of Henle.Decreased clearance of calcium in patients with FHH and hypoparathyroidism when compared with hypoparathyroid controls indicates that relative hypocalciuria in FHH is not dependent on hyperparathyroidism. Since the parathyroid glands in FHH are not appropriately suppressed by calcium, this implies that FHH represents a disorder of abnormal transport of, and/or response to, extracellular calcium in at least two organs, parathyroid gland and kidney.
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PMID:Urinary calcium excretion in familial hypocalciuric hypercalcemia. Persistence of relative hypocalciuria after induction of hypoparathyroidism. 687 59

1. All available evidence for and against the concept of ectopic hyperparathyroidism, including 307 case reports of tumor hypercalcemia, was collated. 2. Of 104 combined cases of tumors of the kidney, lung, liver, head, neck and esophagus, 91 (88%) were in men. 3. The parathyroid glands were examined in 170 of 307 cases and parathyroid hyperplasia or adenoma were described in 34 cases. This high frequency may reflect higher likelihood of reporting such association. 4. Analysis of the histological pattern of tumors associated with humoral hypercalcemia revealed a marked association with certain histological types in different organs, such as clear-cell carcinoma of the kidney and ovary, hepatocarcinoma and cholangiocarcinoma, pheochromocytoma, and squamous-cell carcinoma of the lung, head, neck, esophagus, and urogenital tract. This histological correlation is not compatible with the "random derepression" hypothesis. 5. The existence of tumor humoral hypercalcemia is well documented, as 61 of 74 operated patients sustained remission of hypercalcemia following tumor removal. 6. The evidence for ectopic PTH being produced by tumor is not well documented and is based on conflicting radioimmunoassay results. We have found no case in the literature which fulfilled unequivocally criteria of ectopic production of biologically active PTH. There has been a lack of studies of tumors for the presence of biologically active hypercalcemic factors because only relatively insensitive bioassays are available at present. More information is also required on microscopic bone changes in tumor hypercalcemia as x-ray studies alone are inadequate. 7. On the basis of the present evidence, causes and mechanisms of tumor hypercalcemia are likely to be multiple.
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PMID:Tumor hypercalcemia and "ectopic hyperparathyroidism". 699 43

Dispersed parathyroid cells were employed to study calcium-regulated parathyroid hormone (PTH) release in severe secondary hyperparathyroidism due to chronic renal insufficiency. Cell preparations were obtained from 16 parathyroid glands of 6 patients undergoing subtotal parathyroidectomy for parathyroid bone disease and/or hypercalcemia. The effects of increasing ambient calcium concentration on immunoreactive PTH release in vitro were assessed and compared with results observed in cells prepared from 7 adenomas and 6 normal parathyroid glands. There was no difference in maximal PTH release for the 3 types of tissue (mean +/- SEM, 8.48 +/- 1.9 , 8.1 +/- 3, and 10.1 +/- 0.78 ng/10(5) cells. h respectively). In 14 of 16 hyperplastic glands, 6 of 7 adenomas, and all of the normal glands, PTH release was inhibited more than 50% by 2-3 mM calcium (suppressible glands). Of the normal glands, half of the maximal inhibition of PTH release (the set-point) occurred at less than 1.03 mM calcium in 5 of 6 cases. In 12 of 14 suppressible hyperplastic glands and all of the 6 suppressible adenomas, on the other hand, the set-point was 1.03 mM or higher (p less than 0.01 and P less than 0.002, respectively). Thus, in severe secondary parathyroid hyperplasia due to chronic renal insufficiency, there is frequently an increase in the set-point for calcium without a change in the maximal secretory rate per cell. Abnormal calcium-regulated PTH release at the cellular level, therefore, is not limited to parathyroid neoplasia (i.e. adenoma or primary hyperplasia), but may occur in secondary hyperplasia as well.
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PMID:Abnormal regulation of parathyroid hormone release by calcium in secondary hyperparathyroidism due to chronic renal failure. 705 14

A series of 104 consecutive patients treated at the Massachusetts General Hospital between 1933 and 1978 for primary hyperplasia was reviewed. Early in this period (1933-1958) nine patients were treated by what was the considered subtotal resection (five with clear cell and four with chief cell hyperplasia). Hypercalcemia persisted in four cases; three from inadequate resection and one (case 170) associated with a fifth gland in the mediastinum that was removed at a second stage operation. Later (1959-1978), adequate subtotal resection, leaving 30 to 50 mg of viable hyperplastic tissue, was performed in 28 patients (7 with clear cell and 21 with chief cell hyperplasia). The operation was successful in 27 patients (96%). In one patient (case 442) subtotal resection failed, and hypercalcemia recurred, requiring a second operation. Sixty-seven patients in this series had excision of one, two, or three (but not more than three) glands. Of these 21 (31%) had persistent hypercalcemia after operation and required further surgery. Transient hypocalcemia occurred in 40 patients, permanent hypocalcemia in two. This study shows that subtotal resection, leaving 30 to 50 mg of viable tissue, is the surgical treatment of choice for primary parathyroid hyperplasia. It is effective in the great majority of patients. We have not found total parathyroidectomy with autotransplantation necessary and believe that it should be reserved only for selected cases.
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PMID:Surgical management of hyperparathyroidism due to primary hyperplasia. 706 44

Three hundred thirty-eight consecutive parathyroidectomies for hyperparathyroidism were performed over a 22 year period. There were 53 dialysis patients (31 male and 22 female), 285 patients (165 female and 120 male) with primary hyperparathyroidism, 55 patients (19 percent) with parathyroid hyperplasia, and 230 patients with 236 parathyroid adenomas. The location of the adenomas were right upper in 57, right lower in 59, left upper in 60, and left lower in 60. Forty-three patients of the last 194 operated on had histories of childhood head and neck irradiation (21.6 percent), 34 patients (79.6 percent) had associated thyroid disease, and there were 10 with thyroid carcinomas. In the 285 patients, 54 percent had thyroid disease, and 18 had thyroid carcinomas. Twenty-three patients required reoperation for persistent or recurrent hypercalcemia, and 19 neck reexplorations and 6 mediastinotomies were performed. The identification and biopsy as indicated of all four parathyroid glands at initial neck exploration would have prevented over 70 percent of reoperations.
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PMID:Parathyroidectomy. Review of 338 consecutive cases for histology, location, and reoperation. 712 71

We analyzed, by light microscopy, specimens obtained at parathyroid surgery from 18 members of eight kindreds with familial hypocalciuric hypercalcemia. For comparison, similar analyses were performed with normal parathyroid glands (surgical or postmortem specimens) and with glands from patients with typical primary parathyroid hyperplasia. The average parathyroid parenchymal area in familial hypocalciuric hypercalcemia was 300 per cent of that in normal subjects (0.049 versus 0.15 sq. cm., p less than 0.0005) but significantly less than that in typical primary parathyroid hyperplasia. Thirteen of the 18 subjects with familial hypocalciuric hypercalcemia had one or more enlarged glands. Enlarged parenchymal areas were noted at all ages in familial hypocalciuric hypercalcemia, but there was a spectrum of histologic findings among the glands in each case, within most families, and between families. Mild parathyroid hyperplasia was a feature in most patients with familial hypocalciuric hypercalcemia who had undergone neck surgery. Simple quantitative analyses were useful in identifying parathyroid hyperplasia in the group with familial hypocalciuric hypercalcemia.
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PMID:The parathyroid glands in familial hypocalciuric hypercalcemia. 722 18

The regulation of parathyroid hormone (PTH) secretion by calcium was studied in normal and abnormal parathyroid tissue from five patients with a parathyroid adenoma. Dispersed cells were prepared from the adenoma and from a portion of a normal parathyroid gland and were incubated for two hours with varying concentrations of calcium. PTH release as a function of the concentration of calcium was determined by radioimmunoassay (C-terminal). Cells from the normal glands showed a lower set-point for calcium (the concentration of calcium causing half of the maximal inhibition of PTH release) than those from the adenomas in four of five cases. Moreover, both set-point and maximal PTH release at low concentrations of calcium were significantly lower in normal glands from patients with an adenoma than in normal glands from patients with normal calcium homeostasis (0.77 +/- 0.04 [SEM] versus 0.99 +/- 0.03 mM calcium and 3.4 +/- 0.43 versus 10.1 +/- 0.78 ng/10(5) cells/hr, respectively). These observations may explain, in part, the transient hypocalcemia frequently seen in patients after removal of a parathyroid adenoma. In addition, they suggest that the set-point for calcium and maximal PTH release in normal parathyroid tissue may be altered by prior exposure to chronic hypercalcemia or other physiologic variables. Finally, the "normal" set-point that we have noted previously in parathyroid tissue from some patients with primary parathyroid hyperplasia may be inappropriately high for the hypercalcemia seen in those cases.
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PMID:Abnormal calcium-regulated PTH release in normal parathyroid tissue from patients with adenoma. 728 44

Parathyroid autotransplantation is a known and increasingly utilized procedure. It is indicated in patients with primary parathyroid hyperplasia, in patients with primary hypercalcemia who have normal parathyroid tissue devascularized during surgery, in patients with secondary and tertiary parathyroid hyperplasia, and in patients with total thyroidectomy when normal parathyroid tissue is accidentally or unavoidably removed or completely devascularized. No normal viable parathyroid tissue should be autotransplanted. This procedure was performed in 13 dialysis patients, 27 primary hypercalcemic patients and 77 patients with thyroidectomy. The hypercalcemic patients had autotransplantations into muscle pockets in the volar surface of the forearm, while the thyroidectomy patients had autotransplantation into the sternocleidomastoid muscles. The application of parathyroid autotransplantation is a major technical and physiologic breakthrough in the field of thyroid and parathyroid surgery. It should greatly reduce the morbidity associated with permanent hypocalcemia in this type of extensive surgery.
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PMID:Parathyroid autotransplantation in patients with parathyroid disease and total thyroidectomy. Indications in 117 cases. 728 53


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