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)

Of 365 patients surgically treated for hyperparathyroidism at the University of Toronto hospitals, 3 had hypercalcemia due to an abnormal and ectopic fifth parathyroid gland. Autopsy studies have shown that a fifth gland may be present in 3% to 5% of patients with hyperparathyroidism. The possibility of an abnormal fifth gland as the cause of primary hyperparathyroidism should be considered when four glands of normal size and histology have been found in the neck, and such a gland should be sought in all patients with the diffuse hyperplasia of secondary hyperparathyroidism. The fifth gland is usually in the lower neck or upper mediastinum, frequently within the thymus. If present, it can usually be recognized and excised.
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PMID:Importance of a fifth parathyroid gland in the surgical treatment of hyperparathyroidism. 67 81

In two patients with extensive pulmonary tuberculosis who developed hypercalcaemia and hypokalaemia the hypercalcaemia appeared related to the use of small doses of vitamin D, which suggested patients with tuberculosis were hypersensitive to vitamin D. They were thus similar to patients with sarcoidosis, and it is interesting that the Kveim test result was positive in both cases. The hypercalcaemia was quickly suppressed with steroids. Hyperparathyroidism, thyrotoxicosis, Addison's disease, and multiple myeloma were excluded on clinical grounds and by the appropriate tests. The hypokalaemia was associated with increased renal excretion of potassium, and was probably due to distal tubular damage from hypercalcaemia.
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PMID:Hypercalcaemia and hypokalaemia in tuberculosis. 69 98

Six patients with chronic renal failure on regular dialysis treatment were given low doses (0.5--1.0 microgram/day) of 1alpha-hydroxyvitamin D3, monitoring the serum calcium, inorganic phosphate, immunoreactive parathyroid hormone concentration (IPTH) and alkaline phosphatase activity. The serum calcium rose in all patients after 7 days' treatment, in some subjects to hypercalcemic range; this effect persisted 6--14 days after withdrawal of 1alpha-hydroxyvitamin D3. The elevated serum IPTH rose in the first days of treatment, but later decreased to normal values. It is suggested that active vitamin D metabolites are necessary for normal response of parathyroid glands to variation in serum calcium. Low-dose 1alpha-hydroxyvitamin D3 treatment appears to be a promising method of correcting hypocalcemia and secondary hyperparathyroidism in chronic renal failure. Careful control of serum calcium is necessary, as hypercalcemia may occur even after minute doses of 1alpha-hydroxyvitamin D3.
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PMID:Effects of 1alpha-hydroxyvitamin D3 on serum calcium and immunoreactive parathyroid hormone in patients with chronic renal insufficiency. 70 Sep 46

A prospective series of 200 patients with persistent hypercalcemia had an abbreviated diagnostic work-up consisting of parathormone radioimmunoassay, chest roentgenogram, intravenous pyelography, and serum protein electrophoresis. All patients with hypercalcemia and hyperparathormonism had neck exploration if roentgenograms failed to reveal evidence of ectopic hyperparathyroidism. Serum iPTH proved to be at least 96% accurate in predicting parathyroid disease while at the same time resulting in considerable diagnostic economy. An elevated iPTH was particularly helpful in distinguishing between hypercalcemia due to destruction of bone by malignancy and primary hyperparathyroidism with a coexisting malignancy. Further, measurement of parathormone was useful in evaluation of postoperative hypercalcemia.
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PMID:Serum parathormone in the identification and surgical management of hyperparathyroidism. 70 2

Hypercalcemia occurs in approximately one of every five patients with thyrotoxicosis, and one of seven patients with hypercalcemia and thyrotoxicosis will have hyperparathyroidism as the cause of the serum calcium elevation. While there are no clinical features which permit easy identification of patients with hyperparathyroidism and thyrotoxicosis, determination of serum parathyroid hormone levels may help. Parathyroid hormone levels may be normal or suppressed if hypercalcemia is due to hyperthyroidism alone, and an elevated parathyroid hormone level suggest coexisting hyperparathyroidism.
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PMID:Hypercalcemia in thyrotoxicosis. 71 46

Hyperparathyroidism during pregnancy is clearly associated with an increased incidence of neonatal morbidity and mortality. Although it is impossible to define the precise incidence of this entity, we believe that its occurrence will be seen more frequently with the increasing numbers of female patients who have successfully received renal transplants and with the routine determination of serum chemistries in the nontransplanted pregnant patient. A review of case reports since 1962 of women known to be hyperparathyroid during pregnancy revealed 80 per cent of these pregnancies to be complicated by neonatal tetany, death, or abortion. This review substantiates Ludwig's earlier report [1], which noted a 50 per cent incidence of neonatal complications despite the advances of prenatal and postnatal medical care. There have been only eight reported cases in which parathyroid resection was performed during pregnancy. Successful operation dramatically reduced the incidence of neonatal complications. An adaptive normocalcemic hyperparathyroidism occurs routinely during pregnancy. However, in the hypercalcemic hyperparathyroid pregnancy, transplacental passage of calcium leads to a profound hypercalcemia in the fetus. Since the fetal parathyroid glands are functionally responsive, parathyroid suppression is thought to occur in utero due to high calcium levels. This can lead to neonatal tetany or perhaps permanent neonatal hypoparathyroidism. When a patient presents with significant hypercalcemic hyperparathyroidism during pregnancy, we suggest that an explorative parathyroid operation be performed during the second trimester of pregnancy. After delivery, the baby's course should be carefully monitored with frequent calcium determinations. Cow's milk or other formula feedings high in phosphate content should be avoided in favor of feedings with a calcium:phosphorus ratio similar to that of human milk.
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PMID:Hyperparathyroidism during pregnancy. 76 83

Parathormone levels were determined in 17 patients with functioning renal transplants. In 8 patients recently transplanted, very high serum levels of parathormone were found without obvious relation to the glomerular filtration rate. Hypophosphatemia was also present in these cases. In 9 other patients studied 2-7 years after transplantation the mean level of parathormone was lower than in the previous group but levels above normal were noted in half of the patients, some of which had perfect renal function and normal serum phosphorus. The response to induced hypercalcemia was used as a sensitive test to reveal abnormal responses even in cases which initially had normal peripheral levels of parathormone. From these results, tertiary hyperparathyroidism would appear to be rare although hyperfunctioning parathyroid glands can be demonstrated long after kidney transplantation, even when renal function is close to normal.
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PMID:Evolution of secondary hyperparathyroidism after renal transplantation. 77 58

New information has elucidated many of the biochemical pathways in the formation, release and metabolism of parathyroid hormone (PTH). The hormone is biosynthesized in the parathyroid cells from two distinct precursors, or prohormones, that are modified by specific enzymic cleavages during the synthesis and intracellular transport of the hormonal polypeptide. Release of the hormone from the gland inversely depends on the extracellular calcium concentration, but is regulated over a much narrower range of calcium concentration than was realized previously. This new information points to a pattern of regulation that is more appropriate for homeostasis than was the pattern indicated by earlier studies. The persistence of a basal level of PTH secretion, despite sustained hypercalcaemia, suggests a possible mechanism for the abnormal secretion seen in states of hyperparathyroidism. The discovery of a calium-dependent degradative pathway for PTH in the parathyroid cell indicates that changes in the turnover of PTH may be one means by which calcium regulates the amount of hormone available for secretion. Of the multiple immunoreactive forms of PTH present in the circulation of man and animals, the predominant form in blood appears to be a large biologically-inactive fragment consisting of the middle and carboxy two-thirds of the hormone sequence. At times, smaller biologically-active fragments of PTH may also appear in blood. Most circulating fragments of PTH probably arise from peripheral cleavage of the intact, secreted hormone in kidney and liver, but some forms of the hormone, including prohormones, may also be secreted from the parathyroid gland. The heterogeneity of circulating PTH and the concomitant uncertainties regarding its precise character have introduced difficulties in the interpretation of immunoassay measurements. A further delineation of the pathways and regulation of PTH biosynthesis, secretion and metabolism should lead to the development of more-specific immuno-assays and result in improved diagnosis and management of patients with disorders of the parathyroid glands.
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PMID:New concepts in the formation, regulation of release, and metabolism of parathyroid hormone. 78 74

A case is reported of hypercalcemia persisting for seven years after kidney transplantation, with normocalcemia being achieved after subtotal parathyriodectomy. The finding of post-transplantation hyperparathyroidism of this extreme duration, in association with several other reports of hyperparathyroidism persisting for years after kidney transplantation, raises serious questions about the completeness of parathyroid involution after kidney transplantation. Extensive review of the literature reveals that little is really known about the natural history of parathyroid function and involution after kidney transplantation.
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PMID:Hypercalcemia of seven years' duration after kidney transplantation. 78 70

Sixty-eight patients were observed for a period of up to seven years after transplantation. Serum parathyroid hormone levels were measured in 41 patients; 17 patients had persistent hypercalcemia for a period of from one to seven years. Serum parathyroid hormone levels were elevated in seven of these 17 patients. Serum parathyroid hormone was elevated in 11 of the other 24 patients with normocalcemia. The function of the kidney was not affected either by the state of hypercalcemia or persistent hyperparathyroidism. Aseptic necrosis was significantly present in those of the hypercalcemic group. It is suggested that persistent hypercalcemia is an important precipitating, if not the main, cause of an aseptic necrotic condition of the bones.
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PMID:The high incidence of persistent secondary hyperparathyroidism after renal homotransplantation. 78 41


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