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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-seven hypercalcaemic subjects were identified in three generations of a family. There were no clinical complications of chronic hypercalcaemia, but five had had parathyroid surgery which was unsuccessful in four. Twenty of the twenty-seven subjects were compared with twenty-four normocalcaemic controls from the same family and the findings were also compared with those from forty patients with surgically proven primary hyperparathyroidism. The relation between the serum and urinary calcium levels was studied by means of an oral calcium loading test. The ratio of calcium clearance to creatinine clearance was normal in this family (but elevated in the patients with primary hyperparathyroidism) and the concentration of parathyroid hormone was normal, as was the total urinary excretion of cyclic AMP. Thus, there was no evidence of either suppressed or increased parathyroid activity in this familial condition. Basal urinary calcium excretion was normal under steady-state conditions indicating that the hypercalcaemia could not be attributed to either increased bone resorption or increased calcium absorption from the gut. In accordance with this, the serum levels of 1,25-dihydroxycholecalciferol were normal. The hypercalcaemia in this condition can be accounted for in full by an increase in renal tubular reabsorption of calcium, and thus differs from that of primary hyperparathyroidism in which there is increased production of calcium from gut and/or bone as well as an increase in renal tubular reabsorption of calcium. Although the serum phosphate and renal tubular reabsorption of phosphate were both low in patients with familial benign hypercalcaemia, they were not as low as in patients with the same degree of hypercalcaemia due to primary hyperparathyroidism. The changes in phosphate transport in familial benign hypercalcaemia could be explained as a secondary effect of the increased filtered load of calcium in the kidney. The tendency towards hypermagnesaemia in our patients, which contrasts with a tendency towards hypomagnesaemia in primary hyperparathyroidism, could also be explained as a secondary effect of the abnormality of renal tubular reabsorption of calcium. Increased renal tubular calcium reabsorption and persistent normal functioning of the parathyroid glands in the face of hypercalcaemia remain the sole definite abnormalities of the syndrome.
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PMID:Familial benign hypercalcaemia. Study of a large family. 631 Jun 72

Clinical and biochemical evidence of primary hyperparathyroidism (prim. HPT) is reported in an infant with hypotonia, feeding problems and constipation from birth. Following a partial parathyroidectomy at the age of 12 months, the clinical condition improved. In her sister, mother and three other maternal relatives a familial hypocalciuric hypercalcemia (FHH) was subsequently demonstrated. All were clinically healthy in spite of increased total and ionized serum calcium, normal serum parathyroid hormone concentration, low urinary calcium excretion and normal renal excretion of cyclic AMP. Similar findings appeared in our patient after parathyroidectomy. An autosomal dominant inheritance of FHH is suggested. It is thus demonstrated, that a mother with FHH may give birth to healthy children with FHH as well as to infants with prim. HPT associated with FHH.
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PMID:Primary hyperparathyroidism in infancy associated with familial hypocalciuric hypercalcemia. 631 30

Serum vitamin D metabolites, the renal tubular maximum reabsorptive rate for phosphate (TMP/GFR) nephrogenic cyclic AMP (NcAMPI, and CaE (urinary calcium excretion per litre of glomerular filtrate) were measured in 14 adults with familial hypocalciuric hypercalcaemia (FHH). The findings were compared with analyses in 14 patients with surgically proven primary hyperparathyroidism matched for serum calcium, creatinine clearance and vitamin D status (assessed by serum concentrations of 25 hydroxyvitamin D). Vitamin D metabolites were also measured in 16 normocalcaemic relatives of patients with FHH. The serum concentration of 24,25 dihydroxycholecalciferol was appropriate for the prevailing 25 hydroxyvitamin D and no difference was found between groups. The serum concentration of 1,25 dihydroxycholecalciferol was significantly greater in primary hyperparathyroidism (P less than 0.0005) compared with patients with FHH and their normocalcaemic relatives. TMP/GFR was reduced in both primary hyperparathyroidism (0.53 +/- 0.12 mmol/l GF, mean +/- SEM) and FHH (0.86 +/- 0.14 mmol/l GF). Patients with primary hyperparathyroidism showed an increase in NcAMP output in the urine (38.5 +/- 16 mmol/l GF) which was significantly greater (P less than 0.0001) than the normal NcAMP (13.5 +/- 9.2 nmol/l GF) found in FHH. CaE was low in FHH indicating increased renal tubular reabsorption of calcium. It is concluded that there is no abnormality of vitamin D metabolism in FHH comparable with the changes observed in primary hyperparathyroidism. It is suggested that the biochemical abnormalities in FHH cannot be explained solely upon an increased sensitivity of the renal tubules to the effects of endogenous parathyroid hormone.
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PMID:Familial hypocalciuric hypercalcaemia: observations on vitamin D metabolism and parathyroid function. 631 24

Although small cell carcinoma of the lung has a high incidence of skeletal metastasis and is frequently associated with paraneoplastic syndromes, it is only rarely associated with hypercalcemia. Similarly, the more unusual small cell carcinoma of the pancreas has not been associated with hypercalcemia. The authors describe the first such patient with small cell carcinoma of the pancreas and hypercalcemia. Comprehensive metabolic measurements (fasting calcium excretion, renal phosphorus threshold, 1,25 dihydroxyvitamin D, 25 hydroxyvitamin D levels, nephrogenous cyclic AMP and immunoreactive PTH levels) suggest that although bone metastases were present, the hypercalcemia may have been caused in part by humoral mechanisms.
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PMID:Hypercalcemia in small cell carcinoma of the pancreas. 632 Oct 9

It is proposed that this review will adopt the following format: establishment of hypercalcemia. This demands a discussion of the problem of normal ranges, the usage of either total calcium or ionized calcium in making this decision and where total calcium is used whether adjustment of this value for serum protein concentration should be used and if so, the formulae which have been cited to perform this. Having established hypercalcemia why is it necessary to differentiate this? This will involve reviewing those clinical situations in which differentiation of hypercalcemia has been attempted and will include an attempt to produce an up to date indication of conditions in which hypercalcemia has been described. When hypercalcemia has been established the laboratory tests which have been further used to discriminate will be divided into single tests such as N- or C- terminal parathormone, 1,25- dihydroxycholecalciferol, cyclic AMP; the combination tests which have been used including phosphate clearance, chloride vs. bicarbonate etc. proceeding to those groups which have used discriminant function to help in the decision making; dynamic testing will also be discussed particularly with reference to steroid suppression but will also include other known suppressants such as Mithramycin and Calcitonin. A final section will be included attempting to assess overall the present state of art in differentiating laboratory diagnosis of hypercalcemia and will also attempt to highlight those areas which appear to be most fruitful areas of progress in the future.
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PMID:Differential laboratory diagnosis of hypercalcemia. 638 33

A patient with familial hypocalciuric hypercalcaemia (FHH) is reported. Seven years after total parathyroidectomy he remained hypocalcaemic, with biochemical evidence of hypoparathyroidism (enhanced renal tubular reabsorption of phosphate, low nephrogenic cyclic AMP excretion, and reduced serum concentration of 1,25-dihydroxycholecalciferol in the presence of normal renal function and normal serum 25-hydroxyvitamin D levels). Iv infusions of calcium were given before and 6 years after total parathyroidectomy. The renal tubular reabsorption of calcium was compared in these two situations. No difference was found. Before and after parathyroidectomy there was enhanced renal tubular reabsorption of calcium. It is concluded that the enhanced renal tubular reabsorption of calcium in FHH is independent of parathyroid hormone. Total parathyroidectomy corrects the hypercalcaemia in FHH by a reduction in the input of calcium into the extra-cellular fluid from gut and or bone perhaps as a result of reduced renal synthesis of 1,25-dihydroxycholecalciferol.
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PMID:Familial hypocalciuric hypercalcaemia: evidence for continued enhanced renal tubular reabsorption of calcium following total parathyroidectomy. 647 56

Biochemical and other parameters in VX-2 carcinoma in rabbits were evaluated. VX-2 carcinoma not only produced hypercalcemia but also hypophosphatemia and 25-OH-vitamin D deficiency. An increased turnover of 25-OH-vitamin D seems likely. Serum parathyroid hormone and urinary cyclic AMP did not increase. Hypokalemia occurred in association with hypophosphatemia and lowered blood glucose within 1 week after tumor transplantation. At the end of the experiment glucose and insulin were both below the control range. It is concluded that VX-2 carcinoma in rabbits yields much more complex biochemical alterations than reported before on calcium metabolism.
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PMID:Electrolyte and glucose metabolism in VX-2 carcinoma of the rabbit. 668 51

Since the structural requirements for all known biological activities of parathyroid hormone (PTH(1-84)) are virtually satisfied by the amino-terminal 34 amino acid fragment, PTH(1-34), we investigated whether this fragment could elaborate the overall actions of the intact hormone in the whole animal by comparing the effects of equimolar infusions of each peptide to dogs and rats. Infusion of bovine PTH(1-84) (bPTH(1-84)) at 17 pmol/kg per h for 20 h to three dogs or at 100 and 200 pmol/kg per h to groups of six rats for 5 days produced greater hypercalcaemia (3.02 +/- 0.03, 2.52 +/- 0.07 and 3.24 +/- 0.11 mmol/l respectively) than equimolar infusions of human PTH(1-34) (hPTH(1-34)) (2.61 +/- 0.03, 2.46 +/- 0.05 and 2.71 +/- 0.09 mmol/l respectively). A significant calcium rise was not observed in dogs until after 4 h of PTH infusion. No rise in plasma calcium was apparent in rats, however, until the third day of PTH infusion. Only in parathyroidectomized rats was there a rise in plasma calcium within 24 h of starting an infusion of PTH. The hypercalciuria and plasma phosphate responses in dogs during equimolar infusions of hPTH(1-34) and bPTH(1-84) were not significantly different. However, by day 5 of infusion in rats greater hypercalciuria was produced by bPTH(1-84). Although infusion of hPTH(1-34) and bPTH(1-84) caused rises in urinary cyclic AMP excretion (measured only in the dog) of immediate onset and equal magnitude, bPTH(1-84) tended to produce greater phosphaturia than hPTH(1-34) in both species. If the assumption is correct that the half-lives of hPTH(1-34) and bPTH(1-84) in the circulation are similar and provided that hPTH does not inherently have less biological activity than bPTH, then during equimolar infusions of these peptides into dogs and rats, the greater responses observed with bPTH(1-84) suggest that intact PTH may have a direct action of its own in vivo before being metabolized into smaller biologically active fragments. In additional experiments using parathyroidectomized rats, the infusion rate of bPTH(1-84) required to restore normocalcaemia was 26 pmol/kg per h. Although near-normal calcaemia and intestinal calcium absorption could still be maintained when the infusion rate was increased to 39 pmol/kg per h, hypercalciuria and phosphaturia became apparent.
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PMID:Effects of parathyroid hormone and the synthetic 1-34 amino-terminal fragment in rats and dogs. 684 24

In an attempt to gain insight into the relationship between bone marrow and bone tissue, studies of bone metabolism and quantitative analysis of bone structure were carried out in mice following a transplantation of a granulocytosis-inducing mammary carcinoma. With the progression of the tumor growth and development of granulocytosis, there was a sharp increase in plasma calcium and urine calcium, both reaching over 200% of control values. Hypercalcemia was associated with a significant increase in urinary hydroxyproline (P less than 0.005), an increase in marrow medullary area (P less than 0.05), and an increase in number of endosteal osteoclasts (P less than 0.005), together indicating that the cause of hypercalcemia was an increase in bone resorption. In parallel with hypercalcemia and hypercalcuria, there was an increase in urinary cyclic AMP excretion. The removal of the tumor normalized both blood neutrophil counts and plasma calcium levels, suggesting that a humoral agent from the tumor tissue, rather than tumor metastasis to bones, may be responsible for the phenomena. These studies documented the association of excessive bone resorption in this animal model of tumor-induced neutrophilia; the model may prove useful for studies of tumor-associated hypercalcemia as well as studies of marrow and bone interactions.
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PMID:Hypercalcemia, excessive bone resorption, and neutrophilia in mice bearing a mammary carcinoma. 684 52

Fasting calcium excretion, renal phosphorus threshold, plasma 1,25 dihydroxyvitamin D, immunoreactive PTH, nephrogenous cyclic AMP excretion, and tumor burden were assessed in nine patients with gynecologic neoplasms and hypercalcemia. Gynecologic neoplasms were responsible for hypercalcemia in seven of 34 (20.5%) consecutive patients with malignancy-associated hypercalcemia. The tumor burden in each patient was large. Three of four endometrial carcinomas contained squamous elements. All patients displayed biochemical evidence of nonparathyroid humorally mediated hypercalcemia (bone resorption). Treatment of hypercalcemia did not appear to diminish production of the humoral calcemic factor but eradication of tumor eliminated biochemical evidence of the humoral syndrome. It can be concluded that (1) gynecologic neoplasms are a frequent cause of malignancy-associated hypercalcemia, (2) humoral mechanisms appeared to be responsible for the hypercalcemia in 100% of the patients in this series, (3) squamous features occur with unexpected frequency in hypercalcemic endometrial carcinoma, (4) the presence of hypercalcemia connotes a large tumor burden, and (5) treatment directed at the neoplasm (but not treatment directed at hypercalcemia) may eliminate evidence of ectopic calcemic hormone production.
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PMID:Hypercalcemia associated with gynecologic malignancies: biochemical characterization. 707 51


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