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

The effect of dietary phosphorus (P) on calcium (Ca) and phosphorus metabolism was studied in young female rats. P levels in the semipurified diets ranged from 0.1 to 0.4% (w/w). A level of 0.4% P in the diet is recommended for rats. Kidney calcification was observed in rats fed the 0.4%-P diet whereas P restriction prevented this condition. Rats fed the diet containing 0.1% P, showed severe hypercalciuria, hypercalcemia, reduced growth and impaired bone mineralization. These effects did not occur when the diet contained 0.2 or 0.3% of P. This study suggests that in short-term studies P in the diet of female rats can be restricted to 0.2% so as to prevent nephrocalcinosis without affecting their development.
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PMID:Influence of dietary phosphorus restriction on calcium and phosphorus metabolism in rats. 252 16

Investigation of 44 patients with endogenous hypercorticism (EH) of various degrees of severity showed that the development of osteoporosis was accompanied by changes in the indices of calcium-phosphorus metabolism and calcium regulating hormones. Marked variations in the level of parathyroidin, calcitonin, vitamin D3 were observed in a severe type of EH. All the examinees were characterized by a decrease in the transport form of vitamin D3, which was most noticeable in a mild form of EH. A significant decrease in the concentration of the transport form of vitamin D3 against a background of hypercalcemia and hypercalciuria in mild EH can be regarded as the most informative indicators in early diagnosis of initial symptoms of osteoporosis.
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PMID:[Calcium-regulating hormones in endogenous hypercorticism]. 254 55

Altogether 184 patients with bone, renal or mixed hyperparathyroidism (HPT) presenting primarily were examined for blood levels of parathyroid hormone and indirect indicators of parathyroid function. None of the indices (calcium concentration, phosphorus level, serum activity of acid and alkaline phosphatase, oxyproline excretion with urine, etc.) was changed. The commonest biochemical signs of primary HPT were hypercalcemia, hypersecretion of parathyroid hormone, hyperoxyprolinuria. Biochemical indices deviations occurred more often and were more profound in bone primary HPT and parathyroid adenomas.
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PMID:[Clinico-biochemical parallels in diverse forms of primary hyperparathyroidism]. 258 52

With increasing recognition of problems regarding the use of aluminum hydroxide as a phosphate binder, calcium carbonate has become the medication of choice. Use of calcium has, however, frequently been associated with development of hypercalcemia. At this institution, calcium carbonate powder as a phosphate binder, examination of its efficacy, and the frequency of hypercalcemia with its use were of great interest. Calcium carbonate powder (CalCarb-HD, 2.4 gms elemental calcium/packet) (CalCarb-HD, Lafayette Pharmacal Inc., Fort Worth, TX) was used in the study. Twenty-one end-stage renal disease (ESRD) patients (17 hemodialysis and 4 chronic ambulatory peritoneal dialysis) were chosen and converted from their previous binder (primarily, calcium carbonate tablets) to calcium powder. The dosage was adjusted to keep phosphorus levels at 3.5 to 5.5 mg/dl and calcium less than 11.5 mg/dl. At 2 months, the average calcium level in the 16 patients remaining in the study was 9.2 mg/dl, and the average phosphorus level was 5.2 mg/dl with an average calcium dose of 1.4 packets/day. By 7 months, the 8 patients remaining in the study had an average calcium level of 9.9 mg/dl with an average phosphorus level of 5.5 mg/dl; average calcium dose was 1.8 packets/day. Total episodes of hypercalcemia (calcium greater than 11.5 mg/dl) were two. Calcium carbonate powder appears to be an effective phosphate binder in the ESRD population. The relatively few episodes of hypercalcemia may be related to possible enhanced bioavailability of the compound secondary to its powdered form.
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PMID:Calcium carbonate powder as a phosphate binder. 259 73

Many investigators have shown that calcium carbonate (CaCO3) is an effective phosphate binder which also prevents the potential disabling effects of aluminum (Al) accumulation. However, hypercalcemia may develop in a substantial numbers of patients. Thus, to control serum phosphate (PO4) and prevent hypercalcemia, we performed studies in 21 patients on maintenance hemodialysis in which, in addition to the oral administration of CaCO3, the concentration of calcium (Ca) in the dialysate was reduced from 3.25 to 2.5 mEq/liter. The studies were divided in three periods: I. control, on Al-binders (one month); II. no Al-binders (one month); III. CaCO3 (seven months). Blood was obtained three times/week before dialysis for the first five months of the study and once a week for the remaining four months. During the control period, the mean serum calcium was 8.86 +/- 0.08 mg/dl. The value decreased to 8.65 +/- 0.07 mg/dl when phosphate binders containing aluminum were discontinued, and increased to 9.19 +/- 0.07 mg/dl (P less than 0.001 compared to period II) during oral supplementation with calcium carbonate. The mean serum phosphorus was 5.03 +/- 0.07 mg/dl during the control period, and increased to 7.29 +/- 0.91 mg/dl (P less than 0.001) after phosphate binders were discontinued. It decreased to 4.95 +/- 0.06 mg/dl (P less than 0.001) with the administration of calcium carbonate. During CaCO3 administration, serum Al decreased from 64.2 +/- 8.5 to 37.1 +/- 3.6 and 25.1 +/- 3.0 micrograms/liter (P less than 0.001) at three and seven months, respectively. Serum parathyroid hormone (PTH) decreased by 20%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term effects of calcium carbonate and 2.5 mEq/liter calcium dialysate on mineral metabolism. 261 97

The study shows the gasometric and electrolytic features during the first five day from newborns from toxemic mothers. It is a prospective study, carried out during a four month period at the obstetrics premature ward at the Gynecological-Obstetrics Hospital of "La Raza" Medical Center. Thirty-three newborn babies with evidences of toxemia and who had not received any intravenous therapy were studied. Blood samples were taken and serum calcium, phosphorus and magnesium levels were measured at 24, 48, 72 and 120 hours after birth. The results showed that six patients (18%) were anemic, and another had polycythemia. Twelve others (36%) had plaquetopenia, one had hypercalcemia, another hypocalcemia, and eleven (33%) presented hypophosphatemia. Of the initial 33 patients, 75% presented metabolic acidosis which spontaneously corrected itself within the following 72 hours. Three showed signs of hypernatremia, four hyponatremia, and two others hyperkalemia, with a return to normal levels within the next 24 hours. No chloride alterations were found in any of the patients. Some newborn babies born from toxemic mothers can spontaneously correct their electrolytic and acid-base imbalance within 72 hours of their birth. Electrolytes; toxemia.
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PMID:[Electrolytes in toxemic fetuses]. 261 19

Carbetimer is a new antineoplastic agent whose limiting toxicity consists of dose- and treatment duration-dependent hypercalcemia. We examined the short-term effects of Carbetimer on calcium metabolism on days, 1, 3 and 5 during 11 5-day courses (6.5-8.2 g/m2/day given over daily 2-h infusions, q 3-4 weeks). Blood parameters were measured before and after Carbetimer, whereas urinary parameters were studied in three consecutive 2-h collections before, during and after Carbetimer infusions. Carbetimer effects were similar regardless of the infusion day. We found a consistent decrease of plasma ionized Ca (Ca2+) levels from 4.56 +/- 0.05 mg/dl before infusion to 4.28 +/- 0.06 mg/dl after infusion (P less than 0.001) whereas total serum Ca (corrected for protein levels) did not change. The fall of Ca2+ stimulated parathyroid function, as suggested by the increased plasma PTH levels, the decreased serum phosphorus and TmP/GFR index, or the increased urinary phosphate and cyclic AMP excretion. Carbetimer infusions also induced a marked increase in urinary Ca excretion (expressed as mg Ca/mg creatinine) from 0.093 +/- 0.011 before to 0.359 +/- 0.042 during and 0.177 +/- 0.031 after infusion (P less than 0.011). These changes were best explained by Carbetimer-induced Ca chelation that we confirmed in vitro by incubating Carbetimer at various concentrations in whole blood for 2 h at 37 degrees C, e.g. 2 mg of Carbetimer/ml lowered Ca2+ from 4.82 to 3.20 mg/dl without changing total Ca levels. On the other hand, a direct effect of Carbetimer on bone cannot be excluded since we observed an increase of serum osteocalcin levels from 2.0 +/- 0.3 to 2.5 +/- 0.4 ng/ml after infusion (P less than 0.001). In summary, the short-term effects of Carbetimer on calcium metabolism markedly differ from the long-term effects. They mainly consist of a dose-related calcium chelation leading to a decrease in Ca2+ levels, an increase in urinary Ca excretion and a stimulation of parathyroid function.
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PMID:Short-term effects of Carbetimer on calcium and bone metabolism in man. 263 64

Chronic metabolic acidosis causes a profound disturbance in renal proximal tubule 1OHase activity through perturbation of the normal ionic and hormonal controls of the enzyme activity. A lack of enzyme stimulation in response to hypophosphatemia and a paradoxical response of increased 1OHase activity to increased extracellular phosphorus are the important extracellular markers of deranged P control of 1OHase activity during chronic metabolic acidosis. 1OHase activity is down-regulated during chronic metabolic acidosis by an increase in renal cortical tubule mitochondrial calcium content and a functional abnormality in calcium handling, a reduction in extramitochondrial buffering capacity. There is a defect in PTH regulation of 1OHase during chronic metabolic acidosis, despite PTH levels which are inappropriately normal in relation to ionized hypercalcemia. PTH-directed cAMP accumulation is likely normal as well. Metabolic clearance of calcitriol is increased during chronic metabolic acidosis. Thus, the hormonal stimulus to maintain calcium and phosphorus homeostasis, calcitriol, is so altered by chronic metabolic acidosis that it is easy to understand the profound clinical effects of the acidosis on the skeleton of growing children. Chronic metabolic acidosis has allowed a greater understanding of the complex regulatory physiology that underlies renal proximal tubular 1OHase activity and calcitriol metabolism.
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PMID:Calcitriol metabolism during chronic metabolic acidosis. 266 5

The unusual causes of hypercalcemia have been reviewed. These disorders are rarely derived as the cause of hypercalcemia from the usual tests that one obtains in working up hypercalcemic patients (such as PTH level, phosphorus, urinary calcium). These diagnoses (particularly drug-related hypercalcemia) can be determined only from a careful history. The vast majority of hypercalcemic patients have disease secondary to cancer, hyperparathyroidism, or disorders of vitamin D metabolism. It should be noted that some hypercalcemic patients may have more than one disease. Therefore, before assuming that a hypercalcemic patient with Paget's disease, thiazide ingestion, immobilization, or so forth has hypercalcemia secondary to the primary disorder, hyperparathyroidism and cancer should also be considered. Similarly, serum calcium levels can normalize in some patients with mild hyperparathyroidism or bony metastases with mobilization and/or cessation of thiazide therapy.
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PMID:Unusual causes of hypercalcemia. 267 71

The mammalian thyroid gland is composed of 2 distinct endocrine cell populations concerned with the synthesis of 2 different classes of hormones. Follicular cells secrete the metabolically active iodothyronines whereas the C-(parafollicular) cells are concerned with the production of calcitonin, a hormone that influences blood levels of calcium and phosphorus, and bone cell metabolism. The synthesis of metabolic thyroid hormones is different than in other endocrine glands because the final assembly of hormone occurs within the follicular lumen. This extracellular synthesis of thyroid hormones is made possible by thyroglobulin, a glycoprotein synthesized by follicular cells. The secretion of thyroid hormones under the influence of pituitary thyrotrophin (TSH) from stores in the luminal colloid is initiated by elongation of microvilli and formation of pseudopods. FD&C Red No. 3 is a tetraiodinated derivative of fluorescein which in lifetime studies increases the incidence of thyroid follicular cell adenomas in male Sprague-Dawley rats. The striking changes in circulating levels of thyroid hormones and morphologic evidence of follicular cell stimulation are the result of alterations in the peripheral metabolism of thyroxine. An inhibition by FD&C Red No. 3 of 5'-deiodinase in the liver and kidney would explain the lower serum triiodothyronine (T3) levels. The pituitary, sensing the lowered circulating levels of T3, increased the secretion of thyroid stimulating hormone which resulted in the morphologic evidence of follicular cell stimulation in the long-term studies. Other xenobiotics increase the incidence of thyroid tumors in rodents by a direct effect on the thyroid gland to disrupt 1 of 3 or more possible steps in the biosynthesis of thyroid hormones. Physiologic perturbations alone, such as iodine deficiency or partial thyroidectomy, can disrupt thyroid hormone economy in rodents and, if sustained, increase the development of thyroid tumors. The wide variety of drugs, chemicals, and physiologic perturbations which increase thyroid tumor development appear to act through a secondary (indirect) mechanism to promote tumor development by causing a long-standing hypersecretion of thyroid stimulating hormone. Nodular and/or diffuse hyperplasia of C-cells occurs with advancing age in many strains of laboratory rats and in response to long-term hypercalcemia in certain animal species and human beings. Focal or diffuse hyperplasia often precedes the development of C-cell neoplasms. Radiation and the feeding of diets high in vitamin D resulting in hypercalcemia have been reported to increase the incidence of C-cell tumors in rats.
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PMID:The effects of xenobiotics on the structure and function of thyroid follicular and C-cells. 267 79


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