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 observation of a non-metastatic reactive hepatopathy associated with a hypernephroma in a 39-year-old man who had had fever for 4 months led to a review of the literature and an analysis of basically three aspects of the disorder: a) The various manifestations of carcinoma of the kidney, which include a large number of paraneoplastic clinical symptoms (polycythemia, anemia, prolonged fever, hypercalcemia, hypertension, nefropathy, loss of salt, peripheral neuropathy, and amyloidosis); b) an alteracion of hepatic function known since 1961 which is characterized by an abnormal retention of sulfobromophthalein, increase of alkaline phosphatase, prothrombin decrease, dysproteinemia with hypoalbuminemia, and alpha2-globulin increase. It may or may not be accompanied by enlargement of the liver. c) Criteria of operability of the primary tumor.
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PMID:[Liver disease associated with hypernephroma. A case report (author's transl)]. 45 99

To examine the relative importance of calcium and gastrin in regulation of calcitonin secretion, we administered graded oral doses of calcium to 10 normal men, ages 23-29 yr. Each subject had previously shown an appropriate increase in calcitonin secretion in response to a pharmacologic (0.5 mug/kg) pentagastrin injection. On separate days and in random order, each man drank 250 ml of distilled water containing 0.0, 0.5, 1.5, and 3.0 g of elemental calcium as the gluconate salt. Blood samples were drawn before and at 30, 60, 90, 120, 180, and 240 min after the oral calcium dose. The samples were analyzed for calcium by atomic absorption spectroscopy, and for gastrin and calcitonin by radioimmunoassays of established sensitivity and specificity. Ingestion of water (control) caused no change in any of the three variables. Calcium ingestion resulted in dose-related increases, within the normal range, of all three variables. Immunoreactive gastrin rose promptly, peaking at 30 min, and returning to basal levels or below by 120 min. In contrast, calcium and immunoreactive calcitonin levels rose slowly and in parallel, peaking at 120-240 min. Changes in calcitonin and changes in calcium were strongly and positively correlated, r = 0.73, when all data were pooled. Furthermore, individual linear regressions for changes in calcitonin and calcium levels (calculated separately for the three oral calcium doses in each subject) had positive slopes in 28 out of 30 sets (P < 0.01). The changes in calcitonin concentrations were much more poorly correlated with the corresponding changes in serum gastrin levels; in fact, the regression coefficient was weakly negative, r = -0.20. These results show that, at least in young adult men, changes of ambient calcium concentration within the normal range may be of major importance in physiologic regulation of calcitonin secretion. The findings are consistent with the hypothesis that calcitonin functions to prevent excessive postprandial hypercalcemia.
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PMID:Regulation of calcitonin secretion in normal man by changes of serum calcium within the physiologic range. 50 Aug 34

The authors studied the presence of visceral calcification as evidenced by the visceral uptake of bone-seeking radionuclides during the course of a bone scan among 22 patients with terminal renal failure maintained on dialysis, nine patients with hypercalcemia secondary to malignancy, and nine patients with primary hyperparathyroidism. Uptake by the lungs or stomach was observed in 11 renal failure patients (50%) and in four of those with malignancy and hypercalcemia (44%). None of the patients with primary hyperparathyroidism had evidence of visceral calcification. The serum CaXP product was significantly higher among those with visceral calcification than those without. The results of this study indicate that a CaXP product of 60 represents the saturation product of calcium phosphate in serum above which spontaneous precipitation of this salt may occur in such viscera as stomach and lungs.
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PMID:Visceral calcification and the CaXP product. 71 4

Due to toxic side effects of aluminum-containing agents for treatment of uremic hypophosphatemia, much interest has been focused upon aluminum-free phosphate binder alternatives. From results of experimental studies with calcium acetate, this salt has been suggested as a possible effective and safe phosphate binder. In the present study, calcium acetate was used during a mean of 11 months for serum phosphate control in 30 uremic patients previously treated with aluminum and/or calcium carbonate. Satisfactory control of serum phosphate was achieved during the study (mean phosphate concentration +/- SE: 2.15 +/- 0.12 mmol/l compared to prestudy 2.23 +/- 0.19 mmol/l). Mean serum concentrations of calcium, alkaline phosphatase and parathyroid hormone did not change significantly during the study. Serum aluminum decreased significantly (p less than 0.01). Moderate hypercalcemia was observed in 6 patients. Calcium acetate treatment was withdrawn in 2 patients due to gastrointestinal discomfort. It is concluded that calcium acetate seems to be an effective phosphate binder alternative with relatively few side effects.
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PMID:Calcium acetate used as phosphate binding treatment in uremic hyperphosphatemia. 168 Apr 30

Patients suffering from malignant disease will probably develop some metabolic abnormality of electrolytes. Hypernatremia is defined as an elevation of serum natrium over 150 mEq/l and caused by decrease of water intake, low level of ADH secretion and impaired response of kidney to ADH. Hyponatremia below 135 mEq/l of serum natrium is caused by SI-DAH, sick cell syndrome and increased loss of natrium from the kidney. On the other hand, hyperkalemia is defined as an elevation of serum kalium over 5.0 mEq/l and caused by acute tumor cell lysis syndrome, adrenal and renal insufficiency. Hypokalemia is caused by kalium loss from kidney and hypersecretion of mineral corticoid. Hypercalcemia is found in the high frequency among patients with malignant disease. Hypercalcemia is defined as an elevation of serum calcium over 11.0 mg/dl, although the most important aspect is the level of ionized calcium. The excess calcium causes defective urinary concentration with polydipsia, nausea and vomiting leading to volume depletion. At serum calcium levels about 13.8 mg/dl, there may be rapid deterioration or renal function, dehydration, coma and cardiac arrhythmias. Hypercalcemia is rarely the first manifestation of cancer. There are three principle pathogenic causes of malignant hypercalcemia, 1) hypercalcemia is a feature of several hematological cancers, including Burkitt's lymphoma, T cell leukemia, but most commonly with myeloma. The hypercalcemia in these myeloma patients is due to the secretion of an osteoclast activator, a lymphokine by the myeloma cells. 2) all patients with bony metastases have biochemical evidence of increased bone resorption. However, not all patients with bony metastases develop hypercalcemia. Probably the hypercalcemia is due partially to increased renal tubular reabsorption of calcium, mediated by a humoral factor, with activity similar to that of parathormone. 3) hypercalcemia in the patients without bony metastases is due to increased bone resorption caused by the ectopic secretion by the tumor. Mildly symptomatic patients will benefit from modest salt loading. They are dehydrated and replacement of the extracellular fluid is the first line of treatment. This may require 4-10 l normal saline/24 h. In addition, frusemide will increase calcium excretion. Calcitonin may be given subcutaneously or intravenously to refuse the mobilisation of calcium from bone. Glucocorticoids are unhelpful, but will prolong the effect of calcitonin. A diphosphonate is also useful.
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PMID:[Palliative therapy in cancer. 4. Palliation of the symptoms from a malignant tumor. (2)]. 169 56

Idiopathic hypercalciuria (IHC) is defined by an urinary calcium excretion greater than or equal to 0.10 mmol/kg body weight/day on a free diet in the absence of hypercalcemia. Pak's classification into absorptive and renal forms of IHC is no longer accepted as such. The now proposed "operational" classification of IHC separates dietary IHC, where calcium excretion falls below 0.07 mmol/kg BW/day on moderate dietary calcium restriction, from true IHC, where urinary calcium excretion remains above this value while on a 600 mg Ca diet, with renal and absorptive "presentations". Etiopathogenic mechanisms of IHC are revisited and appear to be multifactorial. They involve endogenous factors, such as disorders of calcitriol biosynthesis (or receptors), bone resorption and/or calcium membrane transport, whose phenotypic expression is enhanced by extrinsic factors, mainly nutritional, such as high animal protein and salt intake. A protocol of laboratory investigation based on these recent data is proposed, together with a stepped therapeutic approach involving a readjustment of nutritional habits combined, when needed, with thiazide diuretics.
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PMID:[Idiopathic hypercalciuria. Biological studies and therapeutic applications]. 183 61

Calcium acetate has many characteristics of an ideal phosphorus binder. It is a readily soluble salt that avidly binds phosphorus in vitro at pH 5 and above. One-dose/one-meal balance studies show it to be more potent than calcium carbonate or calcium citrate. We studied chronic (3-month) phosphorus binding with calcium acetate in 91 hyperphosphatemic dialysis patients at four different centers. All phosphorus binders were stopped for 2 weeks. Calcium acetate at an initial dose of 8.11 mmol (325 mg Ca2+) per meal was then used as the only phosphorus binder. Dose was adjusted to attempt control of predialysis phosphorus level less than 1.78 mmol/L (5.5 mg/100 mL). Final calcium acetate dose was 14.6 mmol (586 mg) Ca2+ per meal. Sixteen patients developed mild transient hypercalcemia (mean, 2.84 mmol/L [11.4 mg/dL]. Initial phosphorus values in mmol/L (mg/dL) were 2.39 (7.4); at 1 month, 1.91 (5.9); and at 3 months, 1.68 (5.2). Initial calcium values in mmol/L (mg/dL) were 2.22 (8.9); at 1 month, 2.37 (9.5); and at 3 months, 2.42 (9.7). Initial aluminum values in mumol/L (micrograms/L) were 2.99 (80.7); and at 3 months were 2.54 (68.4). Initial C-terminal parathyroid hormone (C-PTH) values in ng/mL were 14.6; at 1 month, 11.9; and at 3 months, 13.2. Sixty-nine patients then entered a double-blind study. Phosphorus binders were stopped for 1 week. Calcium acetate (at a dose established in a prior study) or placebo was then administered for 2 weeks. Next, patients were crossed to the opposite regimen for 2 weeks. Initial phosphorus was 2.36 mmol/L (7.3 mg/100 mL) and calcium 2.22 mmol/L (8.9 mg/100 mL).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium acetate control of serum phosphorus in hemodialysis patients. 202 56

Calcium acetate is a potent phosphate binder that causes fewer problems with hypercalcemia and elevated serum aluminum concentrations than other calcium salt or aluminum-binding agents. It exceeds calcium carbonate in its binding ability and is not expensive. These advantages make it an attractive alternative to many of the standard phosphate-binding regimens.
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PMID:Medication review: an alternative phosphate binder--calcium acetate. 206 59

The symptoms which are caused by hypercalcemia are variable and unspecific. In the elderly the functional capacity of homeostatic mechanisms is less than in young people and at the same time the prevalence of diseases which may cause hypercalcemia is greater. One should be aware of the possibility of hypercalcemia in patients presenting vague gastrointestinal and/or psychiatric complaints or symptoms. The prevalence of hypercalcemia in elderly women may well be 3%. Hypercalcemia leads to renal loss of salt and disturbances of renal function. An increasing inability to excrete the calcium overload is the result. Only in primary hyperparathyroidism renal function remains generally normal and moderately increased calcium levels may exist for years without serious consequences. Important causes of hypercalcemia in the elderly are hyperthyroidism, malignant disease and abrupt immobilization with previously elevated skeletal remodelling activity. Thiazide diuretics may precipitate the hypercalcemic state. Diagnosis is relatively simple and is based on a limited package of laboratory tests. Treatment should always begin with the restoration of the extracellular fluid volume. This is followed by inhibition of bone resorption by means of bisphosphonates or corticosteroids and treatment of the underlying disease.
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PMID:[Hypercalcemia in the elderly]. 218 Jan 40

Thionapthene-2-carboxylic acid (TNCA) was previously shown to lower serum calcium concentrations in hypercalcemic rats: however, oral administration of TNCA may cause gastric irritation. We have assessed thionapthene-2-carboxylic acid lysine salt (TNLY) for its effects on serum calcium concentration and survival in rats bearing the hypercalcemic Leydig cell tumor. TNLY (0.6-1.8 mmol/kg/day) produced a marked and prolonged dose-related decrease in serum calcium concentration. At the highest dose of 1.8 mmol/kg/day, hypocalcemia occurred. Effects were sustained for 96 hours or longer. In tumor-bearing rats that were not yet hypercalcemic, pretreatment with TNLY (0.9 mmol/kg/day) did not induce hypocalcemia and the onset of hypercalcemia was prevented. Neither TNLY nor dichloromethylene diphosphonate (CL2MDP), a potent inhibitor of bone resorption, significantly prolonged overall survival. We concluded that TNLY is a potent antihypercalcemic agent that warrants further testing for use in the treatment of hypercalcemic disorders.
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PMID:The effects of thionapthene-2-carboxylic acid-lysine on the hypercalcemia of malignancy in the rat. 252 8


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