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)

Single intravenous infusions of 30 mg aminohydroxypropylidene diphosphonate were given to 16 patients who had malignant hypercalcaemia to assess host tolerance and the effect on serum calcium concentration. Ten of these patients also received intravenous rehydration or corticosteroids, or both. The serum calcium concentrations decreased significantly after treatment with aminohydroxypropylidene diphosphonate. Ten patients became normocalcaemic (normal range, adjusted for serum albumin, 2.25-2.75 mmol/l), two became hypocalcaemic, three showed decreases in serum calcium concentrations of more than 0.75 mmol/l, and one showed a decrease of more than 0.55 mmol/l. Only one patient had a minimum concentration greater than 2.77 mmol/l. Aminohydroxypropylidene diphosphonate was effective in metastatic and non-metastatic hypercalcaemia, and its hypocalcaemic effect was prolonged in some cases. There were no appreciable side effects. Single high dose infusions of aminohydroxypropylidene diphosphonate could replace conventional daily lower dose infusions, but the optimum frequency of high dose infusions remains to be determined.
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PMID:Effect of single high dose infusions of aminohydroxypropylidene diphosphonate on hypercalcaemia caused by cancer. 310 30

In 23 patients with hypoparathyroidism or pseudohypoparathyroidism treated with vitamin D, and in whom the dosage was adjusted downward or upward in response to hypercalcemia or hypocalcemia respectively, assays of serum 25-hydroxyvitamin D (25-OHD) were carried out in addition to the usual serum calcium assays. In 120 assays there was a significant correlation between serum 25-OHD levels and serum calcium levels (corrected for serum albumin). There was, however, no clear distinction between the 25-OHD levels of patients who were hypocalcemic, normocalcemic or hypercalcemic. The highest serum 25-OHD level found in a hypocalcemic patient was 1193 nmol/L and the lowest serum 25-OHD level found in a hypercalcemic patient was 605 nmol/L. It was not possible to predict subsequent episodes of hypocalcemia or hypercalcemia from the serum 25-OHD levels. The 25-OHD assay was found to be useful only in checking compliance. We conclude that the assay of serum 25-OHD is of no more value than serum calcium alone in the management of compliant patients.
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PMID:The value of serum 25-hydroxyvitamin D measurements in hypoparathyroid and pseudohypoparathyroid patients treated with calciferol. 348 79

The effects of thiazide diuretics on serum phosphate concentration, renal tubular threshold for phosphate, and urinary calcium excretion in children with renal hypophosphatemic rickets were studied. There were nine controlled acute studies conducted in five patients, and, in addition, seven long-term studies of up to 26 months were performed. During the acute studies, the children continued to receive the same doses of oral calcitriol and phosphate supplementation as at home. Hydrochlorothiazide, 1.50 to 2.25 mg/kg/d, was used alone in the first four studies; hydrochlorothiazide and amiloride at a dose of 1 mg for each 5 mg of hydrochlorothiazide were used in the other five studies. Administration of the diuretics for four days gave rise to a significant increase in serum phosphate concentration from 3.1 +/- 0.4 mg/dL to 3.7 +/- 0.9 mg/dL (P less than .01) and in tubular threshold for phosphate from 1.31 +/- 0.45 mg/dL to 1.74 +/- 0.60 mg/dL (P less than .01). These changes were accompanied by significant reductions in urinary sodium excretion from 135 +/- 39 mEq/24 h during the control period to 99 +/- 42 mEq/24 h on the fourth day of therapy (P less than .05), fractional sodium excretion from 0.99% +/- 0.42% to 0.81% +/- 0.42% (P less than .05), and urinary calcium excretion from 57.3 +/- 28.9 mg/24 h to 19.0 +/- 13.1 mg/24 h (P less than .01). Fractional excretion of phosphate divided by fractional excretion of sodium after the treatment with diuretics was not significantly different from that observed at the end of the control period. Increments in serum phosphate concentrations were correlated with elevations in serum albumin concentrations (r = .739; P less than .02). As an additional index of intravascular volume contraction, the elevations in serum phosphate concentrations were correlated with the increase in BUN, (r = .793; P less than .01). The addition of amiloride in the last five studies prevented the hypokalemia and alkalosis that had complicated the administration of hydrochlorothiazide. Long-term follow-up studies for a total of 119 therapy-months on six children and one adult, who continued to receive the diuretics concomitantly with calcitriol and phosphate supplementation, showed that they were free of complications except for a transient episode of hypercalcemia and hypercalciuria in one patient. In comparison with the previous period of treatment with calcitriol and phosphate without diuretics, linear growth velocity and healing of the rickets were not changed in two children and improved in the other four after the addition of hydrochlorothiazide and amiloride.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of hydrochlorothiazide and amiloride in renal hypophosphatemic rickets. 388 56

A circadian variation in serum calcium, albumin and PTH concentration in normal subjects has been demonstrated. The levels of the three blood constituents were remarkably constant during the day, but striking night and early morning changes occurred. Serum calcium levels were highest at 8:00 p.m. and reached a nadir between 2:00 and 4:00 a.m. Serum albumin levels were parallel to those of serum calcium. PTH levels began to rise after 8:00 p.m., reached the highest levels between 2:00 and 4:00 a.m., and fell to baseline values by 8:00 a.m. The nocturnal fall in serum calcium levels appears to be secondary to dilution of serum proteins by increasing blood volume. The nocturnal rise in PTH levels appears to be independent of serum calcium levels within the normal range but it can be abolished by induced hypercalcemia. Serum phosphate levels were lowest between 8:00 a.m. and 10:00 a.m. and highest between 2:00 a.m. and 4:00 a.m. The data presented suggest that circadian changes in serum phosphate levels are not mediated in toto by parathyroid hormone but they are exaggerated when the secretion of this hormone is inhibited. They are independent of growth hormone levels and activity but they are greatly modified during a prolonged fast.
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PMID:Circadian rhythm in serum parathyroid hormone concentration in human subjects: correlation with serum calcium, phosphate, albumin, and growth hormone levels. 505 63

Total and ionized calcium and other related parameters were measured in 34 patients with multiple myeloma. Hypercalcemia was not a major feature of the group of patients studied with only three patients exhibiting marked increases in total (Ca total) and ionized (Ca++) calcium concentrations. The Ca++/Ca total ratio was also maintained within relatively narrow limits. No major differences were found in the calcium fractions of patients with different types of multiple myeloma. Serum immunoreactive parathyroid hormone showed no consistent relationship with either the total or ionized calcium concentration. There were no correlations between increased total protein or reduced serum albumin concentrations and changes in total and ionized calcium fractions or Ca++/Ca total ratios. These results imply that in this group of myeloma patients, there was no significant binding of calcium by the monoclonal immunoglobulins.
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PMID:Frequency of calcium binding by monoclonal immunoglobulins in multiple myeloma. 646 28

Serum calcium was prospectively studied in 50 consecutive patients with active pulmonary tuberculosis. Twenty-four of them (48%) developed hypercalcaemia during an observation period of at least 8 weeks. Maximal increase in serum calcium (corrected for serum albumin) occurred three weeks after initiation of treatment, by which time 28% of the patients were hypercalcaemic. The increase in serum calcium was followed by a spontaneous remission. Only two patients developed symptoms related to hypercalcaemia, which promptly responded to steroid administration. No patient received vitamin D supplements before or during the study. No correlation could be found between hypercalcaemia and either the presence of acid-fast bacilli in the sputum or the season of the year. There was a trend for higher serum calcium values in the patients with the more severe radiographic changes on admission. Hypercalcaemia in patients with pulmonary tuberculosis seems to be triggered by chemotherapy. However, the mechanism(s) by which anti-tuberculosis treatment affects calcium metabolism remains uncertain.
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PMID:Serum calcium during chemotherapy for active pulmonary tuberculosis. 688 47

When rats or mice were immunized with sheep red blood cells, bacterial lipopolysaccharides or bovine serum albumin, a proliferative response could be detected in the bone marrow and spleen. This response was associated with a hypercalcaemic phase. Parathyroidectomy, which resulted in a protracted hypocalcaemia, prevented the development of an increase in levels of plasma calcium. This operation also prevented the rise in bone marrow proliferations following antigenic challenge, but did not ablate the normal proliferative response to antigen by cells in the spleen. Antibody production and numbers of antibody-forming cells were not significantly reduced by parathyroidectomy. These results suggest that there is a pool of antigen-insensitive cells in the bone marrow which are stimulated after antigenic challenge. It is postulated that these events were mediated by the development of a parathyroid-dependent hypercalcaemia which stimulates the cells non-specifically. These events may form part of a cellular homeostasis, replacing cells in peripheral lymphoid tissues.
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PMID:Changes in plasma levels of calcium and in bone marrow mitosis after antigenic challenge in rats and mice. 727 2

Alendronate (4-amino-1-hydroxybutylidine-1,1-bisphosphonate), an antiosteolytic agent, is currently under investigation for the treatment of osteoporosis. Earlier studies in animals from this laboratory disclosed that systemically administered alendronate is rapidly taken up by bone tissues to the extent of 60% to 70% of the dose and excreted by the kidney, 30% to 40% in 24 hr, and that renal excretion is the only route of elimination. This study was designed to explore the effect of calcium on plasma protein binding and the renal handling of alendronate. The binding of alendronate to rat plasma was concentration, pH and calcium dependent. The fraction of unbound drug in rat plasma increased from about 3% to 9% over a drug concentration range of 0.2 to 10 micrograms/ml. Supplementation of calcium strongly augmented the binding to serum albumin. The binding of alendronate in plasma increased with increasing pH from about 50% at pH 6.6 to 98% at pH 8.6. The effects of pH on the binding of calcium and of alendronate to serum albumin were qualitatively similar. Under steady-state conditions, the binding of alendronate was substantially lower in hypocalcemic rats but unchanged in hypercalcemic rats. Although hypocalcemia caused a significant decrease in the renal secretion of alendronate, there was no effect on the renal secretion of tetraethylammonium bromide and p-aminohippuric acid. The differential effect of hypocalcemia suggests that calcium may play an important role in the renal handling of alendronate. However, hypercalcemia resulted in a substantial decrease of renal secretion of all three compounds and the decreased renal secretion was associated with a marked decrease in the glomerular filtration rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of calcium in plasma protein binding and renal handling of alendronate in hypo- and hypercalcemic rats. 824 40

We examined 111 patients with acute type- or lymphoma type-adult T-cell leukemia (ATL) and compared them with 106 patients with non-Hodgkin's lymphoma (NHL). In addition to skin involvement and hypercalcemia which are already known to be frequent in ATL, ATL patients showed an higher incidence of hepatic involvement. There was more frequent palpable hepatomegaly, higher total bilirubin, GOT, GPT, lactate dehydrogenase (LDH), and alkaline phosphatase values in ATL than in NHL patients (p < 0.0001). Among 36 autopsied liver samples, invasion of ATL cells was confirmed in 22 cases. ATL patients with impaired hepatic function showed shorter survival times than patients without hepatic dysfunction. Moreover, ATL patients showed a worse performance status (PS), a higher incidence of lytic bone lesions, lower total protein (TP) and serum albumin levels than NHL patients. This invasive characters of ATL cells and consequent impaired general condition seemed to be factors affecting the poor prognosis recorded in ATL.
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PMID:Frequent hepatic involvement in adult T cell leukemia: comparison with non-Hodgkin's lymphoma. 932 95

Evaluation of growth hormone therapy in burns is limited and none is reported from developing countries where burns still carry high mortality. We analysed serial observations on the clinical and biochemical profiles in 13 patients with second and third degree burns who received recombinant human growth hormone (rhGH) (0.5 IU/kg body wt) for 2 weeks in addition to standard conservative treatment and in 9 patients who were managed with standard conservative treatment only. The two groups of patients had burns, comparable in extent and severity. Additional rhGH treatment resulted in improved wound healing (p < 0.001), delayed separation of eschars (p < 0.01), increase in haemoglobin (p < 0.05), serum albumin (p < 0.01), calcium (p < 0.05), phosphorus (p < 0.001), glomerular filtration rate (p < 0.05) and 7 fold elevation in IGF-1. Also, a reduction in weight loss (p < 0.01), nitrogen production rate (p < 0.05), catabolic index (p < 0.01), duration of sepsis (p < 0.01) and hospital stay by 40% (p < 0.01) was noted with rhGH therapy. Transient hypercalcemia (3 patients), albuminuria (2 patients) and elevated blood glucose (one patient) were noted in the rhGH treated group not necessitating any specific therapy. Mortality in rhGH treatment group was 8.3% compared to 44.5% in the "no rhGH" treatment group. These observations suggest significant benefits of short term rhGH treatment in burn patients on conservative management.
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PMID:Effect of growth hormone therapy in burn patients on conservative treatment. 991 74


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