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

Influence of vasoactive intestinal polypeptide, neuropeptide Y, calcitonin gene-related peptide, and substance P was investigated on dispersed parathyroid cells of adult cattle. At a physiological concentration of extracellular calcium, vasoactive intestinal polypeptide stimulated the parathyroid hormone release in a dose-dependent manner, whereas no effects were noted for the other peptides. The dependency of PTH secretion upon extracellular calcium was shifted to the right by vasoactive intestinal polypeptide at 10(-6) mol/l, with a tendency for greater effects at low (0.5 mmol/l) than high concentrations (2.0-3.0 mmol/l) of the cation. Vasoactive intestinal polypeptide significantly enhanced cAMP release of the parathyroid cells, whereas no influence was noted on cytoplasmic calcium or pH within the cells. The results suggest that vasoactive intestinal polypeptide stimulates the PTH release by interaction with cAMP production of the parathyroid cells. This effect may contribute to the development of hypercalcemia in patients with neuroendocrine tumours secreting vasoactive intestinal polypeptide.
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PMID:Vasoactive intestinal polypeptide stimulates parathyroid hormone release by interaction with cyclic adenosine monophosphate production of bovine parathyroid cells. 170 45

Gallium nitrate, a novel drug for the treatment of cancer-related hypercalcaemia, inhibits osteoclast activity but does not affect osteoclast morphology or viability. Limited clinical experience in patients with cancer-related hypercalcaemia indicates that gallium nitrate is effective in restoring normocalcaemia in 75 to 85% of patients and is well tolerated in those with preserved renal function, producing few clinically relevant adverse effects. In comparative clinical trials it proved a more effective antihypercalcaemic agent than calcitonin or etidronate and produced a longer lasting normocalcaemic response. Gallium nitrate would appear to be indicated in symptomatic patients with cancer-related hypercalcaemia who have failed to respond to adequate rehydration.
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PMID:Gallium nitrate. A review of its pharmacological properties and therapeutic potential in cancer related hypercalcaemia. 171 24

Murine gamma-interferon (MuIFN-gamma) is a potent inhibitor of bone resorption induced by interleukin 1 and parathyroid hormone-related protein in vitro. To investigate whether MuIFN-gamma is also effective in vivo, the cytokine was injected s.c. into hypercalcemic, tumor (EC-GI)-bearing nude mice, in which parathyroid hormone-related protein and interleukin 1 alpha are synergistically responsible for causing humoral hypercalcemia. When MuIFN-gamma was injected s.c. at a dose of 1 to 20 x 10(4) units for 5 days consecutively, serum calcium concentrations in the tumor-bearing mice decreased in a dose-dependent manner. The minimal effective dose was 5 x 10(4) units/mouse. Unlike calcitonin, which decreased the serum calcium concentration for only 1 to 2 days despite continuous daily injections, MuIFN-gamma decreased it for more than 7 days even after the injections had been stopped. Human gamma-interferon was completely ineffective. The decrease in serum calcium concentration was accompanied by a decrease in urinary calcium excretion. Histological examination of the femur revealed a decreased number of osteoclasts in the MuIFN-gamma-treated mice. Furthermore, MuIFN-gamma, when injected into nude mice or normal mice at a dose of 15 x 10(4) units for 3 days, almost completely abolished the formation of multinucleated osteoclast-like cells in vitro. These findings suggest that MuIFN-gamma suppresses the formation and maturation of osteoclasts and inhibits osteoclastic bone resorption, resulting in the prolonged decrease of serum calcium concentration seen in hypercalcemic, tumor-bearing nude mice. Therefore, bone resorption inhibitors like MuIFN-gamma, which ameliorate humoral hypercalcemia without an escape phenomenon, are potentially useful for the treatment of malignancy-associated hypercalcemia.
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PMID:Prolonged decrease of serum calcium concentration by murine gamma-interferon in hypercalcemic, human tumor (EC-GI)-bearing nude mice. 172 16

Calcitonin has been used clinically to treat hypercalcemia, Vitamin D intoxication, osteolytic bone metastases and increased skeletal remodeling in Paget's disease. In general calcitonin is given every 6 to 12 hrs intramuscularly or subcutaneously. It has been found in this study that the same results can be achieved by giving calcitonin through eyes as ophthalmic solutions. When 25 microliters of 0.05% calcitonin was given as eyedrops to New Zealand white rabbits, it did not reach the concentration achieved by i.v. administration at the same dose level. The systemic absorption of calcitonin did not reach the level achieved by i.v. administration even though the eyedrop concentrations were increased 2-fold (0.1%) to 10-fold (0.5%). When absorption enhancers such as BL-9 and Brij-78 were added to calcitonin eyedrops, however, the systemic absorption of calcitonin was enhanced markedly. BL-9 (0.5%) increased calcitonin (0.5%) absorption 16-20 fold and raised blood concentration of calcitonin above levels achieved by i.v. injection (25 microliters, 0.05%) with 0.5% calcitonin eyedrops instillation. Effects of Brij-78 (0.5%) were even more impressive. It increases calcitonin absorption 22-24 fold and raised the blood concentration of calcitonin above the levels achieved by i.v. injection (25 microliters 0.05%) with 0.15% and 0.5% calcitonin eyedrops instillation. These results indicate that the therapeutic level of calcitonin can be reached through the ocular route.
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PMID:Systemic administration of calcitonin through ocular route. 173 6

Calcitonin secretion is stimulated by acute hypercalcemia. Furthermore, in the rat, the calcemic response to parathyroid hormone (PTH) is decreased by calcitonin stimulation. However, in renal failure, it is not known if an increase in the serum calcium concentration within the physiologic range of serum calcium stimulates calcitonin and whether the increased calcitonin decreases the calcemic response to PTH. In the present study, four groups of pair-fed rats were evaluated: normals (N); parathyroidectomy (PTX); and two groups with renal failure (RF)--basal serum calcium less than 8.5 mg/dl (RFa) and basal serum calcium greater than 8.5 mg/dl (RFb). Hypocalcemia was induced by parathyroidectomy or in the RFa group, by a high phosphate diet. Increases in the serum calcium were produced by a 48 hour infusion of rat 1-34 PTH. In the RFa and PTX groups, stimulation of calcitonin was observed as the serum calcium increased from hypocalcemia to normal levels of calcium (P less than 0.01). In all four groups, increasing the serum calcium from normal levels to hypercalcemia increased the serum calcitonin level (P less than 0.05). The relationship between serum calcitonin and calcium was best expressed as a sigmoidal curve. In the two groups with basal hypocalcemia, PTX and RFa, the calcitonin-calcium curve was shifted to the left of the N and RFb groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sigmoidal relationship between calcitonin and calcium: studies in normal, parathyroidectomized, and azotemic rats. 174 20

This study was conducted in order to establish whether C cells, which are responsible for secretion of calcitonin within the thyroid gland, change either in volume or morphology under conditions of chronic hypercalcemia in primary hyperparathyroidism. Out of 106 primary hyperparathyroid patients undergoing surgery, in 11 cases the thyroids were excised and examined for changes in the C cell. As a control group we used thyroids removed in another 14 cases undergoing thyroidectomy or laryngectomy. Calcitonin in the C cell was observed by optical microscope after immuno staining using the indirect peroxidase-labeled antibody technique. C cells are not evenly distributed within the thyroid. However, there is excellent positive correlation (p less than 0.001) between the C-cell index, which is the average of two tissue samples excised from the area at the border between the upper 1/3 and middle 1/3 of the thyroid lobe (the area where most C cells are found), and the total number of C cells. The C-cell index can thus be used as an indicator of the total number of C cells in the thyroid. The number of C cells decreased (p less than 0.01) as the level of calcium in serum increased. In patients with primary hyperparathyroidism, this decrease in C cells was significantly greater (p less than 0.025) than in the controls. Focal C cell hyperplasia and diffuse C cell hyperplasia were present in both the control group and primary hyperparathyroid group, but there was no significant difference between the two groups as to the frequency of occurrence. For both these conditions the rate of occurrence was considered within normal ranges for C cell morphology. We concluded that the decrease in C-cell count in primary hyperparathyroidism patients with chronic hypercalcemia is due to consumption of calcitonin in the C cell.
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PMID:[Immunohistochemical studies on the thyroid C-cells in primary hyperparathyroidism]. 176 Nov 42

In hospitalized patients primary hyperparathyroidism (HPT) and neoplasms account for more than 90% of all hypercalcemias. Measurements of parathyroid hormone, particularly when combined with dynamic tests using calcitonin and EDTA have a high specificity and sensitivity in the differential diagnosis of hypercalcemia but are time-consuming and costly for screening purposes. Most chemical autoanalyzers beside serum calcium also measure serum chloride, phosphate and albumin. In order to evaluate how these simple variables could differentiate between HPT and hypercalcemia due to malignant disorders, 110 measurements from HPT subjects and 111 measurements from cancer patients with hypercalcemia were used. Serum chloride was best among the simple variables to separate the two disorders and classified 84% of the hypercalcemic subjects correctly. When serum phosphatase and albumin were added giving the formula (serum chloride-84) x (albumin-15)/phosphate, only 3% of the cancer and 4% of the HPT subjects were misclassified when borderline values (400-500) were excluded (5% of the sample). In conclusion, while other more sensitive and expressive tests exist to establish the cause of hypercalcemia the above mentioned formula is a cheap and easy screening test for a preliminary diagnosis.
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PMID:Serum chloride in the differential diagnosis of hypercalcemia. 177 37

We report a case of severe hypercalcaemia in a 16-year-old patient, 24 weeks after immobilization for quadriplegia. The biochemical and histomorphometric parameters showed increased osteoclastic resorption and decreased osteoblastic formation. Hydration, chair sitting, salmon and porcine calcitonin, sodium etidronate were unable to normalize the hypercalcaemia. The new antiosteoclastic agent, 3-amino-1 hydroxypropylidene-1, 1-bisphosphonate (AHPrBP), was effective in normalizing serum calcium and biochemical parameters of osteoclastic activity within five days. Bone histomorphometry showed a marked reduction in osteoclastic activity after AHPrBP treatment, as well as a drastic depression of osteoblastic activity, presumably due to the reduction of bone turnover. This case represents to our knowledge, the first successful use of AHPrBP in the treatment of immobilization hypercalcaemia.
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PMID:Aminohydroxypropylidene bisphosphonate (AHPrBP) treatment of severe immobilization hypercalcaemia in a young patient. 179 Jun 47

A child with acute lymphoblastic leukemia, spinal osteoporosis with vertebral compression fractures, and hypercalcemia appearing early in the course of the hematologic disease was followed for two and a half years. Bone mineral density (BMD), measured by single photon absorptiometry at the radial shaft, was within normal limits for age and sex. However, x-rays of vertebrae and vertebral BMD, measured by dual photon absorptiometry, showed marked demineralization. Despite leukemic remission, the spinal osteoporosis became worse and the patient required aggressive treatment for eight months. Treatment included 50 units of calcitonin subcutaneously every other day, 1,000 mg/day of oral calcium, and 3,000 IU/day of vitamin D. The back pain disappeared quickly, and laboratory controls showed a significant diminution of bone turnover. No new compression fractures occurred. Eighteen months later, the patient continued in remission and menarche had occurred. Dual photon absorptiometry revealed a significant "catch up" of the lumbar spine BMD. X-ray examination showed a marked remodeling of the vertebral bodies. BMD measurements in this child indicate that bone loss affected the trabecular bone compartment or occurred only at active bone marrow sites. The rapid clinical amelioration and objective biochemical, densitometric, and radiologic evidence of bone improvement warrant further clinical trials on similarly affected patients.
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PMID:Vertebral compression fractures at the onset of acute lymphoblastic leukemia in a child. 183 Feb 97

We report our experience of the presentation and management of symptomatic hypercalcaemia in advanced lung cancer. Between 1981 and 1987, 55 patients required urgent admission due to rapid clinical deterioration accompanied by significant hypercalcaemia (greater than 2.75 mmol l-1). Forty patients (72%) had squamous cell cancer, five small cell, three large cell, two adenocarcinoma and five unclassified. Thirty-five had evidence of bony metastases. Symptoms were categorized for each patient on the basis of being either potentially attributable to hypercalcaemia or not. All patients were rehydrated but specific treatment schedules over the period varied [1981-1985: steroids, calcitonin, mithramycin; 1985-1987: aminohydroxypropylidene bisphosphonate (APD)]. Treatment resulted in a significant reduction in the prevalence of all systems except for pain and nausea/vomiting; the greatest effect being seen on central nervous system and renal tract symptoms (75 and 80% reduction respectively; P less than 0.005 pre- versus post-treatment). Overall, 45 patients (82%) had a biochemical response; serum calcium fell from 3.28 +/- 0.33 mmol l-1 (mean +/- SE) to a nadir of 2.54 +/- 0.36 mmol l-1 (P less than 0.001). Twenty-five (49%) patients were discharged home. We conclude that despite the poor life expectancy of this group of patients (median survival 42 days) treatment of hypercalcaemia is worthwhile as it results in a significant symptomatic improvement.
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PMID:Symptomatic hypercalcaemia in lung cancer. 183 17


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