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)

Vitamin D has complex effects in bone: it stimulates matrix formation and bone maturation but also enhances osteoclastic activity and may influence differentiation of bone cell precursors. Calcitonin inhibits the function of osteoclasts, reducing bone resorption, thus, the combination of vitamin D and calcitonin could result in a positive bone balance. We tested the hypothesis that chronic treatment with high doses of vitamin D (150,000 U/week), moderate doses of salmon calcitonin (120 MRC U/week), and adequate Ca supplementation (1 g/day) could be beneficial in osteoporosis. Thirteen women with postmenopausal osteoporosis received this treatment for 2-6 years (mean 3.5 years). No side effects, hypercalcemia, or hypercalciuria occurred. There was marked reduction in bone pain. The fracture rate in 11 patients with vertebral compression fracture was 240/1,000 patient years, threefold lower than the reported 834 fractures for untreated patients of similar age. Single photon bone densitometry of the radius did not change. Iliac crest bone biopsies obtained at the initiation and conclusion of the study showed a 43% increment in trabecular bone volume (P = 0.0003), without changes of the normal osteoid thickness, surface, and volume. Because single photon densitometry reflects mostly cortical bone, the data suggest that the combination of vitamin D and calcitonin increases trabecular bone mass and prevents the fall of cortical bone mass in osteoporosis. Previous reports suggest that calcitonin alone or with small doses of vitamin D increased bone mass for about 2 years. The present study suggests a prolonged beneficial effect of the combination of high doses of vitamin D with rather moderate (less than 150 MRC U/week) doses of calcitonin in postmenopausal osteoporosis.
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PMID:Effect of calcitonin and vitamin D in osteoporosis. 250 3

Calcium, injected to rats, elicits a rapid increase in translatable calcitonin mRNA, by acting probably at the post-transcriptional level, as no change in calcitonin mRNA could be detected by hybridization assay. In this study we have measured calcitonin mRNA extracted from rats subjected or not to acute hypercalcemia and pretreated or not with actinomycin D. Calcitonin mRNA was quantified by its ability to direct the synthesis of calcitonin (CT) precursors in a cell free system and by hybridization to a 32P cDNA probe specific for CT mRNA. Actinomycin D, injected 5 hours before calcium administration, decreased the incorporation of 3H adenine in liver and thyroid, but did not inhibit the rise in plasma levels of calcium and CT (measured by radioimmunoassay). The antibiotic was able to inhibit the eightfold increase in translatable mRNA elicited by calcium administration in the control animals. Hybridizable CT mRNA levels were not modified by the treatments. Thus the increase in translatable CT mRNA after calcium stimulation is independent of CT secretion and is probably due to post-transcriptional modifications involving the expression of other gene(s).
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PMID:Actinomycin D inhibits the rapid increase in translatable calcitonin mRNA provoked by acute calcium stimulation. 258 74

A 57-year-old female was admitted to our hospital with general lassitude, loss of appetite, nausea, upper abdominal pain, thirst, polydipsia and polyuria. On admission, she had an asymmetrical pear-shaped tumor in the right supraclavicular region and severe hypercalcemia. Plasma C-PTH was elevated to 22.72ng/ml. Plasma calcitonin was also elevated to 336 pg/ml. She died of respiratory and cardiac failure of two weeks after admission without any positive response to the treatment, including hemodialysis. Pathohistologically, the tumor was a parathyroid adenoma. The concentrations of C-PTH, intact PTH and calcitonin in the tumor tissue were markedly high: 4.56 micrograms/g wet, 13.9 ng/g wet and 50.7 ng/g wet, respectively. Immunohistologically, the tumor cells and the fibrous stroma were stained strongly positive to rabbit anti-human calcitonin antibody and rabbit anti-human N-PTH antibody by indirect immunoperoxidase staining. Calcitonin-producing tumors, except for medullary thyroid carcinoma are rarely reported. To our knowledge, this is the first report of such a calcitonin-producing parathyroid adenoma associated with primary hyperparathyroidism.
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PMID:A case of calcitonin-producing parathyroid adenoma with primary hyperparathyroidism. 258 94

Severe hypercalcemia is a potentially life-threatening complication of several diseases. Most commonly it is caused by cancers that enhance bone resorption. Impaired renal calcium excretion resulting from a combination of volume contraction and calcium-induced renal injury (nephrocalcinosis) plays a critical role in the genesis and aggravation of hypercalcemia. Treatment of hypercalcemia is based on treating the underlying disease, restoring extracellular volume, correcting electrolyte deficiencies (potassium and magnesium), and reducing bone resorption. Several measures are available to reduce bone resorption, of which the most efficacious are the bisphosphonates and plicamycin (mithramycin). One of these agents in combination with volume expansion can reduce serum calcium concentrations to near normal in most patients within 3 to 6 days. Because of the delayed hypocalcemic action of these agents, they should be administered early. Calcitonin has a more modest hypocalcemic action than the bisphosphonates or plicamycin but has a more rapid effect. Combining calcitonin with plicamycin or a bisphosphonate can enhance the rate of decline of the serum calcium level. Bone resorption also can be reduced by getting patients out of bed to stand or walk. Glucocorticoids may be effective in patients with hypercalcemia associated with high levels of vitamin D, such as sarcoidosis, some lymphomas, or vitamin D intoxication. Patients with mild to moderate hypercalcemia may be asymptomatic. Therapy in these patients should be directed at the primary disease as well as at preventing complications that could raise the level of serum calcium. Efforts should be made to prevent volume contraction and prolonged bed rest. Sedatives and narcotic analgesics, by reducing activity and oral intake, can raise serum calcium levels. In the future it may be possible to predict which patients with cancer are likely to develop accelerated local tumor-mediated or humorally mediated osteolysis. For example, high circulating levels of PTH-like peptides in patients with lung cancer might suggest a greater risk of developing hypercalcemia. These patients could be monitored more closely by periodically measuring urinary calcium. Another prophylactic approach would be to treat patients at risk of developing hypercalcemia with drugs, such as the bisphosphonates, that inhibit bone resorption.
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PMID:Treatment of hypercalcemia. 267 75

The calcitonin (CT) gene encodes at least 3 peptides: CT, the 21-aminoacid carboxyl-terminal flanking peptide (katalcin or PDN-21) and CT-gene related peptide. Normal thyroid C-cells as well as malignant ones co-secrete CT and PDN-21 in response to hypercalcemia, so assay of PDN-21 may be an usefull method to assess C-cells secretion. Because of our knowledge no data are available on PDN-21 values in children, we measured this peptide in healthy children and in spasmophilia (Sp), a disease that has been related to CT deficiency. We studied 16 healthy children (9 males, 7 females; aging from 3.0 to 11.6 years) and in 21 patients with diagnosed Sp (8 males, 13 females, aging from 4.6 to 13.0 years). PDN-21 were assayed in whole serum by RIA using synthetic human PDN-21 for standards, 125I-PDN-21 for tracer and specific antiserum. CT was measured the serum of the same subjects by RIA using an ultrasensitive methods. In healthy children PDN-21 serum values were 12.3 +/- 2.0 pg/ml and no significant differences were found between males and females. Children with Sp showed slow higher PDN-21 concentrations (14.0 +/- 1.4 pg/ml) than normals, but the difference was not statistically significant. Also CT values were not significantly different between normal children (21.4 +/- 3.7 pg/ml) and patients with spasmophilia (22.5 +/- 1.8 pg/ml). A high significant positive relation was found between katalcacin and CT levels in normals as well as in spasmophilics. The physiological effects of PDN-21 are actually unknown.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Katacalcin levels in healthy children and children with spasmophilia]. 268 35

The effect of salmon calcitonin (0.25 MRC mU/g body wt) was investigated on the serum calcium and inorganic phosphate levels of the frog. Rana tigrina. The hormone evokes hypocalcemia (on Day 1 and Day 3) which is followed by a significant hypercalcemia on Day 10. Thereafter, the level of calcium decreases again on Day 15. Calcitonin induces hypophosphatemia (on Day 3 and Day 5). Thereafter, hyperphosphatemia is recorded on Day 10. Normal serum phosphate value is achieved by Day 15. The results obtained in R. tigrina have been discussed in relation to the increased calcium deposits in the paravertebral lime sacs and to the possible enhanced secretion of the parathyroid glands.
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PMID:Influence of calcitonin administration of serum calcium and inorganic phosphate level of the frog, Rana tigrina. 273 50

The authors compared the effect of synthetic salmon calcitonin and synthetic somatostatin (SRIF) and hypercalcaemia on an oral glucose tolerance test (OGTT) in healthy subjects in relation to changes of insulin (IRI), somatotrophin (HGH) and cortisol levels. Calcitonin--100 U--in an intravenous infusion in the course of OGTT markedly altered the pattern of the blood sugar curve and of IRI levels. After the initial retardation of the rise of the blood sugar and IRI levels during the 15th and 30th min, the values of both variables increased parallel during the 120th and 180th min, as compared with the control examination after saline. SRIF--500 micrograms--administered in an intravenous infusion altered the pattern of the blood sugar and IRI curves in a similar way as calcitonin, however during the 120th and 180th minute when the blood sugar levels rose significantly the IRI levels did not rise. The curve of HGH levels on infusion with calcitonin displayed a typical three-phase course, as during the control OGTT. During infusion of SRIF the HGH levels were insignificantly but constantly reduced during the first 60 mins. of the OGTT and thus the typical three-phase shape of the curve was impaired. Calcitonin significantly raised the cortisol levels throughout the OGTT, while SRIF caused their slight decline during the 120th min. Hypercalcaemia induced by infusion of 13.3 mg Ca/kg body weight did not alter significantly the blood levels of glucose, IRI and HGH, but caused a significant rise of the cortisol level throughout the OGTT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of calcitonin, somatostatin and hypercalcaemia on metabolic and hormonal indicators during an oral glucose tolerance test (OGTT). 288 8

Calcitonin gene-related peptide (CGRP) in the thyroid has a dual localization to nerve fibers around blood vessels and follicles and to parafollicular (C) cells. CGRP was found to coexist with substance P (SP) in most of the nerve fibers; a few CGRP fibers seemed to lack SP, and a few SP fibers seemed to be devoid of CGRP. In the C cells, CGRP coexisted with calcitonin (CT). Cervical vagotomy (extirpation of the nodose ganglion) eliminated approximately 50% of the CGRP/SP fibers in the thyroid without any overt influence on CGRP/CT in the C cells. Removal of the superior cervical ganglion or chemical sympathectomy (6-hydroxydopamine treatment) affected neither thyroid CGRP/SP nerve fibers nor CGRP/CT-storing C cells. CGRP nerve cell bodies were numerous in the jugular-nodose ganglionic complex (notably in the jugular portion); in many of them, CGRP coexisted with SP. A few scattered CGRP nerve cell bodies also occurred in the laryngeal ganglion, whereas none was found in the thyroid ganglion. Hypercalcemia evoked by vitamin D2 treatment, which is known to degranulate thyroid C cells, reduced the thyroid content of both CGRP and CT. As tested in mice in vivo, CGRP and SP alone or together had no effect on basal or TSH- or isoprenaline-induced thyroid hormone secretion. Vasoactive intestinal peptide-stimulated iodothyronine release, on the other hand, was enhanced by CGRP, but not by SP. SP had no effect on combined vasoactive intestinal peptide-CGRP-stimulated iodothyronine release. These findings suggest that CGRP participates in the control of thyroid hormone secretion and that, like CT, CGRP in the C cells is under control of the serum calcium level.
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PMID:Calcitonin gene-related peptide in thyroid nerve fibers and C cells: effects on thyroid hormone secretion and response to hypercalcemia. 309 6

Paget's disease of bone is often discovered incidentally, but can have extensive metabolic and local mechanical complications. Treatment is not required for all patients and should only be undertaken for certain indications, and with a clear understanding of the three types of drugs available. Bone pain unmanageable with analgesics and pathologic fractures are the most common indications, while neurologic symptoms, hypercalcemia and congestive heart failure are less frequent ones. Calcitonin or mithramycin is used for the more urgent indications, and calcitonin or the diphosphonate, etidronate sodium (EHDP), for the more chronic ones. The drugs are generally efficacious and well tolerated.
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PMID:Paget's disease of bone: clinical features and treatment. 315 5

After 7 days in air on wet filter paper mudskippers had normal body weight and normal levels of plasma sodium, potassium, and phosphate. They were, however, significantly hypercalcemic. The hypercalcemia could be reduced by the daily intraperitoneal injection of synthetic eel calcitonin (1.67 microgram kg-1 day-1) and this effect was dose dependent with a maximal response at a dose of 3.33 micrograms kg-1 day-1. Calcitonin had no effect on plasma calcium levels of fish held in water but did induce significant hyperphosphatemia whether the fish were held in water or in air on wet filter paper with this effect being greater under the latter conditions. The hypocalcemic action of calcitonin was restricted to conditions under which the fish displayed patent hypercalcemia. Under no conditions did calcitonin produce significant hypocalcemia so it appears that the action of synthetic eel calcitonin in the mudskipper, Periophthalmodon schlosseri, is dependent upon the presence of excess plasma calcium and is thus more accurately described as being anti-hypercalcemic rather than hypocalcemic.
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PMID:Effects of calcitonin on plasma calcium and phosphate in the mudskipper, Periophthalmodon schlosseri (Teleostei), in water and during exposure to air. 338 5


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