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)

Calcitonin and its carboxyl-terminal flanking peptide (PDN-21), also encoded by the calcitonin gene, were measured by RIA in unextracted serum of normal subjects and patients with primary hyperparathyroidism and surgically verified and suspected medullary thyroid carcinoma. Serum PDN-21 was detectable (greater than 0.005 ngeq/ml) in the large majority of normal subjects (92%), and the values increased significantly more in men than women (4.8- and 2.0-fold, respectively; P less than 0.01) in response to 1-min iv calcium injections. Calcitonin was detectable (greater than 0.025 ngeq/ml) in only 25% of normal subjects before iv calcium and became measurable after iv calcium in 88% of men and 41% of women. In patients with chronic hypercalcemia due to primary hyperparathyroidism, PDN-21 and calcitonin were within normal limits. In normal subjects, iv pentagastrin (0.5 microgram/kg BW) did not increase PDN-21, and calcitonin remained undetectable. In 41 medullary thyroid carcinoma patients, basal PDN-21 and calcitonin levels were increased similarly, and they were stimulated in response to iv calcium or iv pentagastrin. In 5 siblings of medullary thyroid carcinoma patients, PDN-21 and calcitonin were increased in response to iv pentagastrin, and we suspect C-cell hyperplasia or medullary thyroid carcinoma. In conclusion, a diagnostically useful RIA for the measurement of PDN-21 in unextracted serum which complements calcitonin measurements has been developed.
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PMID:Diagnostic evaluation of measurements of carboxyl-terminal flanking peptide (PDN-21) of the human calcitonin gene in human serum. 390 67

Calcitonin was detected by RIA in sera from four marine species, leopard sharks (Triakis semifasciata), horn sharks (Heterodontus francisci), thornback rays (Platyrhinoides triseriata), and kelp bass (Paralabrax clathratus). These animals have levels of calcitonin and calcium higher than freshwater and terrestrial species have. The administration of salmon calcitonin to bass (4 micrograms/kg BW) produced hypocalcemia and hypophosphatemia as has been reported for other bony vertebrates. In marked contrast, calcitonin produced a prompt hypercalcemia in sharks; the average was 9.8% increase in serum calcium in nine animals with no attendant change in phosphorus. These findings demonstrate that calcitonin can increase serum calcium in sharks. Because shark skeleton is composed of cartilage, this hypercalcemic effect of calcitonin does not require a bony skeleton.
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PMID:Calcitonin produces hypercalcemia in leopard sharks. 396 31

Pulmonary cancers produce many hormonal polypeptides. There is a tumor-specific pattern to the appearance of abnormal adrenal function and inappropriate secretion of vasopressin, which are frequently found in small cell undifferentiated carcinoma but occur only very rarely, if at all, in squamous tumors. Humoral hypercalcemia, on the other hand, occurs almost entirely in squamous tumors and is rarely if ever seen in small cell or large cell tumors or in adenocarcinoma. In contrast, "big ACTH" and beta lipotropin are found in the plasma and tumor extracts of lung cancers of all types. Calcitonin and the beta chain of human chorionic gonadotropin are also found in the plasma of a considerable portion of patients with all histological types of lung cancers.
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PMID:The pattern of ectopic hormone production in lung cancer. 627 Sep 16

The etiology of tumor-induced hypercalcemia was investigated in a transplantable Leydig cell tumor of the Fischer rat. In this model, serum calcium rose from a baseline of 10.4 +/0 0.3 mg/dl to 12.5 + 0.4 mg/dl at day 10 and 16.4 +/- 1.3 mg/dl (p less than 0.001) at day 13 post transplant. Urinary calcium also increased from 1.52 +/- 0.17 mg/d to 3.52 + 0.72 mg/d (Day 12, p less than 0.01). Serum phosphate decreased from a baseline of 7.5 +/- 0.3 mg/dl to 5.5 +/- 0.6 mg/dl at day 13 (p less than 0.05). At day 13 serum immunoreactive parathyroid hormone levels fell 76% from baseline (p less than 0.01). Calcitonin increased from 59 +/- 2 pg/ml to 88 +/- 9 pg/ml (p less than 0.02). The plasma prostaglandin E metabolite, 13,14-dihydro-15-keto-PGE2 increased from 407 +/- 103 pg/ml to 647 +/-62 pg/ml (p less than 0.05) and the active Vit D compound 1,25(OH)2D increased from 94.8 +/- 5.2 pg/ml to 162.3 +/- 11.8 pg/ml (p less than 0.01). Urinary cyclic AMP did not decrease in parallel with the parathyroid hormone level and, in fact, increased from 146 +/- 3 nmol/d to 172 +/- 27 nmol/d (NS). Administration of the cyclooxygenase inhibitor indomethacin (20 mg/Kg/d) or hydrocortisone (50 mg/Kg/d) did not prevent the development of hypercalcemia. This model is similar to many patients with humoral hypercalcemia of malignancy who demonstrate suppression of parathyroid hormone with elevated urinary cyclic AMP excretion and may prove useful in the understanding of the responsible mechanisms.
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PMID:Hypercalcemia in association with a Leydig cell tumor in the rat: a model for tumor-induced hypercalcemia in man. 628 3

It is proposed that this review will adopt the following format: establishment of hypercalcemia. This demands a discussion of the problem of normal ranges, the usage of either total calcium or ionized calcium in making this decision and where total calcium is used whether adjustment of this value for serum protein concentration should be used and if so, the formulae which have been cited to perform this. Having established hypercalcemia why is it necessary to differentiate this? This will involve reviewing those clinical situations in which differentiation of hypercalcemia has been attempted and will include an attempt to produce an up to date indication of conditions in which hypercalcemia has been described. When hypercalcemia has been established the laboratory tests which have been further used to discriminate will be divided into single tests such as N- or C- terminal parathormone, 1,25- dihydroxycholecalciferol, cyclic AMP; the combination tests which have been used including phosphate clearance, chloride vs. bicarbonate etc. proceeding to those groups which have used discriminant function to help in the decision making; dynamic testing will also be discussed particularly with reference to steroid suppression but will also include other known suppressants such as Mithramycin and Calcitonin. A final section will be included attempting to assess overall the present state of art in differentiating laboratory diagnosis of hypercalcemia and will also attempt to highlight those areas which appear to be most fruitful areas of progress in the future.
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PMID:Differential laboratory diagnosis of hypercalcemia. 638 33

The authors investigated the effect of acute hypercalcaemia induced by a 2-hour intravenous infusion of calcium gluconate (8.9 mg Ca2+/kg b. w.) on the lactotrophic secretory reserve assessed by the test with insulin hypoglycaemia (delta PRL) and the effect of an intravenous bolus of 50 IU synthetic salmon calcitonin on the lactotrophic secretory reserve assessed by means of the TRH test (delta PRL). Acute hypercalcaemia inhibits PRL levels stimulated by insulin hypoglycaemia (p less than 0.01) as well as delta PRL (p less than 0.01). Calcitonin reduces PRL levels at rest and TRH stimulated levels (p less than 0.05 and p less than 0.01, respectively) as well as delta PRL (p less than 0.01). The prolactin inhibiting effect of calcitonin resembles markedly the effect of hypercalcaemia. The exact mechanism of these changes and the physiological impact of calcitonin on the regulation of PRL secretion is not known.
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PMID:Hypercalcaemia and calcitonin inhibit prolactin secretion. 644 27

Experimental studies have suggested that in primary hyperparathyroidism (HPT) the cells of the hyperfunctioning parathyroid tissue retain some capacity for stimulation and that an increase in secretion of parathyroid hormone (PTH) can occur when the extracellular calcium concentration is lowered within the hypercalcaemic range. We have tested this hypothesis in 23 patients with HPT, 10 patients with hypercalcaemia of other origin (7 of whom had disseminated malignant disease) and 17 normal subjects. In all three groups a single injection of 100 MRC units of salmon calcitonin caused a reduction in serum calcium of approximately 3 to 5%. In the hypercalcaemic patients this reduction was correlated to the basal calcium level (r = -0.57, P less than 0.01). In the patients with HPT, although they all remained hypercalcaemic, the decrease in serum calcium was associated with a mean increase in serum PTH of 10%. Only in 2 patients did such an increase fail to occur despite an adequate decrease in serum calcium. These 2 patients had high basal PTH levels and the lack of response might have been due to a high degree of autonomous parathyroid function. Calcitonin also reduced serum calcium and increased serum PTH in normal subjects. None of the patients with hypercalcaemia of other origin than primary HPT displayed a secretory PTH response to serum calcium reduction. Thus, this test could be of practical clinical value, particularly in patients with borderline PTH values. A calcitonin-induced rise in PTH while serum calcium is lowered within the hypercalcaemic range strongly suggests primary HPT.
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PMID:A stimulation test with calcitonin for differential diagnosis of hypercalcaemia. 649 90

Because calcitonin administration has been shown to decrease the serum calcium level in certain hypercalcemic conditions, 10 patients on maintenance dialysis with renal osteodystrophy and persistent hypercalcemia were treated with salmon calcitonin for 3 months. While plasma calcium concentrations were reduced by calcitonin therapy in four patients, therapy was ceased in two patients due to a worsening of their hypercalcemia, although in another two patients the initial worsening of the hypercalcemia settled with continued therapy. No significant changes in calcium levels occurred in the remaining two patients. Analysis of the data suggests that a hypocalcemic effect of calcitonin was most likely in the presence of osteomalacia, while predominant osteitis fibrosa favored a hypercalcemic response. Calcitonin administration caused a mean increase in parathyroid hormone (PTH) secretion 3.6 +/- 1.5 to 6.5 +/- 1.7 ng/ml; p less than 0.05) after 6 weeks of therapy. Three patients reported improvement in their bone pain. These studies show that despite possible symptomatic and morphological effects of calcitonin, its hypocalcemic effect in patients with renal osteodystrophy and hypercalcemia is inconsistent.
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PMID:Effect of calcitonin on hemodialysis patients with hypercalcemia and renal osteodystrophy. 653 90

Forty patients with various neoplasias and radiological and scintigraphic evidence of multiple osteolytic lesions were studied between March 1979 and December 1981 at the Savona Oncology Service. All of them were treated with chemo and/or hormone therapy, plus 100 UMRC salmon calcitonin a day for 20 days a month until a clinical improvement was observed. The parameters for evaluation were: radiography and scintigraphy of the skeletal segment involved, blood calcium, alkaline phosphatase, intensity of pain, and restriction of function. An assessment was made before and after calcitonin management. Blood calcium fell in all cases even in the range of those initially normal. Alkaline phosphatase decreased in 83.3% and pain disappeared or was less severe in 87.50%. Good results were also observed with regard to restriction of function. Good recalcification of some osteolytic lesions was noted in 7 cases (17.5%). Calcitonin thus proved effective in the correction or prevention of damage caused by hypercalcaemia, and was particularly useful in the reduction of pain and functional damage. Its analgesic effect often appeared at an early stage.
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PMID:[Use of calcitonin in neoplastic osteolysis]. 683 60

A cervical lymph node enlarged since 3 weeks was to be removed in a 12-year-old boy, whose only complaint was slight fatigue. Routine screening revealed hypercalcemia of 7.3-8.1 mval/l. This rose to 9.2 mval/l despite furosemide-induced high fluid turnover and prednisone while diagnostic evaluation proceeded. Serum phosphate was low consistently. Malignancy, vitamin D-intoxication, immobilisation and familial conditions could be ruled out as causes. Highly elevated serum-parathormone levels inspite of hypercalcemia, and ultrasonography of the neck were the most helpful evidence of a parathyroid adenoma. Calcitonin was effective in lowering serum-calcium to 6-7 mval/l preoperatively.
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PMID:[Asymptomatic, excessive hypercalcemia n a 12-year-old boy]. 685 83


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