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

The hypercalcemia observed during the acute calcitonin test reflects the size and the activity of the osteoclastic population throughout the entire skeleton. Several calcitonins of animal origin (pork, salmon) have already been used for this test in human pathology, but the results can be flawed by the presence of anti-calcitonin antibodies. The authors demonstrate that human synthetic anti-calcitonin in man has a hypocalcemia effect identical to salmon synthetic calcitonin, with an equipotential dose for the rat. The systematic study of acute salmon calcitonin in various osteopathies makes it possible to note a certain number of paradoxical responses with prolonged hypercalcemia in the hours following injection. This is observed especially in the "hyperosteoidosis states" and the authors attempt to give it a physiopathological explanation. Finally, the acute salmon calcitonin test can be used as a mean of surveillance of the anti-osteoclastic activity of the disphosphonates in the treatment of Paget's disease.
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PMID:[The hypocalcemia test, using human and salmon synthetic calcitonins. Paradoxical hypercalcemic responses. Responses in patients with Paget's disease treated with EHDP]. 11 60

Albright in 1944 described a syndrome of hypercalcaemia in patients immobilized following fractures through bones affected with Paget's disease. This paper reports a further two cases in which this syndrome was considered the cause of hypercalcaemia with fatal outcome. Both patients had parathyroid adenomata. The literature is reviewed, and it is argued that no firm evidence for the existence of this syndrome has ever been put forward. The finding of hypercalcaemia in Paget's disease of bone should prompt an exhaustive search for its cause.
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PMID:Hypercalcaemia in Paget's disease of bone. 28 35

Thyrocalcitonin (TCT) is useful as a diagnostic and therapeutic agent in selected human diseases. Elevated plasma levels of TCT occur in patients with medullary carcinoma of the thyroid gland. Asymptomatic relatives of these patients harboring microscopic foci of tumor may have abnormal plasma levels of TCT in the basal state or after provocative stimuli. In both instances the plasma levels of TCT can be used in the diagnosis and management of this thyroid neoplasm. Elevated plasma levels of TCT have also been described recently in subjects with certain extrathyroidal neoplasms or renal failure. Moderate elevations are seen during normal pregnancy and in the neonatal period. Although exogenous TCT has actions on several organs, including bone, the kidneys and the gastrointestinal tract, its physiological role in man, if any, is still unknown. The recently reported measurements of TCT in normal subjects should facilitate the clarification of this issue. TCT has been used as a therapeutic agent in Paget's disease of bone, hypercalcemia of diverse etiologies, osteopenia and several other skeletal disorders. The dramatic improvement of patients with Paget's disease has been a unique therapeutic action of TCT. The therapeutic responses in hypercalcemic subjects given TCT are encouraging but more information is needed about the pharmacology of the hormones in these subjects before conclusions can be formed. At present the therapeutic role of TCT in osteopenia is hypothetical and the results of ongoing and future studies are needed to determine its effects.
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PMID:Clinical aspects of thyrocalcitonin. 109 26

A patient with histologically proven coexistent Paget's disease of the bone and parathyroid adenomatosis is described. She developed coma associated with hypercalcemia and underwent successfully surgical removal of two parathyroid adenomata. The differential diagnosis of hypercalcemia in patients with this rare association is discussed and the importance of early surgical treatment is stressed. A review of similar reported case is presented.
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PMID:Coma due to hypercalcemia in a patient with Paget's disease and multiple parathyroid adenomata. 114 50

We treated four hypercalcemic cancer patients by nasal hCT, 3 x 2 mg daily, which has been reported to be active in Paget's disease at lower doses. Only one patient became normocalcemic and mean (+/- SEM) calcium levels fell from 11.6 +/- 0.2 mg/dl before therapy to 10.7 +/- 0.6 mg/dl 2-3 days after starting hCT. The tolerance was excellent but, because of insufficient efficacy, we do not recommend this form of therapy for cancer hypercalcemia.
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PMID:Nasal human calcitonin for tumor-induced hypercalcemia. 139 70

A patient with extensive Paget's disease of bone presented with severe bone pain, hypercalcaemia and a large osteolytic lesion of the femur which developed during long-term therapy with etidronate. Treatment with pamidronate normalized serum calcium concentration and induced a complete biochemical remission. The osteolytic lesion was grafted with bone chips. A recurrence of the Paget's disease was associated with clear autonomous hypercalcaemic hyperparathyroidism. Five years after removal of 3 1/2 hyperplastic parathyroid glands, the patient remains in complete clinical and biochemical remission. These findings illustrate the pitfalls encountered in the management of Paget's disease and the value of combining medical and surgical interventions.
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PMID:Paget's disease with osteolytic lesions: combining medical and surgical treatments. 143 68

Pamidronate [aminohydroxypropylidene diphosphonate disodium (APD), disodium pamidronate] is an orally and intravenously active amino-substituted bisphosphonate which produces potent and specific inhibition of bone resorption at doses devoid of any significant detrimental effect on bone growth and mineralisation. Clinical trials indicate that pamidronate is effective in a variety of conditions characterised by pathologically enhanced bone turnover, including Paget's disease, hypercalcaemia of malignancy, osteolytic bone metastasis, steroid-induced osteoporosis and idiopathic osteoporosis. Pamidronate is highly effective in restoring normocalcaemia in patients with hypercalcaemia of malignancy associated with bone metastases but, in common with other bisphosphonates, is marginally less effective against humoral hypercalcaemia of malignancy. Comparative studies in this area have suggested that, at therapeutic doses, pamidronate has a more pronounced calcium-lowering action than etidronate (etidronic acid) and clodronate (clodronic acid) and provides a longer period of normocalcaemic remission. In Paget's disease arrest and, in some patients, reversal of the progression of osteolytic lesions by pamidronate is associated with a sustained reduction in bone pain, improved mobility and a possible reduced risk of bone fracture. In patients with osteolytic bone metastasis pamidronate reduces skeletal morbidity and slows the progression of metastatic bone destruction. Long term use of low-dose pamidronate in conjunction with conventional antiosteoporotic therapy may halt bone loss in steroid-induced and idiopathic osteoporosis. Pamidronate appears to represent a valuable addition to the drugs currently available for the treatment of symptomatic Paget's disease and cancer-associated hypercalcaemia, and shows promise in the treatment of osteolytic bone metastasis and osteoporosis.
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PMID:Pamidronate. A review of its pharmacological properties and therapeutic efficacy in resorptive bone disease. 170 54

The geminal bisphosphonates are a new class of drugs characterised by a P-C-P bond. Consequently, they are analogues of pyrophosphate, but are resistant to chemical and enzymatic hydrolysis. The bisphosphonates bind strongly to hydroxyapatite crystals and inhibit their formation and dissolution. This physicochemical effect leads in vivo to the prevention of soft tissue calcification and, in some instances, inhibition of normal calcification. The main effect is to inhibit bone resorption, but in contrast to the effect on mineralisation, the mechanism involved is cellular. These various effects vary greatly according to the structure of the individual bisphosphonate. The half-life of circulating bisphosphonates is very brief, in the order of minutes to hours. 20% to 50% of a given dose is taken up by the skeleton, the rest being excreted in the urine. The half-life in bone is far longer and depends upon the turnover rate of the skeleton itself. Bisphosphonates are very well tolerated; the relatively few adverse events that have been associated with their use are specific for each compound. Bisphosphonates have been used to treat various clinical conditions, namely ectopic calcification, ectopic bone formation, Paget's disease, osteoporosis and increased osteolysis of malignant origin. The three compounds commercially available for use in tumour-induced bone disease are in order of increasing potency, etidronate, clodronate and pamidronate. Most data have been obtained with the latter two agents. By inhibiting bone resorption, they correct hypercalcaemia and hypercalciuria, reduce pain, the occurrence of fractures, as well as the development of new osteolytic lesions, and in consequence improve the quality of life. In view of these actions, of their excellent tolerability and of the fact that they are active for relatively long periods, these compounds are, after rehydration, the drugs of choice in tumour-induced bone disease and an excellent auxiliary to the drugs used in oncology.
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PMID:Bisphosphonates. Pharmacology and use in the treatment of tumour-induced hypercalcaemic and metastatic bone disease. 172 40

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

In patients with either Paget's disease or hypercalcaemia associated with malignancy (HCM) we have assessed the parathyroid response to pamidronate therapy, both by immunoassay of serum intact parathyroid hormone PTH (1-84) and by measurement of indirect parameters of PTH bioactivity, tubular maximum reabsorption of phosphate (TmPO4/GFR) and nephrogenous cyclic AMP (NcAMP). In 12 patients with Paget's disease, therapy with pamidronate produced a small but significant decrease in adjusted serum calcium within the reference interval which was accompanied by a progressive increase in PTH (1-84) secretion and a corresponding fall in TmPO4/GFR and increase in NcAMP. In 12 patients with HCM pretreatment, PTH (1-84) concentrations were suppressed, whilst mean TmPO4/GFR was reduced and NcAMP was increased, compatible in most patients, with parathyroid hormone-related peptide (PTHrP) driven hypercalcaemia. Therapy with pamidronate produced the expected fall in serum calcium but caused an increase in PTH (1-84) secretion in the presence of absolute hypercalcaemia. The initial subnormal TmPO4/GFR decreased further to a nadir on day 5, and there was a corresponding further increase in NcAMP. By day 7, however, when PTH (1-84) concentrations were maximal, there was a significant paradoxical rise in TmPO4/GFR and a corresponding decrease in NcAMP. These data are consistent with a variable trigger point for PTH (1-84) secretion, one consequence of which is a reduction in the risk of hypocalcaemia following pamidronate. The results have major clinical implications for the interpretation of PTH (1-84) measurements in patients who are being treated or about to be treated for bone disease or for hypercalcaemia of malignancy (HCM).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Direct and indirect assessment of the parathyroid hormone response to pamidronate therapy in Paget's disease of bone and hypercalcaemia of malignancy. 184 62


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