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

In a prospective investigation, a large kindred (twenty-one subjects) with unexplained association of familial hypocalciuric hypercalcaemia and idiopathic interstitial lung disease was studied. Serum calcium was increased in fifteen patients (the youngest being 7 years old) and was associated with hypo- or normocalciuria. The abnormalities were not age-dependent. The serum concentrations of parathyroid hormone, 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3 and calcitonin were normal. In twelve patients the diffusing capacity (DLCO) and/or DLCO per unit lung volume was less than 75% predicted. This was often accompanied by a vital capacity of less than 80% predicted, and increased Tiffeneau index, and a reticulo-micronodular pattern with high diaphragm on chest X-ray. The decrease in DLCO was more pronounced in older non-smoking as well as smoking subjects (P less than 0.02) suggesting a progressing interstitial disease with age. The fibrosing alveolitis, which had been confirmed by open lung biopsy in three subjects, could not be attributed to sarcoidosis, collagen-vascular disease, or exogenous causes. The disturbances in the calcium homeostasis and in the diffusing capacity of the lung coexisted in seven of the twenty-one patients. Apparently, both abnormalities were inherited following an autosomal-dominant pattern but with a different penetration in each person, and seemed not be causally related to each other.
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PMID:Coexistence of hypocalciuric hypercalcaemia and interstitial lung disease in a family: a cross-sectional study. 392 83

High daily oral doses of 10 micrograms 1 alpha-hydroxycholecalciferol (1 alpha-OHD3) administered to adult rats produced toxic effects such as loss of body weight, hypercalcemia and bone resorption. However, small (0.09 microgram) and moderate (0.9 microgram) daily doses of 1 alpha-OHD3 did not produce toxic effects during six weeks of observation. Serum calcium level was only slightly raised, but bone mass, bone mineral and organic matter contents, including collagen and nucleic acids of the cortical bone matrix, significantly increased, while the amount of glycosaminoglycans was reduced. Treatment with small daily doses of 1 alpha-OHD3 (0.09 microgram/day for six weeks) produced a more pronounced effect on the variables studied than did the moderate dosage (0.9 microgram). 1 alpha-OHD3 promotes new bone formation in the mature rat skeleton after conversion to 1,25 dihydroxycholecalciferol [1,25(OH)2D3] in the liver, probably by exerting a direct effect on bone tissue rather than through indirect hormonal events.
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PMID:Effect of 1 alpha-hydroxycholecalciferol on bone mass and composition of cortical bone in adult male rats. 616 32

Calciphylaxis is a local tissue calcific reaction at the site of an injection of challenger substance given a critical time period after the oral administration of a sensitizer substance such as dihydrotachysterol (DHT), vitamin D or parathormone. Cutaneous calciphylaxis is readily induced in the rat but not in the mouse and this may be because, in the latter, the challenger substance is absorbed rapidly by macrophages. In the rat the administration of 500 micrograms/0.1 ml of DHT followed after 24 h by the subcutaneous (SC) injection of ferric chloride (FeCl3) (30 micrograms/0.1 ml) is followed rapidly by calcification of the SC site. There is an early transient acute inflammatory reaction with the incrustation of collagen fibres by the iron salt and an apparent exudation of calcium and phosphate ions from the bloodstream. These ions also become associated with collagen fibres. Two days after injection macrophages and multinucleated giant cells become the dominant cells. Calciphylaxis is a useful experimental model of ectopic calcification and is associated with an initial hypercalcaemia. The diphosphonates ethane-1-hydroxy-1, 1-diphosphonate (EHDP) and dichloromethylene diphosphonate (Cl2MDP) are effective inhibitors of the calciphylactic reaction when administered prior to the initiation of the experimental procedure.
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PMID:Cutaneous calciphylactic reactions in the mouse and the rat and the effects of diphosphonates on the reaction in the rat. 623 Apr 25

Experimental chronic renal failure (CRF) in rats gave rise to azotemia, hyperphosphatemia, reduction in the proportion of the diaphyses, decrease in them of calcium, phosphorus and hydroxyproline, and to the lowering of the calcium content in the epiphyses. Administration to the animals of 0.025 microgram of 1,25-dioxycholecalciferol (1,25(OH)2D3) a day did not make the indicators under consideration return to normal. At the same time 1,25(OH)2D3 enhanced the degree of hyperphosphatemia and demineralization of the epiphyses, provoked moderate hypercalcemia and dramatically enhanced calcinosis in the aorta and in the remainder of the kidney. Administration of 24,25-dioxycholecalciferol (24,25(OH)2D3) in a dose of 0.25 microgram made the majority of the indicators return to normal, increasing the proportion of the diaphyses and the content in them of calcium and phosphorus, reducing the blood phosphorus content and the degree of azotemia. Furthermore, 24,25(OH)2D3 raised the collagen content in the diaphyses and epiphyses. A higher dose of 24,25(OH)2D3 (1.25 microgram) did not appear more effective. In none the doses applied, 24,25(OH)2D3 produced hypercalcemia or calcinosis. Combination of 1,25(OH)2D3 in a dose of 0,025 microgram and 24,25(OH)2D3 in a dose of 1,25 microgram slightly reduced the hypercalcemic, hyperphosphatemic and calcinosis-inducing effects of 1,25(OH)2D3, completely prevented osteoporotic alterations in the diaphyses, but enhanced the demineralization in the epiphyses, which may point to the advisability of reducing the doses of these metabolites on combined use. The data obtained indicate that 24,25(OH)2D3 is a more effective and safer agent for correcting the disturbances of the phosphorus-calcium metabolism and osseous lesions in CRF than 1,25(OH)2D3.
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PMID:[Effect of 24,25-dioxycholecalciferol on calcium-phosphorus metabolism and bone tissue in rats with experimental renal failure]. 633 22

We describe a study of a boy with neonatal severe primary hyperparathyroidism (NSPHP) and alkaptonuria born to related parents of Turkish origin. The clinical and chemical courses (e.g. of mineral metabolism, of urinary excretion of amino acids and collagen metabolites) in response to various therapeutic approaches including total parathyroidectomy (PTX) are reported. Urinary excretion of calcium was unusually low before and immediately after PTX, and later during an inadvertent vitamin D intoxication. It corresponded to values typical for patients with familial hypocalciuric hypercalcemia (FHH), an autosomal dominant disorder. Both parents and one sibling had episodes of hypercalcemia with inappropriately high parathormone levels; in the father there was also relative hypocalciuria consistent with FHH. On the basis of the genetic and pathophysiologic data reported here, we speculate that homozygosity for the 'FHH-gene' is the cause of the life-threatening manifestation of NSPHP, whereas heterozygosity for the same gene leads to FHH, by comparison a mild disorder. The association of the two very rare recessively transmitted disorders, alkaptonuria and NSPHP, is unique; close linkage of the two genes, one coding for homogentisic acid oxidase, the other for the unknown gene product defective in NSPHP, can be suspected.
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PMID:Neonatal severe primary hyperparathyroidism and alkaptonuria in a boy born to related parents with familial hypocalciuric hypercalcemia. 654 41

Calcification and ossification of soft tissues occurs as a response to a variety of injuries such as atherosclerosis, myositis ossificans, and caseous necrosis. These injuries and others have as a unifying characteristic persistent necrotic tissue elements. Normal tissues may calcify under conditions of hypercalcemia or hyperphosphatemia. The initial mobilization of Ca and P following injury is rapid, as observed in calcergy. The mitochondria of cells, normally a storehouse of Ca, become preferential sites of precipitated Ca when cells are irreversibly injured, and act as foci of progressive calcification. Collagen fibers undergo calcification directly, principally when they are located within devitalized sites such as prosthetic heart valves, and direct calcification of collagen may predominate generally in dystrophic calcification. VArious porous sponges act as foci for calcification and ossification, and the utilization of porous implants may provide for the development of therapeutically useful calcifying and ossifying biomaterials.
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PMID:Mineralization of connective tissue surrounding implanted devices. 733 Nov 58

Hypercalcemia is the most common paraneoplastic syndrome associated with cancer. This paper addresses the etiology and pathogenesis of hypercalcemia of malignancy and discusses the relative contributions of local and humoral effects on bone and renal calcium homeostasis. The roles of parathyroid hormone-related protein and other osteolytic cytokines are outlined. New biochemical markers that enable more specific monitoring of the response of bone metastases to treatment are introduced, including urinary excretion of the collagen crosslinks pyridinoline and deoxypyridinoline. The clinical management and prevention of hypercalcemia is systemically outlined, including indications for bisphosphonate, glucocorticoid, and calcitonin therapy. The results of recent trials of bisphosphonate therapy for the prevention of tumor progression and its subsequent problems such as bone pain, fracture, and hypercalcemia also are discussed.
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PMID:Hypercalcemia and bone resorption in malignancy. 763 18

Parathyroid hormone (PTH) plays a central role in regulation of calcium metabolism. For example, excessive or inappropriate production of PTH or the related hormone, parathyroid hormone related protein (PTHrP), accounts for the majority of the causes of hypercalcemia. Both hormones act through the same receptor on the osteoblast to elicit enhanced bone resorption by the osteoclast. Thus, the osteoblast mediates the effect of PTH in the resorption process. In this process, PTH causes a change in the function and phenotype of the osteoblast from a cell involved in bone formation to one directing the process of bone resorption. In response to PTH, the osteoblast decreases collagen, alkaline phosphatase, and osteopontin expression and increases production of osteocalcin, cytokines, and neutral proteases. Many of these changes have been shown to be due to effects on mRNA abundance through either transcriptional or post-transcriptional mechanisms. However, the signal transduction pathway for the hormone to cause these changes is not completely elucidated in any case. Binding of PTH and PTHrP to their common receptor has been shown to result in activation of protein kinases A and C and increases in intracellular calcium. The latter has not been implicated in any changes in mRNA of osteoblastic genes. On the other hand activation of PKA can mimic all the effects of PTH; protein kinase C may be involved in some responses. We will discuss possible mechanisms linking PKA and PKC activation to changes in gene expression, particularly at the nuclear level.
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PMID:Signal transduction pathways mediating parathyroid hormone regulation of osteoblastic gene expression. 796 63

Twenty-six cases of adult T-cell leukemia/lymphoma (ATLL) were identified between 1983 and 1991 in Martinique (French West Indies). There were 14 men and 12 women, all of mixed racial descent and born in Martinique. Their ages ranged from 23 to 95 years. The main clinical and laboratory features at initial presentation were peripheral lymphadenopathy (22 cases), hepatomegaly (11 cases), splenomegaly (10 cases), cutaneous lesions (12 cases), hypercalcemia (16 cases), refractory infection by Strongyloides stercoralis (12 cases), and pre-existing autoimmune disorders (4 cases). All patients had absolute lymphocytosis with circulating pleomorphic abnormal lymphocytes. The prognosis was poor, with most patients (20 cases) surviving for less than 6 months. Although the overall clinicopathologic features of ATLL in this series are similar to those described in previous reports, we observed three additional points of interest: a high association with Strongyloides infection, an increased incidence of tropical spastic paresis/HTLV-1 associated myelopathy (TSP/HAM) among the relatives of the patients (5 cases), and the presence of prior collagen vascular diseases.
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PMID:Adult T-cell leukemia-lymphoma: a clinico-pathologic study of twenty-six patients from Martinique. 811 52

The mechanism of crystal deposition in joints varies with the chemical nature of the crystal. Crystallisation of monosodium urate, characteristic of gout, requires a neutral pH and supersatured tissues, which is the basis for the clinical definition of the upper limit of normal blood uric acid level. The appearance of crystals also is dependent on time since crystallisation of monosodium urate is very slow. Inhibitory or promoting factors could intervene and explain rare cases of gout without hyperuricemia or the rapid crystallisation which seems to characterise some types of drug-induced gout. Crystal deposits of calcium pyrophosphate dihydrate form mainly in the cartilage where they seem favoured by ageing or by trauma, which could deplete cartilage of crystallisation inhibitors, notably proteoglycans. High pyrophosphate levels within cartilage also play an important role. The appearance of these pyrophosphates in the interstitial cartilagenous medium would be in large part due to the activity of an ectoenzyme, nucleoside triphosphate pyrophosphatase; increased activity of this ectoenzyme could be responsible for some chondrocalcinosis. Chronic hypercalcaemia can also be involved in the pathogenesis of cartilage deposition of calcium pyrophosphate dihydrate by raising the calcium-pyrophosphate product, or by decreasing the activity of alkaline phosphatase, an enzyme responsible for breakdown of extracellular pyrophosphates. The pathophysiology of calcium phosphate deposits is poorly understood. For some authors, these deposits occur within matrix vesicles, but for others, within collagen fibres. Increase in the calcium-phosphate product can also be a cause, for example, during renal osteodystrophy or vitamin D intoxication.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mechanism of crystal deposition in the joints]. 817 67


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