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)

Immunoreactive PGE2 was determined in 11 surgically removed malignant tumors. When compared to adjacent non-malignant tissues PGE2 content was significantly higher in the neoplastic tissues. These findings support the view that PG may play a role in cell proliferation and/or vascular supply to tumor tissues. The hypothesis was also discussed that PGE2 may represent a tumor against host defense since it can decrease spontaneous and antibody dependent cytotoxicity. PGE2 may also play a role in tumor induced osteoporosis and hypercalcemia. If this hypothesis is correct PGE2 synthesis inhibitors may be employed as auxiliary antitumor agents.
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PMID:Prostaglandin E2 production by human tumors. Defense mechanism against the host? A preliminary report. 658 44

From January 1, 1971, to December 31, 1982, 242 patients with uncomplicated biochemical or asymptomatic hyperparathyroidism underwent operative therapy at the Massachusetts General Hospital. They represent 36.1 percent of the 670 total operative cases during this period. Before 1971, from 1941 to 1970, there were only 33 hyperparathyroid patients with asymptomatic hyperparathyroidism who underwent surgery. The initial surgical procedures included 88 unilateral and 134 bilateral cervical explorations. There were 19 patients who underwent reexploration, including 15 referrals and 4 patients who had their primary operation at the Massachusetts General Hospital. There were no deaths, no recurrent nerve injuries, and only one patient with protracted but temporary postoperative hypocalcemia. Four patients (1.7 percent) had persistent hypercalcemia and therefore, must be considered treatment failures. The procedure resulted in normocalcemia in 238 of the patients (98.3 percent). The mean serum calcium level decreased from a preoperative value of 11.1 to 8.9 mg/100 ml the serum phosphorus level increased from 2.8 to 3.9 mg/100 ml postoperatively. Pathologic examination revealed 201 adenomas (83.1 percent), 39 hyperplasias (16.1 percent), 2 patients with normal glands (0.8 percent), and no carcinomas. The size of the abnormal glands appeared to correlate with the degree of hypercalcemia. Patients with marked hypercalcemia generally had a large gland that was more easily identified than the gland patients who had milder disease in whom it was smaller, harder to locate, and more difficult to distinguish pathologically from a normal gland. In general, patients with milder disease (serum calcium less than 11 mg/100 ml) should be followed expectantly. In some of these patients, there is doubtless progressive exacerbation of hypercalcemia, increases in the parathyroid hormone level, osteopenia, or renal insufficiency which ultimately requires surgical intervention. In others, there is apparently severe biochemical, asymptomatic hyperparathyroidism as manifested by a serum calcium level greater than 11 mg/100 ml, an increased parathyroid hormone level, increased 24 hour urinary calcium excretion greater than 150 mg, progressive loss of bone mass, or deterioration of renal function. These latter patients should be operated on without delay. For patients who risk the long-term complications of hyperparathyroidism and menopausal patients who are potentially threatened by postmenopausal osteoporosis, surgery is likely to be beneficial. For those whose compliance with therapy or follow-up poses a significant logistic problem, surgical therapy is often the best solution.
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PMID:Management of asymptomatic hyperparathyroidism. 671 53

Bone biopsy specimens from the iliac crest were obtained during surgical operations from 45 patients with rheumatoid arthritis (RA) and 41 with osteoarthritis (OA). Control material was obtained from 20 cases of sudden death due to cardiovascular disease. By both conventional histology and image analysis techniques about a quarter of all patients showed some osteoporosis. This was equally common among the OA and RA patients. It was more common among those with transparent skin and those taking corticosteroids. The only case showing mild osteomalacia suffered from OA. No gross differences were apparent between the groups in relation to plasma biochemical studies, diet, or exposure to sunlight. These results are in striking contrast to the high incidence of osteomalacia in RA reported from the west of England; moreover they do not confirm reports of hypercalcaemia among rheumatoid subjects. We conclude that the differences regarding osteomalacia are due to selection of cases. We find no evidence that osteomalacia is specifically associated with RA.
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PMID:Incidence of metabolic bone disease in rheumatoid arthritis and osteoarthritis. 674 98

For 2 weeks 27 patients with hypercalcemia received a standard oral treatment with (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate (APD) as the sole agent. Results were grouped according to causes of hypercalcemia and compared with effects of APD in 13 normocalcemic patients with Paget's disease of bone and 7 with osteoporosis. In 12 hypercalcemic patients with osteolytic bone lesions and in the 20 normocalcemic patients, the mean serum calcium decreased to final levels that were subnormal and significantly lower than those obtained after treatment of 8 patients with primary hyperparathyroidism. In 3 patients with myeloma and in 4 tumor patients without bone lesions, serum calcium did not always decrease to the normal range. Implications of these observations for the mechanism of hypercalcemia are discussed.
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PMID:Efficacy of amino-hydroxypropylidene bisphosphonate in hypercalcemia: observations on regulation of serum calcium. 681 19

Mineral retention was measured during 39 metabolic balance studies in 34 patients with nutritional osteomalacia or late rickets; they were divided into 5 treatment groups consisting of oral vitamin D, artificial ultra-violet irradiation, 25-hydroxycholecalciferol (calcifediol), 1 alpha-hydroxycholecalciferol (alfacalcidol) and 1 alpha, 25-hydroxycholecalciferol (calcitriol). With the 1 alpha-hydroxylated derivatives, initial dosage of 2 to 6 micrograms daily was required to achieve optimal healing rates by comparison with other responses. Mineral retention was markedly enhanced by supplementation with microcrystalline hydroxyapatite compound (MCHC); untreated X-linked hypophosphataemic rickets healed in 7 weeks on 10 micrograms alfacalcidol daily and 6 grams MCHC daily without developing hypercalcaemia. By contrast, adult-presenting hypophosphataemic osteomalacia developed early hypercalcaemia on the same treatment; additional phosphate supplementation, without changing other treatment, abolished hypercalcaemia and improved calcium retention. A long-term crossover trial of the vitamins D in 6 patients with hypoparathyroidism suggested that relative potencies were as follows (assigning to vitamin D an arbitrary potency of l): vitamin D2 (or D3) l: dihydrotachysterol (DHT) 3: calcifediol 10: alfacalcidol 750: calcitriol 1500. The two-fold superiority of calcitriol over alfacalcidol was evident. Calcifediol and vitamin D controlled plasma calcium at comparable levels of circulating 25-hydroxyvitamin D (25-OH-D), elevated 25-OH-D persisting at least 1 to 2 years after discontinuing long-term (greater than 4 years) vitamin D. In 2 patients with myositis ossificans progressiva treated with 10 to 20 micrograms calcitriol daily, hypercalcaemia was minimized by a low-calcium diet supplemented with cellulose phosphate, suggesting that bone resorption did not play a major role in vitamin D intoxication. Net mineral loss was documented in a young male patient but not in a menopausal female, suggesting that calcitriol treatment was not likely to produce post-menopausal osteoporosis.
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PMID:Calcitriol dosage in osteomalacia, hypoparathyroidism and attempted treatment of myositis ossificans progressiva. 689 16

Studies on post-menopausal osteoporotic patients indicate that 1,25-(OH)2 D3 concentrations are no different from those in age-matched normal subjects and the data suggest that the malabsorption of calcium found in many osteoporotic patients cannot generally be attributed to low plasma 1,25-(OH)2 D3 levels. The effects are discussed of three different therapies - sex hormones alone, vitamin D metabolites alone and a combination of both - on calcium balance and peripheral bone loss in treated compared with untreated osteoporotic patients. The results indicate that combined therapy with a vitamin D metabolite and an oestrogen is more effective in inhibiting the rate of bone resorption in post-menopausal osteoporosis than treatment with either agent used alone, and should be regarded as the treatment of choice at the present time. It is suggested that, using this regimen which is suitable for patients up to about 65 years of age, calcium supplementation is not required, provided daily calcium intake is reasonably adequate, and may even be undesirable by increasing the risk of hypercalcaemia.
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PMID:The vitamin D metabolites in the pathogenesis and management of osteoporosis. 689 17

The clinical course of three patients with cutaneous T-cell lymphoma (CTCL) in whom skeletal disease developed is presented and the literature on skeletal involvement in these disorders is reviewed. Three separate types of skeletal manifestations occurred: (1) osteolytic lesions, (2) osteoblastic lesions, and (3) diffuse osteoporosis. Hypercalcemia was present in two cases. Tumor cells from two patients in short-term culture secreted osteoclast-activating factor(s). Both of these patients had pathologic evidence of osteoclast activation in bone sections. Thus, the tumor cells in certain patients with CTCL may derive from a monoclonal proliferation of a T-cell subset capable of producing humoral bone-resorbing factor(s) similar to those demonstrated in cultures of mitogen- and antigen-activated normal lymphocytes. Since skeletal lesions are unusual, it would follow that other T-cell subsets account for pathologic cell proliferation in most patients with CTCL.
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PMID:Skeletal manifestations in cutaneous T-cell lymphomas. 697 76

A double-blind comparative study of 1 alpha-OHD3 and placebo was performed on 37 patients with osteoporotic hip fracture without clinical osteomalacia. 1 alpha-OHD3, in a dose of 1 microgram/day together with 2.5 g CaCO3, did not heal osteoporosis as judged from determinations of bone mineral density and histomorphometric analyses during four months of treatment. However, 1 alpha-OHD3 seemed to have an effect on fracture healing as concluded from the posttreatment alkaline phosphatase level. Hypercalcemia was common, occurring in six out of 19 patients treated with 1 alpha-OHD3. It is concluded that treatment of osteoporosis with 1 alpha-OHD3 and calcium is ineffective and potentially dangerous because it frequently causes hypercalcemia.
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PMID:Treatment of osteoporosis with 1-alpha-hydroxycholecalciferol and calcium. 698 71

After baseline studies, 21 patients with osteoporosis were treated with human parathyroid hormone fragment (PTH 1-34) given as once-daily subcutaneous injections for 6-24 months. The dose used did not cause hypercalcaemia even in the first few hours after injection. Calcium and phosphate balances improved in some patients, but there was no significant improvement in the group values. There were, however, substantial increases in iliac trabecular bone volume: the mean increase, confirmed by repeat blind measurements, was 70% above mean baseline volume. The new bone was histologically normal. Those patients who had the largest increases in 47Ca-kinetic and histomorphometric indices of new bone formation showed the greatest increases in trabecular bone volume, suggesting that treatment with human parathyroid hormone fragment caused a dissociation between formation and resorption rates that was confined to trabecular bone. Since vertebrae are four-fifths composed of trabecular bone, this hormone fragment may prove useful in treating patients with the crush fracture syndrome.
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PMID:Anabolic effect of human parathyroid hormone fragment on trabecular bone in involutional osteoporosis: a multicentre trial. 699 32

Normal calcium regulation depends on the complex interactions of several systems. The specific calcium regulating hormones, parathyroid hormone, calcitriol and calcitonin, affect calcium and phosphorus concentration and supply by acting on bone, kidney and intestine. The changing concentration and supply of ions not only regulate these hormones, but may also influence the function of the target organs, particularly bone, directly. Systemic hormones such as growth hormone and somatomedins, glucocorticoids, sex hormones and thyroid hormone are essential for skeletal growth and development and interact with calcium regulators. Prostaglandins and osteoclast activating factor may be important in local regulation of bone. Disorders of calcium regulation are common, particularly hypercalcemia; however, measurements of parathyroid hormone are not yet ideal and the factors which produce hypercalcemia in malignancy have not been identified. The role of calcium regulating hormones in the pathogenesis and treatment of osteoporosis is controversial. Solution to these problems may be dependent on the identification of additional factors which influence mineral metabolism.
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PMID:Calcium regulation. 703 24


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