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

Sarcoidosis of the kidneys and liver without radiologically demonstrable lung involvement in a 44-year-old woman was shown to be the cause of a hypercalcaemia syndrome. The hypercalcaemia was presumably due to an increased production of 1,25-(OH)2-vitamin D3 which--like the increased angiotensin converting enzyme--is produced in the epithelioid and giant cells. Corticoid treatment normalized serum calcium and ACE levels and improved renal function. These observations demonstrate that measurement of ACE and 1,25-(OH)2-vitamin D3 levels is helpful in the differential diagnosis of hypercalcaemia, in view of the possibility of sarcoidosis, and should be among the diagnostic tests.
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PMID:[Angiotensin-converting enzyme and 1,25-dihydroxyvitamin D3 in hypercalcemia of unknown origin]. 284 36

Topical application of 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3], an active form of vitamin D3, was previously shown to inhibit the induction of ornithine decarboxylase (ODC) and tumor promotion by tumor promoters in mouse skin. In the present study, this observation in skin was extended to other tissues, such as the stomach, colon, and liver, using 1 alpha-hydroxyvitamin D3 [1 alpha (OH)D3], which is converted to 1 alpha,25(OH)2D3 in the liver without hormonal control and thus evokes the systemic effects, if any, of 1 alpha,25(OH)2D3. When mice were given 1 alpha (OH)D3 at a dose of 5 micrograms by gastric tube, their plasma level of 1 alpha,25(OH)2D3 increased to a peak of about 18-fold the normal level after 12 h, followed by hypercalcemia (about 14 mg/dl), which reached a peak on Days 2 to 3. In 1 alpha (OH)D3-treated mice, induction of epidermal ODC by 12-O-tetradecanoylphorbol-13-acetate was markedly inhibited, the inhibition being maximal 2 to 4 days after 1 alpha (OH)D3 administration. ODC induction in the glandular stomach mucosa of rats by NaCl, a tumor promoter in stomach carcinogenesis, was also inhibited dose and time dependently by 1 alpha (OH)D3. Similarly, 1 alpha (OH)D3 treatment of rats markedly inhibited the induction of ODC in the colon mucosa by deoxycholate, a tumor promoter of colon carcinogenesis, and of ODC in the liver by phenobarbital, a promoter of liver carcinogenesis. These results suggest that an active form of vitamin D3 has a systemic inhibitory effect on induction of ODC activity by tumor promoters.
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PMID:Systemic inhibition of tumor promoter-induced ornithine decarboxylase in 1 alpha-hydroxyvitamin D3-treated animals. 362 Nov 89

1 alpha,25-Dihydroxyvitamin D3 [1 alpha,25(OH)2D3], a hormonally active form of vitamin D3, was found to inhibit the promotional phase of 7,12-dimethylbenz[a]anthracene-induced skin carcinogenesis in female Sencar mice. Topical application of 1 alpha,25-(OH)2D3 once a week at a dose of 1 micrograms or less, a tolerable dose from hypercalcemia, dose dependently inhibited tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). When 1 micrograms of 1 alpha,25(OH)2D3 was applied 30 min before 5 micrograms of TPA, the times required for 50 and 100% tumor incidence were delayed about 2.5 and 7 weeks, respectively, and the number of tumors per mouse was decreased by 25-30%. This inhibitory effect was more pronounced when examined by a two-stage promotion protocol, in which a single application of 5 micrograms of TPA (Stage I) was followed by repeated applications of 5 micrograms of mezerein once a week for 19 weeks (Stage II). When 1 alpha,25(OH)2D3 at 1 micrograms was applied at Stage I + II or Stage II, tumor formation was markedly suppressed, resulting in decrease of about 70-80% in the incidence and 87-90% in the number of tumors per mouse. Application of 1 alpha,25(OH)2D3 at Stage I only did not inhibit tumor formation, indicating that 1 alpha,25(OH)2D3 specifically inhibited Stage II promotion. These results are in good agreement with the previous and present findings that 1 alpha,25(OH)2D3 inhibited induction of epidermal ornithine decarboxylase by TPA and mezerein. The possibility that 1 alpha,25(OH)2D3 suppressed tumor promotion by killing initiated cells rather than inhibiting promotion was ruled out by an experiment in which TPA was applied to the 1 alpha,25(OH)2D3 alone-treated animals.
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PMID:Inhibition of tumor promotion in mouse skin by 1 alpha,25-dihydroxyvitamin D3. 384 Apr 12

The amount of induced hepatic metallothionein (MT) and the alterations of calcium (Ca) and lead (Pb) concentrations in plasma, liver, kidney, and spleen were compared in male mice after iv, ip, and sc injections of lead acetate at a dose of 30 mg Pb/kg body wt. The amount of hepatic MT at 1 day was in the order of ip greater than iv greater than sc injection approximately 0, despite the hepatic Pb concentration in the order of iv greater than ip greater than sc injection. Heat-stable Pb-binding MT was not detected following any injection route. After the iv injection, a transitory hypercalcemia with hyperphosphatemia was observed. As for the tissue Pb concentration after the iv and ip injections, liver and spleen showed a high concentration, while kidney concentration was relatively low. The high tissue Pb was accompanied by an increase of tissue Ca in most cases. Only 10 to 15% of the total Pb accumulated in the liver at 1 day was recovered from the supernatant fraction after ultracentrifugation. The increase of hepatic Ca was ascribed to that in the sediment fraction. After the sc injection, the tissue Pb concentration was very low and no alterations were observed in tissue Ca concentrations.
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PMID:Induction of metallothionein after lead administration by three injection routes in mice. 396 11

The urine-concentrating mechanism was studied in chronic hypokalemia (seven dogs given a low K(+), high NaCl diet plus injections of deoxycorticosterone acetate [DOCA]) and chronic hypercalcemia (seven dogs given vitamin D). In the potassium-depleted dogs, muscle, serum, and urine K(+) fell markedly, but glomerular filtration rate (GFR) and body weight varied little. Maximum urine osmolality fell in all dogs (mean decrease = 45%); however, solute-free water reabsorption (T(CH2O)) at high rates of solute excretion remained normal in three of four dogs. Free water excretion (C(H2O)) increased normally or supranormally as a function of increasing Na(+) delivery to Henle's loop in six dogs so tested. Hypercalcemia of several weeks duration caused a decrease in both GFR (mean 36%) as well as in maximum urine osmolality (mean 57%). Maximum T(CH2O) was not invariably depressed; in fact, when the values were adjusted for the reduced number of functioning nephrons (T(CH2O)/C(In)), four of seven studies were normal. C(H20)/C(In) increased normally (or supranormally) with increasing fractional Na delivery to Henle's loop in four of five dogs.I conclude that the lowered maximum urine osmolality in these hypokalemic and hypercalcemic dogs was not related to abnormal water reabsorption from the collecting ducts. Although not specifically measured in this study, it is very likely that solute accumulation in the renal medulla was reduced. This probably was not caused by abnormal delivery of sodium to, nor reabsorption of sodium from Henle's loop. It is likely that a more subtle defect exists in the countercurrent mechanisms for establishing a steep concentration gradient in the renal medulla. In the few hypercalcemic dogs in whom GFR was very low, I believe that injury to, and blockage of medullary tubules could account for most of the reduction in maximum U(Osm). Although not specifically ruled out, there is no evidence here to suggest that high serum Ca(+) or low serum K(+) per se causes a defect in sodium and water reabsorption in the mammalian nephron.
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PMID:Urine concentration and dilution in hypokalemic and hypercalcemic dogs. 543 74

Sarcoidosis is a systemic disease with predominantly pulmonary manifestations. Its frequency in Denmark is higher than previously assumed; on the basis of studies in two different areas the annual incidence was a least 10 cases/100,000 population. Because several cases remain undetected, the real incidence may be higher. The aetiology is unknown. Pathoanatomically the disease is characterized by the appearance of non-caseous epithelioid cell granulomas. The initial process in the lungs is presumably a non-granulomatous interstitial inflammation (alveolitis) with an accumulation of activated T-lymphocytes and mononuclear macrophages. Subsequent there is transition to organized granulomas and in some patients further development into fibrosis. The immunological abnormalities in peripheral blood suggest a stimulation of the humoral immunity and a inhibited cellular immunity. However, there is increasing evidence that the alveolitis may be an expression of increased cellular immunity manifesting at local sites of granuloma formation. ACE is a protein which in non-sarcoid individuals is associated with the endothelial cells, converting angiotensin I into angiotensin II and contributing to the bradykinin degradation. In sarcoidosis ACE is present in alveolar macrophages, epithelioid and giant cells. It can thus be considered as a marker for abnormal macrophage activity in the disease and has been introduced as a diagnostic tool. On examination of a widely compounded patient material we found elevated SACE in approx. 60% of sarcoidosis patients, compared with 1% in other conditions. Judged by these results, there was more than 90% probability that a patient with elevated SACE had sarcoidosis; however, a normal SACE did not preclude sarcoidosis. In newly detected sarcoidosis SACE was elevated in 50% of the patients, whereas elevated SACE was more frequent in patients with chronic active sarcoidosis (duration greater than 2 years). There was a large overlap between SACE values when the CXR stages were compared, a result which is comparable with other series. Two clinical manifestations exhibited peculiar enzyme patterns: in EN SACE was generally normal initially and subsequently increased to elevated values, and in hypercalcaemic sarcoidosis patients SACE was elevated in all. SACE was not elevated in EN of other aetiology or in non-sarcoid hypercalcaemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical and biochemical aspects of sarcoidosis. With special reference to angiotensin-converting enzyme (ACE). 609 1

Angiotensin converting enzyme was measured in the serum of 52 patients with sarcoidosis, 67 healthy control subjects and 64 patients with pulmonary and non-pulmonary diseases. The patients with sarcoidosis were classified on clinical grounds as having active or inactive disease. In 26 patients with active sarcoidosis not taking corticosteroids the mean serum ACE was significantly higher than in normal controls (P less than 0 . 001). 73% of these patients had elevated serum ACE. Only two out of 12 (17%) patients with inactive sarcoidosis not taking corticosteroids had elevated serum ACE. Serum ACE was normal in patients taking oral corticosteroids for longer than two weeks. Eighty per cent of patients with active sarcoidosis with radiological evidence of pulmonary parenchymal involvement had an elevated serum ACE compared to 25% in patients with normal chest X-rays and 60% of those with bilateral hilar lymphadenopathy. All sarcoid patients with hypercalcaemia had elevated serum ACE whereas only half of those with normal serum calcium had elevated ACE. In the patients with other thoracic and granulomatous conditions serum ACE was normal or rarely marginally elevated. Serum ACE appears to be of value in the diagnosis of active sarcoidosis.
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PMID:A clinical evaluation of serum angiotensin converting enzyme in sarcoidosis. 625 51

Radioactive imaging agents are chemically designed for selective distribution. Another approach to selectivity is to find stable compounds that favorably influence this distribution. Using a rat model of myocardial necrosis, we studied effects of various stable compounds (as a single, large dose or fractionated into short series) on the ratio, uptake of Tc-99m pyrophosphate (PPi) by the target lesion/uptake by the principal nontarget, bone (L/B). Vitamin D3s ability to increase L/B was mediated by the hypercalcemia and hyperphosphatemia that it caused. The hypercalcemia was accompanied by increased [Ca] in the lesion. In contrast, pulse doses of desoxycorticosterone acetate (DOCA) at 7 and 6 hr before killing increased uptake by lesion, increasing L/B from 0.19 +/- 0.03 to 0.45 +/- 0.08 (p less than 0.01), with no change in serum [Ca] and minimal changes in serum [P], [Na], and [K]. DOCA also increased the lesion-to-blood ratio from 6.5 +/- 0.07 to 15.4 +/- 3.9 (p less than 0.05). These results encourage further study of DOCA's effect and investigation of other stable drugs that may influence distribution of other imaging agents.
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PMID:Effect of vitamin D3, other drugs altering serum calcium or phosphorus concentrations, and desoxycorticosterone on the distribution of Tc-99m pyrophosphate between target and nontarget tissues. 626 65

An elderly man with diabetes mellitus and end-stage renal disease managed with continuous ambulatory peritoneal dialysis (CAPD) was hospitalized with peripheral vascular insufficiency; he developed hypercalcemia and became mentally obtunded. Lowering dialysate Ca from 3.5 mEq/L to 2.5 mEq/L, stopping calcium acetate, and ultimately hemodialysis with calcium-free dialysate did not lead to reversal of the hypercalcemia or improvement of his symptoms. The intact parathyroid hormone PTH level was 187 pg/mL, a value rarely associated with significant osteitis fibrosa. A search for other causes of hypercalcemia was unrevealing, and a iliac crest bone biopsy was done. The latter showed osteitis fibrosa, and the patient underwent parathyroidectomy. The hypercalcemia reversed quickly, and his mental symptoms slowly improved. The discussion reviews the probable causes of hypercalcemia in diabetic patient undergoing CAPD with 3.5 mEq/L dialysate calcium and using calcium-containing phosphate binders, with hyperparathyroidism certainly not the usual cause. The reason for the occurrence of significant hyperparathyroidism in the face of only modest elevation of PTH is considered. The value of bone biopsy in resolution of this problem is apparent.
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PMID:Symptomatic hypercalcemia in a diabetic patient undergoing continuous ambulatory peritoneal dialysis: value of bone biopsy in the diagnosis and management. 748 41

Acute exposure of rats to strontium or fluoride by i.p. injection of sodium fluoride or strontium chloride resulted in a systemic response in which changes occurred in the plasma electrolytes and metabolites. Strontium resulted in a rapid but temporary hypercalcaemia while fluoride produced a temporary hypocalcaemia. There was no significant hypophosphataemia after fluoride and only a transient hypophosphataemia with strontium. There was some indication of kidney damage and a general stress response following fluoride injection. These results do not support the hypothesis that interglobular dentine is associated with hypophosphataemia or hypoplastic enamel with hypocalcaemia and are in conflict with the observation that the formation of interglobular dentine following the injection of lead acetate is associated with hyperphosphataemia and hypercalcaemia.
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PMID:Changes in the plasma electrolytes and metabolites of the rat following acute exposure to sodium fluoride and strontium chloride. 760 52


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