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)

Hypercalcemia with adult T-cell leukemia (ATL) is chiefly caused by an excessive production by tumor cells of parathyroid hormone-related protein (PTHrP). We have previously reported hypercalcemic patients with solid tumors to excrete a large amount of the C-terminal fragments of PTHrP (C-PTHrP) into their urine. To elucidate whether PTHrP production correlates with or predicts the development of hypercalcemia, we studied the urinary excretion of C-PTHrP in 36 ATL patients. The urinary excretion of C-PTHrP was in the normal range (< 0.40 nmol equivalent to PTHrP (109-141)/g creatinine) in HTLV-1-positive carriers (n 3), ATL patients in complete remission (n 2) and chronic type ATL patients (n 2). It was marginally increased in seven patients in partial remission, and gradually increased as the disease progressed. In 20 patients who died without or with hypercalcemia, it was increased to 1.98 +/- 0.69 (n 9) and 7.6 +/- 2.1 nmol/g creatinine (mean +/- SD, n 11, P < 0.01), respectively. Urinary C-PTHrP excretion was significantly correlated with serum calcium and LDH levels as well as with CD25-positive cells in the peripheral blood. In four patients whose urinary excretion had been serially determined, it increased prior to the development of hypercalcemia. The findings suggest the urinary excretion of C-PTHrP to be of use as a predictor of the development of hypercalcemia in ATL patients. In ATL patients whose urinary excretion of C-PTHrP is progressively increasing, the serum calcium concentration should be carefully monitored to prevent hypercalcemic crisis.
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PMID:Urinary excretion of parathyroid hormone-related protein as a predictor of hypercalcemia in patients with adult T-cell leukemia. 146 94

A sixty nine-year-old woman was admitted to the hospital because of further examination of hypercalcemia. On July 1990, she complained of general fatigue and loss of appetite. She was pointed out to have hypercalcemia (15.1mg/dl), urolithiasis, and renal insufficiency. CT films of the chest showed swelling of the mediastinal lymphnodes and CT of the abdomen nephrocalcinosis. Ga-scintigraphy demonstrated an abnormal accumulation of gallium in the mediastinum. Levels of the parathyroid hormone was normal. Levels of the serum calcium (13.7mg/dl), angiotensin converting enzyme (30.4IU/L) and 1.25 (OH)2D (87PG/ml) were elevated. Giant cells were found in the biopsy specimen of the lung. A significant relationship between the serum calcium and creatinine were observed (r = 0.76, p < 0.02). Proximal fractional reabsorption of sodium showed to be suppressed (47.7%), and distal fractional reabsorption of sodium showed to be normal (88.4%). From these findings hypercalcemia and urolithiasis was suggested to result from sarcoidosis. The hypercalcemia and renal insufficiency improved with corticosteroid therapy.
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PMID:[A case of sarcoidosis with hypercalcemia, urolithiasis, nephrocalcinosis and renal insufficiency]. 148 16

A retrospective review of 25 patients who underwent orthotopic liver transplantation was performed to relate the prevalence and preferred sites of microscopic calcium deposition seen at autopsy to clinical parameters, namely, hypercalcemia, hypercalcemia, hyperphosphatemia, and renal failure. Microscopic foci of calcification were noted in 84% of patients, and hypercalcemia was noted in 68%. Multiple regression analysis demonstrated that the number of microscopically calcified organs depended in part on the peak total serum calcium level and the duration of hypercalcemia and that the peak total serum calcium level depended in part on the peak phosphorus level and the quantity of calcium administered intraoperatively. Univariate analysis showed that peak phosphorus level was partially dependent on the peak creatinine level. The data suggest that hypercalcemia and postoperative ectopic calcification are common and related occurrences following hepatic transplantation and that intraoperative manipulations of serum calcium levels and renal failure partially, but not entirely, account for this phenomenon.
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PMID:Tissue calcification after orthotopic liver transplantation. An autopsy study. 152 56

Bone mineral content (BMC) and testosterone levels were evaluated and compared in 10 hypogonadal males and 10 normal, age-matched controls. In 6 of the subjects an investigation was also carried out into the effects of testosterone administration on lumbar BMC, calcitonin (CT) response to hypercalcaemia, osteocalcin (BGP) and the fasting urinary calcium/creatinine and hydroxyproline/creatinine ratios. Our results confirm that male hypogonadism is characterized by a low BMC and that testosterone administration is able to improve this parameter and to increase both basal BGP and CT response to hypercalcaemia. Testosterone therefore probably acts on bone tissue through both a direct action on osteoblast cells and an improvement in CT secretion.
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PMID:Effect of testosterone on bone in hypogonadal males. 152 31

Among aminohydroxybisphosphonate derivatives, alendronate (3-amino-1-hydroxybutylidene-1,1-bisphosphonate) has proved efficacious in diseases with increased bone resorption. However, the effective dose in the treatment of malignant hypercalcemia is not clearly established. In 2 randomized studies, we investigated the effects of alendronate and of clodronate (dichloromethylene bisphosphonate) given as a single infusion in 82 rehydrated patients with malignant hypercalcaemia. Various doses of alendronate or clodronate soon produced a significant fall in plasma calcium (Ca), accompanied by a dose-dependent decrease in the fasting urinary Ca/creatinine ratio, taken as a reflection of bone resorption. During the next 5 days, plasma Ca and fasting urinary Ca/creatinine ratio were lower in the group treated with alendronate than in the clodronate group. The renal handling of Ca was similar in both groups. Because of relapsing hypercalcaemia, some patients received an infusion of alendronate approximately 2 weeks after the first infusion; this normalized the urinary Ca/creatinine ratio in 44% of the cases at day 3. At that time, the plasma Ca was below 2.70 mmol/l in 33%. Our results indicate that alendronate decreased bone resorption and calcaemia in cancer patients in a dose-dependent manner.
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PMID:Effect of a single infusion of alendronate in malignant hypercalcaemia: dose dependency and comparison with clodronate. 153 72

A 27-year-old man was admitted to hospital because of weight loss, fatigue and lack of appetite over the previous few weeks and cervical lymphadenopathy. Chest X-ray demonstrated several patchy infiltrates in both lungs. There was also evidence of progressive renal failure (creatinine concentration: 3,0 mg/dl) and hypercalcaemia (2,8 mmol/l). Bronchoalveolar lavage and renal biopsy confirmed sarcoidosis. Fundoscopy revealed eye involvement (several circumscribed, partly confluent, whitish nodules). Wegener's granulomatosis was excluded because no anticytoplasmic antibodies were demonstrated. Administration of steroids (at first daily 60 mg methylprednisolone) quickly resulted in a normal blood calcium level and normal renal function. These findings suggest that the early stage of sarcoidosis consists of in principle reversible functional changes. The differential diagnosis from systemic diseases is often difficult. If sarcoidosis is suspected one must search for rare organ manifestations so that therapy can be started as soon as possible.
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PMID:[Kidney failure as a consequence of sarcoidosis]. 155 74

Parathyroid activity, bone aluminum (Al) metabolism, bone histology, and clinical bone disease were studied in 55 successfully grafted kidney recipients at transplantation (Tx) and after 1 yr of immunosuppression with a low dose corticosteroid and a high dose cyclosporin-A regimen. Symptoms of Al-related bone disease disappeared after Tx. Serum Al and stainable bone Al decreased. The rate of Al removal from the bone surfaces was independent of graft function (creatinine range, 62-415 mumol/L) and bone turnover. Osteoblast activity and bone formation rate increased, while mineralization lag time normalized. Indices of bone resorption remained elevated, indicating persisting hyperparathyroidism. Eighteen percent of the recipients had posttransplant hypercalcemia, most likely caused by incomplete involution of hyperplastic parathyroid glands, while 53% had normocalcemic hyperparathyroidism related to impaired graft function. Cortical thickness decreased, while cancellous bone volume remained stable after Tx; both indices correlated significantly at follow-up with their respective values at Tx. None of 46 radiologically examined recipients had aseptic bone necrosis 1 yr after Tx.
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PMID:Aluminum metabolism and bone histology after kidney transplantation: a one-year follow-up study. 156 61

Alterations in renal calcitriol synthesis are important in the pathogenesis of secondary hyperparathyroidism in patients with progressive renal failure. Many of the manifestations of secondary hyperparathyroidism can be reversed by treatment with 1 alpha-hydroxylated vitamin D sterols, such as calcitriol and 1 alpha-hydroxyvitamin D3, but some studies suggest that such treatment accelerates the rate of progression of renal disease in patients with mild to moderate renal failure. Thus, calcitriol and 1 alpha-hydroxyvitamin D3 have been used infrequently in this group of patients. A review of more than 20 clinical reports indicates that the use of calcitriol or 1 alpha-hydroxyvitamin D3, in daily doses of 0.25-0.5 microgram, is rarely associated with hypercalcemia, hyperphosphatemia, or impairment in renal function. If such complications arise, they are usually reversible when treatment with vitamin D sterols is withdrawn and serum calcium levels return to pretreatment values. There is evidence that calcitriol impairs creatinine secretion by the renal tubule; thus, serum creatinine levels may increase and measurements of creatinine clearance may fall during calcitriol therapy in patients with mild to moderate renal failure without any change in true glomerular filtration rate. Daily oral doses of 0.25-0.50 microgram of calcitriol or 1 alpha-hydroxyvitamin D3 are well tolerated, and they can reverse the biochemical and histologic features of secondary hyperparathyroidism. Calcitriol therapy may be particularly valuable in patients recognized to be at higher risk of developing progressive secondary hyperparathyroidism as their renal failure slowly advances.
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PMID:The use of 1,25-dihydroxyvitamin D3 in early renal failure. 158 May 87

In order to investigate the relationships between serum calcium, urate and kidney function, serum calcium, urate, creatinine and urea were measured at 100 occasions in hypercalcemic cancer patients together with 113 preoperative measurements in HPT subjects and 106 measurements in normocalcemic control persons. When compared to normocalcemic control subjects (serum urate 336 +/- 110 mumol/l) both HPT subjects (356 +/- 98 mmol/1, p less than 0.006) and the cancer patients (407 +/- 179 mmol/l, p less than 0.001) showed raised levels of serum urate. While serum urate was correlated to serum creatinine in all groups (r = 0.40-0.59, p less than 0.0001) a significant correlation to serum calcium was only seen in the HPT group (r = 0.28, p less than 0.004). This relation persisted also after correction for age, sex and serum creatinine in the multiple regression analysis. Serum creatinine was similar in all groups but significantly correlated to serum calcium only in the HPT subjects (r = 0.29, p less than 0.003). Serum urea was not significantly correlated to serum calcium in any of the groups but was elevated in the cancer group (8.3 +/- 4.4 vs 6.2 +/- 2.9 mumol/l in the control group, p less than 0.0001). This elevation in serum urea seen in the cancer patients might rather be explained by dehydration or catabolism than an impaired kidney function. In conclusion, while serum urate is related to the kidney function both in normo- and hypercalcemia, it also seems to be related to the hypercalcemia in HPT subjects but not in cancer patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum urate and renal function in different forms of hypercalcemia. 163 24

The damara mole rat, Cryptomys damarensis, is a strictly subterranean dwelling herbivorous rodent that in its natural habitat has no access to any obvious source of cholecalciferol (D3). We examined the effects of D3 supplementation, at physiological and supraphysiological doses, on calcium metabolism, plasma concentrations of calcium and alkaline phosphatase (ALP) and D3 metabolites. Animals not receiving a D3 supplement maintained normal plasma calcium concentrations. In addition, they exhibited a high apparent fractional mineral absorption efficiency (91%) and maintained a positive mineral flux. The serum concentration of 25-(OH)D3 was undetectable (less than 5 nmol/l) and that of 1,25-(OH)2D3 was 41 +/- 10 pmol/l. Supplementation at a physiological dose of D3 resulted in increased plasma concentrations of D3 metabolites, food intake, apparent fractional absorption efficiency and apparent fractional retention efficiency. Despite the 1.8-fold increase in food intake, body mass remained constant suggesting that the enhanced energy intake was dissipated in catabolic processes. Plasma calcium and ALP concentrations were not significantly altered with physiological doses of D3. The group given supraphysiological doses of D3 exhibited hypercalcaemia, increased creatinine concentrations and markedly increased ALP levels. These data indicate that a pathological response to D3 intoxication occurred and that hepatic and renal excretory functions were impaired. It appears, therefore, that these animals function optimally at the low concentrations of D3 metabolites found naturally. Supplementation at both physiological and supraphysiological doses of D3 may disadvantage the damara mole rat.
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PMID:Effect of oral cholecalciferol supplementation at physiological and supraphysiological doses in naturally vitamin D3-deficient subterranean damara mole rats (Cryptomys damarensis). 166 May 17


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