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)

In this problem-oriented review of abnormalities associated with cancer, we have emphasized distinctive diagnostic points related to pathogenesis for each condition and outlined how the approach to management is determined by pathogenesis. For abnormalities of the complete blood count, it is important to distinguish between abnormalities directly related to marrow malignancy and abnormalities associated with extramarrow malignancy. Hemopoietic tumors consist of developmentally deficient blood cells produced by a clonal population of malignant stem cells. Tumors infiltrating marrow cause overcrowding in the limited marrow microenviroment. Extramarrow malignancies cause blood abnormalities, but the potential for normal marrow function is present. Abnormalities of blood cells secondary to therapy are usually clearly identified by consideration of clinical history. The initial differential diagnosis for hypercalcemia is malignancy. An aggressive diagnostic approach may be needed to identify the neoplasm, and therapy should incorporate measures to prevent renal failure. Hypoproteinemia and hyperproteinemia may be caused by neoplasia. Monoclonal gammopathies should be identified and may be associated with hyperviscosity syndrome. Hypoglycemia in the adult animal is most frequently caused by insulin-secreting tumors, but it has also been associated with hepatic and other tumors. Increased blood urea nitrogen, creatinine, lipase, amylase, and liver enzyme activities may also be caused by malignancy. Inadequate urine concentrating ability may be caused by hypercalcemia or malignancy-associated renal insufficiency. Hematuria in older animals is suggestive of urinary tract neoplasia. Exfoliated tumor cells may be identified in the urine sediment of these patients.
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PMID:Laboratory abnormalities in patients with cancer. 219 37

We have previously shown that cyclosporin A (CsA) produces high bone remodeling with resorption exceeding formation and loss of bone volume in the rat. This may have important clinical implications where CsA is widely used in organ transplantation. 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) is a bone mineralizing hormone which also has immune modifying properties. Consequently, we studied the effect of combined CsA and 1,25(OH)2D3 administration over 28 days in four groups of rats. Group A received vehicle (n = 10), group B CsA (15 mg/kg) (n = 10) alone, group C 1,25(OH)2D3 plus CsA (n = 15), and group D 1,25(OH)2D3 alone (20 ng/100 g) (n = 15). Rats were bled periodically at day 0, 7, 14, and 28 and Ca, parathyroid hormone (PTH), 1,25(OH)2D, osteocalcin (bone Gla-protein, BGP), BUN, and creatinine were measured. Rats were sacrificed on day 28 and bones were examined histomorphometrically. Compared to controls, CsA resulted in significant elevation of BGP and a transient increase in 1,25(OH)2D with excess bone remodeling and loss of bone volume. 1,25(OH)2D3 administration produced hypercalcemia, a significant rise in BGP, with suppression of PTH and increased osteoid volume. Combined therapy prevented the loss of bone volume probably due to increased osteoid tissue and enhanced osteoblast activity. Renal dysfunction, a side-affect of CsA, was not a factor. In conclusion, 1,25(OH)2D3 combined with CsA restores bone volume which is accompanied by increases in serum calcium and BGP.
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PMID:1,25 Dihydroxyvitamin D3 modifies cyclosporine-induced bone loss. 222 90

Familial benign hypercalcaemia has also been termed familial hypocalciuric hypercalcaemia because a major feature of this condition has been a relative hypocalciuria in relation to the hypercalcaemia, such that the calcium to creatinine clearance ratio is less than 0.016. The following is a report of a small kindred of patients with familial benign hypercalcaemia in which two of the affected members have frank hypercalciuria.
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PMID:Familial benign hypercalcaemia: hypercalciuria and hypocalciuria in affected members of a small kindred. 222 87

Immobilization-related hypercalcaemia is an uncommon but important condition being associated not infrequently with both urolithiasis and osteoporosis. In this study 5 patients who had been immobilized for a mean of 3 months and had a mean adjusted serum calcium of 3.15 mmol/l were treated with doses of intravenous pamidronate ranging between 10 mg and 45 mg. All patients became normocalcaemic by day 3. Patients 1-3 mobilized shortly after treatment and remained normocalcaemic. In those patients who continued to be immobile hypercalcaemia recurred after an interval of several weeks. Retreatment with pamidronate again resulted in normocalcaemia. No side effects were noted with treatment. All of the patients studied had increased rates of bone resorption as shown by elevated urinary hydroxyproline/creatinine ratios (median:range) of 0.101:0.045-0.180 (normal less than 0.033) and elevated calcium/creatinine ratios of 2.50:0.69-3.63 (normal less than 0.50). None of the patients in this study had any of the usual risk factors for developing immobilization-related hypercalcaemia though all 5 patients had problems with significant sepsis which we postulate may have lead to cytokine release which in turn contributed to the development of hypercalcaemia. We conclude that pamidronate (at doses as low as 10 mg) is safe and effective in immobilization-related hypercalcaemia and suggest that sepsis should be added to the list of risk factors for development of this syndrome.
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PMID:Immobilization-related hypercalcaemia--a possible novel mechanism and response to pamidronate. 226 2

The long-term safety and efficacy of synthetic 1,25-(OH)2D3 (calcitriol; Rocaltrol) in the treatment of women with type 1 osteoporosis is being assessed in a randomized trial. Patients were allocated in double-blind fashion to 1,25-(OH)2D3 or matching placebo. Initially, the calcium intake was adjusted to 1,000 mg/d. The study protocol called for increasing the dose of 1,25-(OH)2D3 until patients developed either hypercalcemia or hypercalciuria. However, in order to maintain a higher dose of calcitriol on a long-term basis, the calcium intake had to be reduced to 600 mg/d in those receiving calcitriol; if that was not successful in eliminating hypercalcemia and hypercalciuria, then the dose of 1,25-(OH)2D3 was reduced as necessary. During the hypercalcemic phase, the indices of bone resorption decreased significantly, demonstrating that calcium absorption is solely responsible for hypercalcemia. The maintenance dose was established after 8 to 10 weeks, and the 24-hour urine calcium and creatinine clearance remained constant throughout the remainder of the study period. On a calcium intake of 600 mg/d, the long-term maintenance dose of 1,25-(OH)2D3 averaged 0.675 micrograms/d. Long-term therapy on an average dose of 0.675 micrograms/d was not associated with nephrotoxicity.
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PMID:Metabolic effects of synthetic calcitriol (Rocaltrol) in the treatment of postmenopausal osteoporosis. 232 68

The effects of oral calcitriol (0.25 and 0.50 micrograms/d), together with calcium (1 g/d), on calcium absorption and bone resorption were measured in postmenopausal osteoporotic women with calcium malabsorption. Radiocalcium absorption was significantly improved and urinary hydroxyproline/creatinine excretion significantly reduced on both doses, but the higher dose caused an unacceptable incidence of hypercalcemia. In 49 patients treated for an average of 15 months with the lower dose, there was a nonsignificant gain in forearm bone mass of 0.4 +/- 0.3 mg/cm/mo (approximately 1/2% per annum) compared with a significant decrease in 17 untreated patients of 3.8 +/- 1.3 mg/cm/mo (approximately 5% per annum).
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PMID:Calcium and calcitriol therapy in osteoporotic postmenopausal women with impaired calcium absorption. 232 73

The relationship of sarcoidosis to renal insufficiency is not widely known by pathologists or clinicians. During an 8-year period beginning in 1980, we observed six patients with sarcoidosis and clinically significant renal insufficiency (serum creatinine, greater than 260 mumol/L). In one of these patients with long-standing sarcoidosis, renal insufficiency was attributed to unrelated primary renal disease until renal biopsy specimen showed interstitial noncaseating granulomas. The four patients with renal insufficiency at presentation differed from the typical patient with sarcoidosis because they were white men who lacked the usual clinical constellation of skin, eye, and pulmonary involvement. All four had noncaseating granulomas on their initial biopsy (bone marrow [3 patients], and lymph node [1 patient]), suggesting each had sarcoidosis, yet each had two or more follow-up biopsies before the diagnosis of sarcoidosis was accepted and appropriate therapy initiated. One of these four patients underwent long-term antifungal and antituberculous therapy. The major causes of renal insufficiency in these six patients were complications of hypercalcemia and interstitial granulomatous nephritis. Except in one patient with nephrocalcinosis, prednisone therapy resulted in a dramatic fall in serum creatinine level with resolution of hypercalcemia. Sarcoidosis is a rare, but treatable, cause of renal insufficiency. Early recognition by clinicians and pathologists may spare patients from undergoing unnecessary biopsies and result in more timely initiation of therapy.
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PMID:Renal insufficiency in sarcoidosis. A clinical and pathologic study. 233 57

The increasing detection of asymptomatic hypercalcaemic patients by biochemical screening has led to an increase in the number of patients referred for neck exploration. Familial Hypocalciuric Hypercalcaemia (FHH) has emerged as an important condition to distinguish from primary hyperparathyroidism as a cause of hypercalcaemia. Patients with FHH are usually asymptomatic, have similar biochemical findings to primary hyperparathyroidism, but fail to respond to parathyroid surgery. We have studied 15 members of a large kindred with FHH. The initial diagnosis was made in the propositus after a failed neck exploration for presumed primary hyperparathyroidism. Of the 7 affected members, 2 had recurrent acute pancreatitis and 2 had incidental malignant disease with no evidence of bony involvement. Measurement of the calcium: creatinine clearance ratio provides a good method of identifying hypercalcaemic patients who might have FHH. A ratio of less than 0.013 is an indication to screen first-degree relatives before considering neck exploration.
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PMID:The importance of distinguishing familial hypocalciuric hypercalcaemia from asymptomatic primary hyperparathyroidism prior to neck exploration. 235 Aug 91

The pathogenesis, prognosis, and reversibility of renal failure were assessed in 494 consecutive, previously untreated patients with multiple myeloma. For patients with a similar extent of disease, the presence or degree of azotemia did not adversely affect prognosis. Hypercalcemia and/or Bence Jones proteinuria explained the renal failure in 97% of patients. After treatment with a combination of hydration and chemotherapy, normal renal function was achieved in 51% of patients, reversibility usually being rapid and occurring more often in those with slight elevation of serum creatinine. Myeloma control was much more important for survival prolongation than reversal of renal failure, supporting the prompt institution of effective therapy for the underlying malignancy.
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PMID:Renal failure in multiple myeloma. Pathogenesis and prognostic implications. 238 64

A 60-year-old man with adult T cell leukemia had been suffering from intractable hypercalcemia resistant to saline hydration, intravenous administration of furosemide, elcatonin, prednisolone and phosphate, and also hemodialysis. Since there was one report suggesting that bleomycin could act as an anticalcemic agent, peplomycin, a new derivative of blerivative of bleomycin, was given at a dose of 10 mg/day by continuous intravenous infusion for 3 days and rapid normalization of serum calcium and creatinine levels resulted. The mechanism of this antihypercalcemic effect is not clear, but peplomycin directly inhibit bone resorption.
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PMID:[Peplomycin for hypercalcemia in a patient with adult T cell leukemia]. 242 35


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