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

Severe hypercalcemia is a potentially life-threatening complication of several diseases. Most commonly it is caused by cancers that enhance bone resorption. Impaired renal calcium excretion resulting from a combination of volume contraction and calcium-induced renal injury (nephrocalcinosis) plays a critical role in the genesis and aggravation of hypercalcemia. Treatment of hypercalcemia is based on treating the underlying disease, restoring extracellular volume, correcting electrolyte deficiencies (potassium and magnesium), and reducing bone resorption. Several measures are available to reduce bone resorption, of which the most efficacious are the bisphosphonates and plicamycin (mithramycin). One of these agents in combination with volume expansion can reduce serum calcium concentrations to near normal in most patients within 3 to 6 days. Because of the delayed hypocalcemic action of these agents, they should be administered early. Calcitonin has a more modest hypocalcemic action than the bisphosphonates or plicamycin but has a more rapid effect. Combining calcitonin with plicamycin or a bisphosphonate can enhance the rate of decline of the serum calcium level. Bone resorption also can be reduced by getting patients out of bed to stand or walk. Glucocorticoids may be effective in patients with hypercalcemia associated with high levels of vitamin D, such as sarcoidosis, some lymphomas, or vitamin D intoxication. Patients with mild to moderate hypercalcemia may be asymptomatic. Therapy in these patients should be directed at the primary disease as well as at preventing complications that could raise the level of serum calcium. Efforts should be made to prevent volume contraction and prolonged bed rest. Sedatives and narcotic analgesics, by reducing activity and oral intake, can raise serum calcium levels. In the future it may be possible to predict which patients with cancer are likely to develop accelerated local tumor-mediated or humorally mediated osteolysis. For example, high circulating levels of PTH-like peptides in patients with lung cancer might suggest a greater risk of developing hypercalcemia. These patients could be monitored more closely by periodically measuring urinary calcium. Another prophylactic approach would be to treat patients at risk of developing hypercalcemia with drugs, such as the bisphosphonates, that inhibit bone resorption.
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PMID:Treatment of hypercalcemia. 267 75

Aluminium-containing phosphate binders were replaced by a calcium and magnesium carbonate-containing antacid in 20 patients on long-term haemodialysis, over a three-month period in all of them, for 12 months in ten. After two months the serum aluminium level fell (mean +/- SD) from 3.0 +/- 1.6 to 1.4 +/- 0.5 mumol/l (P less than 0.001). After three months the serum phosphate level had fallen from 1.8 +/- 0.4 to 1.5 +/- 0.4 mumol/l (P less than 0.05), while during the same period parathormone (PTH-NH2) fell from 1.4 +/- 1.4 to 0.8 +/- 0.7 ng/ml (P less than 0.05). Serum total calcium concentration rose after two months from 2.2 +/- 0.2 to 2.4 +/- 0.2 mmol/l (P less than 0.001). In a third of patients the uraemic acidosis was corrected, standard bicarbonate rising from 18 +/- 2 to 21 +/- 3 mmol/l (P less than 0.05). Serum pH, potassium, sodium, magnesium and alkaline phosphatase did not change significantly. Hypercalcaemia was an expected disadvantage: repeated symptom-free episodes of hypercalcaemia occurred in six of 20 patients during the first three months and in a further two up to 12 months. These episodes were successfully controlled by a reduction of CaCO3/MgCO3 dosage and readministration of Al(OH)3. Extraosseous calcifications were not observed.
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PMID:[Replacement of aluminum-containing phosphate binders by calcium and magnesium carbonates in long-term hemodialysis]. 270 34

Disorders of fluid and electrolyte metabolism in elderly diabetics were studied. High frequency of hyperkalemia (20.8%), hypomagnesemia (14.6%), hypocalcemia (13.7%), hyperphosphatemia (8.6%), hyponatremia (8.1%) and hyperchloremia (7.2%) was observed among 332 elderly diabetics. Furthermore, hyperkalemia, hyperphosphatemia, hyponatremia, hyperchloremia, hypercalcemia and hypermagnesemia were more frequent in diabetics with renal insufficiency (serum Cr greater than or equal to 1.5 mg/dl) than in diabetics with normal renal function (serum Cr less than or equal to 1.4 mg/dl). In addition, statistically significant negative correlation were observed between plasma glucose levels and serum levels of sodium and chloride in diabetics with normal renal function. These results clearly demonstrated that the most important causal factor of electrolyte disorders in elderly diabetics might be the renal dysfunction due to diabetic nephropathy and/or nephrosclerosis. Moreover, glucose intolerance is also one of the causal factors for hyponatremia and hypochloremia. Disorders of fluid and electrolyte metabolism were manifest in 31 diabetic patients with hyperosmolar non-ketotic coma. The frequency of patients with abnormally elevated serum levels of sodium, potassium and chloride, and patients with abnormally lowered serum levels of calcium was high in this morbid state. Water and sodium deficit, examined in 11 cases of hyperosmolar non-ketotic coma, was 4780 +/- 2100 ml (107 +/- 43 ml/kg body weight) and 290 +/- 170 mEq (6.8 +/- 4.2 mEq/kg body weight), respectively. However, no significant deficit of potassium was observed in the patients. Statistically significant positive correlations between water deficit and serum Cr levels and with serum effective osmolarity were observed. However, there were no significant correlations between water deficit and plasma glucose levels, serum sodium levels and serum osmolarity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Disorders of fluid and electrolyte metabolism in elderly diabetics]. 279 74

Theophylline, with its narrow therapeutic margin, is a common cause of iatrogenic and deliberate overdose. Most cases of self-poisoning are with sustained release preparations, with peak concentrations occurring up to 12 or more hours after overdose. Toxic symptoms are often seen at concentrations above 15 mg/L. Theophylline is metabolised within the cytochrome P-450 system, with an average total body clearance of 50 to 60 ml/min. Clearance is, however, affected by many factors such as other drugs or disease, and in overdose zero order kinetics may result in prolonged half-lives. Toxicity is characterised by agitation, tremor, nausea, vomiting, abdominal pains, seizures, and tachyarrhythmias. Hypokalaemia and metabolic acidosis are more profound in acute toxicity, and hypercalcaemia is usually present. Seizures occur at lower concentrations after chronic over-medication than after acute overdose. Gastric lavage should be performed in all patients presenting early, and an oral multiple dose charcoal regimen started with 50 to 100g charcoal, repeating with 50g doses and checking theophylline concentrations at 2- to 4-hour intervals. Multiple dose charcoal can be expected to double the clearance of theophylline, being as effective as a haemodialysis. Of the invasive techniques available, charcoal haemoperfusion is the most effective, increasing clearance 4- to 6-fold. Supportive care is particularly important. The aggressive supplementation of potassium, treatment of emesis with droperidol and ranitidine, and treatment of tachyarrhythmias and hypotension (possibly with propranolol), together with oral multiple dose charcoal may obviate the need for haemoperfusion. Seizures suggest increased morbidity and mortality. Charcoal haemoperfusion should be considered if plasma concentrations are greater than 100 mg/L in an acute intoxication or greater than 60 mg/L in a chronic intoxication. The decision to haemoperfuse should not be based on plasma concentrations alone, but an overall evaluation of the patient's laboratory and clinical status.
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PMID:Role of extracorporeal drug removal in acute theophylline poisoning. A review. 330 69

We describe a patient who initially formed calcium-containing renal stones owing to gouty diathesis and hypocitraturia. On therapy with 300 mg. allopurinol and 60 mEq. potassium citrate daily serum uric acid decreased from 9.2 to 5.8 mg. per dl., urinary pH increased from less than 5.5 to 6.6 and urinary citrate increased from 223 to 1,005 mg. per day. Four months later while still on this medical regimen, the patient presented with hypercalcemia (13.4 mg. per dl.), high serum 1,25-dihydroxyvitamin D (65 pg. per ml.) and hypercalciuria (598 mg. per day), which subsequently were found to result from sarcoidosis. Prednisone therapy normalized the disturbances in calcium metabolism. During 33 months of combined treatment with 7.5 to 10 mg. prednisone a day, allopurinol and potassium citrate, the patient was free of stones and he had normal urinary calcium, pH and citrate. However, a calcium stone formed 1 month after discontinuation of prednisone therapy, although treatment with allopurinol and potassium citrate was continued. The patient had marked hypercalciuria of 447 to 465 mg. per day, despite normal urinary pH, citrate and uric acid. This case represents calcium stone formation in a patient with 2 separate etiologies for stone disease, that is gouty diathesis and sarcoidosis. Therapeutic regimens directed at the correction of both metabolic disturbances were required to control renal stone formation.
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PMID:Gouty diathesis and sarcoidosis in patient with recurrent calcium nephrolithiasis. 337 3

After 7 days in air on wet filter paper mudskippers had normal body weight and normal levels of plasma sodium, potassium, and phosphate. They were, however, significantly hypercalcemic. The hypercalcemia could be reduced by the daily intraperitoneal injection of synthetic eel calcitonin (1.67 microgram kg-1 day-1) and this effect was dose dependent with a maximal response at a dose of 3.33 micrograms kg-1 day-1. Calcitonin had no effect on plasma calcium levels of fish held in water but did induce significant hyperphosphatemia whether the fish were held in water or in air on wet filter paper with this effect being greater under the latter conditions. The hypocalcemic action of calcitonin was restricted to conditions under which the fish displayed patent hypercalcemia. Under no conditions did calcitonin produce significant hypocalcemia so it appears that the action of synthetic eel calcitonin in the mudskipper, Periophthalmodon schlosseri, is dependent upon the presence of excess plasma calcium and is thus more accurately described as being anti-hypercalcemic rather than hypocalcemic.
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PMID:Effects of calcitonin on plasma calcium and phosphate in the mudskipper, Periophthalmodon schlosseri (Teleostei), in water and during exposure to air. 338 5

There are a variety of water and electrolyte disorders in patients with cancer. These disorders occur during the growth of tumors, generally as a consequence of inadequate intake and absorption of electrolytes, renal failure secondary to tumor or rapid tumor destruction and production of metabolically active substances by the tumor. In this paper, the electrolyte abnormalities associated with cancer were reviewed. Hyponatremia is one of the most common clinical electrolyte abnormalities in advanced cancer. Some patients may have hyponatremia, in spite of increased total body sodium and absence of a defect in water diuresis. This status is designated as "sick cell syndrome" or "essential hyponatremia". In addition, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in association with various tumors has been described. This syndrome is principally due to water retention, but can also be due to continuous urinary loss of sodium, and hypo-osmolality. Hypercalcemia is associated with coexistent primary hyperparathyroidism, prostaglandin (PGE2) or osteoclast-activating factor. It now seems likely that ectopic PTH is rarely the cause of hypercalcemia in nonparathyroid cancer. There are no data supporting the ectopic production of vitamin D-like substance as an important factor in the hypercalcemia of cancer. There are three general categories in which patients with hypercalcemia and cancer may be placed: those with bone metastases, those without bone metastases of solid tumors and those with hematologic malignancies. Hypokalemia is associated with ectopic ACTH- and insulin--producing tumors, and is often found in patients with mucin-secreting, potassium-losing adenocarcinoma of the colon.
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PMID:[Electrolyte abnormalities associated with cancer: a review]. 352 93

The factors responsible for the frequent occurrence of hypertension in patients with primary hyperparathyroidism have not been elucidated. Suggested mediators have included hypercalcemia, renal insufficiency, and increased plasma renin activity. However, experimental results have not been reported in any species that test the hypothesis that sustained hypertension in this clinical syndrome is due to consequences of parathyroid hormone (PTH) excess versus unrelated factors (e.g., primary hypersecretion of other hormones, NaCl sensitivity, genetic factors). Moreover, no systematic evaluation of the renin or adrenal cortical responses to chronic PTH excess has been reported in any species. Accordingly, the present studies assessed the effects of chronic (12 days) continuous intravenous b-(1-34) PTH infusion in normal human subjects (n = 4). PTH infusion resulted in persistent hypercalcemia and hypertension, reversible during a 4-8-day recovery period. Transient but significant increases in urinary tetrahydroaldosterone excretion and plasma cortisol concentration were observed as hypercalcemia and hypertension developed. No significant changes in plasma potassium concentration or plasma renin activity were observed, suggesting that hypercalcemia-induced transient hypersecretion of ACTH was responsible for both cortisol and aldosterone responses. The present results suggest that hypertension associated with clinical primary hyperparathyroidism results from either direct or indirect effects of PTH excess, per se, and requires neither the long-term consequences/complications of the clinical disorder (e.g., severe nephrocalcinosis, renal insufficiency) nor primary hypersecretion of additional hormones. These results are consistent with the hypothesis that hypercalcemia alone or in combination with at least permissive levels of PTH can generate short-term, but persistent (12 days) hypertension in human subjects and thus may be the initiating mechanism for hypertension in clinical primary hyperparathyroidism.
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PMID:Chronic continuous PTH infusion results in hypertension in normal subjects. 354 30

In 93 children, end-stage renal disease was treated with the new dialytic methods of continuous ambulatory peritoneal dialysis (CAPD) or continuous cycling peritoneal dialysis (CCPD) over 5 years. Modality survival rates at 36 months with CAPD, CCPD, or both were 20%, 93%, and 87%, respectively. Use of CCPD as the primary dilaytic method increased during the study period. The peritonitis rate was one episode per 11.8 patient treatment months and was similar with both CAPD and CCPD. Gram-positive organisms were cultured in 34% of these episodes of peritonitis. Staphylococcus aureus peritonitis was associated with a recurrence rate of 40% and led to catheter replacement in 45% of the episodes. Peritoneal membrane failure necessitating switching to hemodialysis was related to peritonitis in three patients. Of the 74 peritoneal catheters that required replacement, 70% were infected. Serial serum levels of urea nitrogen, potassium, calcium, phosphorus, albumin, and alkaline phosphatase remained stable, whereas serum creatinine level rose slightly over time. Episodes of hyperkalemia, hypercalcemia, and hyperphosphatemia were observed at a frequency of one episode per 12.2, 4.6, and 2.5 treatment months, respectively. Blood transfusions were required in once per 1.5 and 3.3 treatment months in seven anephric patients and in 35 patients with their own kidneys, respectively (P = 0.05). In prepubertal patients who received CAPD or CCPD for greater than 1 year, little or no improvement in growth occurred in relationship to either chronologic or bone age.
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PMID:Five years' experience with continuous ambulatory or continuous cycling peritoneal dialysis in children. 365 81

In order to determine the prevalence of rhabdomyolysis-associated acute renal failure (RM-ARF) and assess the effect of oliguria on biochemical features in this condition, 127 cases of ARF seen over 18 months were reviewed. Eleven cases of RM-ARF were seen, a prevalence of 8.6% of all cases of ARF. There were ten males and one female (age range 15-72 years) with precipitating events being trauma in three, coma in two, infection in two and other causes in five. Ten had concurrent clinical or historical evidence of dehydration, two had mild hypokalemia, and one abused alcohol. Serum and urine myoglobin by radioimmunoassay were greater than 800 ng/l in all cases tested. False negative tests for urine myoglobin by o-tolidine reaction after (NH4)2SO4 extraction occurred in four cases. Despite attempted forced saline diuresis and urinary alkalinisation, seven became oliguric and required dialysis for 12-81 days. Initially (pre-dialysis) oliguric patients had significantly higher maximum serum levels of potassium, phosphate, and rate of rise of creatinine, significantly lower trough levels of calcium, and no significant difference in peak creatine phosphokinase or uric acid levels than non-oliguric patients. Two subjects developed recovery phase hypercalcemia, four required fasciotomy for compartment syndromes, three sustained permanent nerve damage, and three required limb amputation. Ten survived, with a mean creatinine clearance of 96 ml/min after nine to 30 months. RM-ARF is common, may be clinically occult and show false negative urine myoglobin tests. Hyperkalemia, hyperphosphatemia, and hypocalcemia are more common in oliguric than in non-oliguric RM-ARF, but both have a good prognosis with appropriate medical and surgical management.
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PMID:Rhabdomyolysis and acute renal failure. 386 39


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