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

Bilateral dense rings in the renal medulla were found on noncontrasted computed tomography in a patient with marked hypercalcemia and suspected primary hyperparathyroidism. The rings were not present on plain radiographs and were obscured on contrasted scans, and may represent occult nephrocalcinosis. Associated findings--renal insufficiency induced by hypercalcemia and interstitial nephritis--may be reversible with early recognition of this CT finding.
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PMID:Renal medullary "rings": possible CT manifestation of hypercalcemia. 670 30

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

Renal and systemic magnesium metabolism has not been adequately characterized in states of prolonged PTH excess in humans. Whereas acute experimental PTH administration uniformly results in enhanced renal magnesium reabsorption in many species, including humans, numerous clinical reports have documented renal magnesium wasting in human primary hyperparathyroidism. The possibility has been raised, therefore, that secondary consequences of sustained hyperparathyroidism (eg, hypercalcemia, nephrocalcinosis) might override the direct renal effects of PTH. Accordingly, the present studies assessed the effects of chronic (12 days) continuous intravenous (IV) b-(1-34)-PTH infusion in four normal human subjects on plasma, urinary, and intestinal magnesium and calcium homeostasis under metabolic balance conditions. Chronic PTH infusion resulted in a steady-state of hypercalcemia, hypercalciuria, and persistent negative calcium balance, which returned to baseline values in a recovery period. In contrast to plasma calcium concentration, plasma magnesium concentration was not altered by PTH infusion. Significant hypermagnesuria was observed during the period of PTH administration (control, 8.21 +/- 0.43 mEq/24 hours; PTH days 7-12, 10.75 +/- 0.74 mEq/24 hours, P less than 0.05) resulting in an initial, but transient, negative magnesium balance. During days 7-12 of PTH administration, net intestinal magnesium absorption increased sufficiently to result in a return to control magnesium balance. These findings suggest that hypermagnesuria associated with clinical primary hyperparathyroidism results from either direct or indirect effects of PTH excess, per se, and does not require the long-term consequences or complications of the clinical disorder (eg, nephrocalcinosis, renal insufficiency, acidosis).
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PMID:Renal and systemic magnesium metabolism during chronic continuous PTH infusion in normal subjects. 673 67

Four families with familial hypocalciuric hypercalcaemia were studied. The probands presented with abdominal pain, which in three was due to acute pancreatitis; in two the condition was life threatening. Serum concentrations of calcium, magnesium, phosphate, and immunoassayable parathyroid hormone, urinary calcium excretion, and the rate of renal tubular reabsorption of phosphate were measured; the findings were compared with results in 10 patients with primary hyperparathyroidism matched for serum calcium concentration to establish differences between the diseases. Familial hypocalciuric hypercalcaemia should be suspected in patients with hypercalcaemia in whom daily urinary calcium excretion is below 5 mmol (200 mg) provided renal insufficiency, vitamin D deficiency, and ingestion of drugs that reduce calcium excretion have been excluded. Most cases appear to run a benign course, but some may suffer considerable morbidity. Surgical treatment should be reserved for patients with severe complications, when all parathyroid tissue should be removed.
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PMID:Familial hypocalciuric hypercalcaemia and acute pancreatitis. 678 29

The incidence of side effects from antacids is low, but patients with renal insufficiency are at risk to develop alkalosis with high doses of calcium carbonate or magnesium hydroxides, or to develop hypercalcemia due to insufficient calcium elimination by the kidneys.--A great potential exists for drug interactions with antacids. In most instances, the effectiveness of other drugs is decreased in the presence of antacids, but effectiveness may be increased for L-dopa (less degradation in stomach) or quinidine (renal elimination reduced). Interactions at the absorption level can be avoided by administering the antacid one hour after intake of the other drugs (one hour after meals) which is also the optimum dosing schedule to ensure good antacid effect. Interactions through changes of urine pH are not eliminated by observing special dosing time schedules, but by modifying the dose or by selecting alternative drug treatment.
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PMID:[Metabolic effects of antacids and interactions with other drugs]. 685 4

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
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PMID:[Electrolyte metabolism and emergency]. 688 72

Forty-five patients met the criteria for the diagnosis of multiple myeloma in a retrospective chart review from 1975 to 1980. Renal insufficiency with peak serum creatinine concentration greater than 1.5 mg/dL involved 69% of all patients. Renal insufficiency was reversible in 55% of the cases. Treatment of hypercalcemia and/or chemotherapy for multiple myeloma was associated with reversibility in 88% of cases. Once renal insufficiency occurred in patients with multiple myeloma, those with reversible renal failure had a duration of survival fourfold longer (11.4 v 2.8 months) than those with irreversible renal insufficiency. In conclusion, reversible renal insufficiency from hypercalcemia or the myeloma process itself develops in a majority of patients with multiple myeloma. If therapy reverses the renal dysfunction, a greater life expectancy occurs. Patients with multiple myeloma and renal insufficiency should, therefore, be examined for reversible causes of renal dysfunction, since if found and treated, a substantial improvement in prognosis is achieved.
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PMID:Reversible renal insufficiency in multiple myeloma. 713 57

Sarcoidosis may involve the kidneys in several ways. Most commonly, aberrations of calcium metabolism, including hypercalcemia, hypercalciuria, and nephrocalcinosis, are responsible for the renal manifestations of sarcoidosis. Granulomatous infiltration of the renal interstitium may also produce severe derangements of renal function. Glomerulonephritis can occur with sarcoidosis, although the pathogenesis remains unclear. Besides renal insufficiency and frank renal failure, nephrotic syndrome, nephrolithiasis, hypertension, and a variety of tubular defects may complicate sarcoidosis. The sensitivity of "sarcoid nephropathy" to corticosteroids usually warrants therapeutic trial.
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PMID:Renal manifestations of sarcoidosis. 722 44

A 64-year-old man died of IgD plasmocytoma only two months after onset of first symptoms. The course of the disease was characterized by marked renal insufficiency, hypercalcaemia with cardiac arrhythmias and bone destruction, in addition to raised phosphate concentration and alkaline phosphatase activity. The electrophoresis diagram was unremarkable and had no M-peak. But immunoelectrophoretic analysis of serum demonstrated a IgD paraprotein; in addition there was a monoclonal light chain, type lambda. At post-mortem the diagnosis of plasmocytoma was made; in addition there was renal amyloidosis.
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PMID:[IgD plasmocytoma: clinical and differential diagnostic features (author's transl)]. 723 6

Over a period of 6 1/2 years hypercalcemia has been diagnosed in 86 patients. In 55.8% of cases a malignant tumor was the cause of the elevated calcium levels, and in 22.1% of cases primary hyperparathyroidism (p.Hp.) was diagnosed. In the remaining 19 patients hypercalcemia was related to renal insufficiency (5 patients), vitamin-D intoxication (4) and thiazide therapy (3), while other, rarer causes were identified in 7 cases. As expected, bronchial and breast carcinomas were most frequent (52%) in the malignancy group. In patients below age 40 malignancy was never responsible for the hypercalcemia, but in patients over 50 malignancy was present in 65%. Of the patients with solid tumors 54.8% had skeletal metastases, while other organ metastases were found in 33.3% of these. The occurrence of a hypercalcemia in patients with malignancy is associated with a poor prognosis since over 60% of the patients died within as little as one month and over 90% within a year after the occurrence of hypercalcemia. Renal function impairment in hypercalcemia was significantly more marked in the patients with malignancy than in patients with p.Hp. and was closely related to the calcium levels. Pharmacological reduction of the blood calcium level produced a distinct improvement in renal function in 70% of the patients treated. The current hypothesis on the pathogenesis of hypercalcemia among carcinoma patients is briefly discussed.
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PMID:[Hypercalcemia in hospitalized patients. Diagnostic and prognostic aspects]. 731 56


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