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 (12.0 to 18.3 mg/dl) was detected in 3 cats that had eaten a rodenticide that contained cholecalciferol. Clinical signs included lethargy, anorexia, vomiting, and polydipsia. Treatment with furosemide and fluids administered IV resulted in normalization of the serum calcium concentration and in remission of the clinical signs in 2 cats. One cat with a serum calcium concentration of 18.3 mg/dl did not have clinical signs, was not treated, and was reportedly normal 9 months after initial examination. We attributed the uniformly favorable outcome of exposure to the rodenticide in these cats to the small quantity of the toxin ingested.
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PMID:Hypercalcemia associated with rodenticide poisoning in three cats. 284 90

Carbetimer, a new synthetic low molecular weight polyelectrolyte with a novel structure displayed antitumor activity in a number of animal tumor model systems and in vitro investigations. Based on these findings it was brought to a phase I clinical trial in patients with advanced malignant disease after failure of conventional treatment or with no conventional treatment available. Forty-eight patients received 98 courses. The schedule was a one hour i.v. infusion every four weeks. The starting dose was 180 mg/m2 and dose escalation was performed according to a modified Fibonacci formula up to 16,690 mg/m2. At least three patients were treated at each dose level and each patient was eligible to receive repeat courses at the same dose, until progressive disease or dose-limiting toxicity intervened. No hematological toxicity was encountered. Some adverse effects such as reversible proteinuria, hypercalcaemia, pain at infusion site, nausea and vomiting and fatigue were seen partly in a dose-related manner but did not represent the maximum tolerated dose (MTD). The limiting toxicity at the highest dose level of 16,690 mg/m2 consisted of ocular symptoms ('light flashes') accompanied by a modest decrease of blood pressure and nausea or vomiting during a one hour infusion. 16,690 mg/m2/1 hour was considered the MTD. There were four deaths on study, all considered disease-related. Fourteen patients had stable disease for more than two courses, which, however, could also be explained by the natural course of disease. No clear-cut antitumor responses were noted in our study center. The recommended dose for phase II trials derived from our results is 12,550 mg/m2/2 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase I trial of the polyelectrolyte carbetimer administered i.v. once every four weeks. 319 84

A 45-year-old female manifested lower abdominal fullness and symptoms of hypercalcemia with nausea, vomiting, and thirst. Physical examination showed a right ovarian mass and laboratory data demonstrated hypercalcemia (14.6 mg/dl). The radiographic findings confirmed a right ovarian tumor without any evidence of bone metastasis. Tests revealed that her PTH, nephrogenic urinary cyclic AMP, and 1-25 (OH)2 Vitamin D were not high but that her prostaglandin E2 (PGE2) was elevated. After correction of her calcium elevation with infusion and prednisolone, right oophorectomy with tumor excision was performed. A histological examination of the tumor revealed a mucinous cysto-adenocarcinoma. The postoperative course has been uneventful, with normal calcium and PGE2 values. This case illustrates that hypercalcemia associated with an ovarian carcinoma (Malignancy-associated hypercalcemia) can be mediated by the patient's PGE2 in part.
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PMID:[A case of hypercalcemia with ovarian carcinoma]. 323 Jun 42

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

The history of illness of an eight-year-old boy is presented. Fifteen days old he had been hospitalized because of vomiting, diarrhoea and prolonged jaundice. Alpha 1-antitrypsin deficiency (genotype PiZZ) was diagnosed. At the age of nearly eight complaints started, such as headache, apathy, nausea and vomiting. Sarcoidosis was diagnosed on account of hypercalcemia (3.48-3.68 mmol/l), an elevated serum angiotensin converting enzyme (60 U/l), a positive Kveim test and the fact that other diseases could be excluded. The prognosis of a combination of a serious alpha 1-antitrypsin deficiency and sarcoidosis is discussed. This combination, as far as we have been able to trace, has not been described before.
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PMID:[A patient with type ZZ alpha 1-antitrypsin deficiency and hypercalcemia caused by sarcoidosis]. 349 14

An adult Keeshond had clinical signs associated with hypercalcemia, including inappetence, polyuria, polydipsia, and vomiting. Blood biochemical findings and urinary clearance studies were consistent with a diagnosis of primary hyperparathyroidism. Histomorphometric analysis of trabecular bone in an iliac crest biopsy indicated increased bone remodeling activity. Surgical exploration of the neck revealed an oval mass, which was removed by blunt dissection. Histologic diagnosis was parathyroid gland adenoma. The dog died because of renal failure on the eighth postoperative day. This report defines primary hyperparathyroidism in the dog, thus facilitating diagnosis for the veterinary clinician.
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PMID:Primary hyperparathyroidism in a dog: biochemical, bone histomorphometric, and pathologic findings. 380 43

In a 26-year-old patient admitted to the emergency ward with acute abdomen, all the symptoms--nausea, vomiting, indeterminate abdominal pain, constipation, renal failure, polyuria and polydipsia--could be explained by calcium intoxication syndrome. Investigation revealed generalized sarcoidosis. Under medical treatment with prednisone all the pathologic findings rapidly regressed. The pathogenesis of hypercalcemia in sarcoidosis, and particularly the disorder of vitamin D metabolism with raised levels of 1,25-dihydroxycholecalciferol, are discussed.
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PMID:[Acute hypercalcemia syndrome in sarcoidosis]. 384 Sep 13

Hypercalcaemia can be caused by many disorders, but is most commonly due to primary hyperparathyroidism in outpatients, and to malignant disease in hospital inpatients. When mild (less than 3 mmol/L) it does not cause symptoms, but can have long term effects such as renal calculi. It is important that the aetiology of the hypercalcaemia be established, as it can reflect serious disease. In most patients the correct diagnosis can be suspected from clinical history and examination, and confirmed by laboratory tests and x-rays. The most difficult diagnostic problem is the patient with negative clinical findings, mild hypercalcaemia and mild renal impairment, when the parathyroid hormone level is normal or slightly elevated. When hypercalcaemia is severe (greater than 3.5 mmol/L), it can cause vomiting, polyuria, dehydration and renal impairment, and is then an important therapeutic problem. Therapy includes treatment of the cause, such as radiotherapy for malignant disease or surgery for primary hyperparathyroidism. In addition, it is usually necessary to treat the hypercalcaemia itself, and the initial step is always rehydration. If the plasma calcium concentration remains high, drug treatment must be added, the most effective and reliable agent being intravenous mithramycin. Aminohydroxypropylidene diphosphonate (APD), though less studied, may be equally useful in this situation. Glucocorticoids are not always effective, and phosphate may cause renal damage, particularly when given intravenously. For long term treatment of malignant hypercalcaemia, oral glucocorticoids and phosphate are often effective, and can be given in combination. When primary hyperparathyroidism cannot be corrected surgically, the hypercalcaemia (and hypercalciuria) are probably best treated with a low calcium diet and cellulose phosphate, a regimen also effective for the hypercalcaemia of sarcoidosis.
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PMID:Hypercalcaemia. What does it signify? 394 Aug 49

Thirteen patients with hypercalcaemia due to carcinoma received inorganic phosphate, orally or intravenously, as palliative treatment for their high serum calcium levels. The serum calcium promptly fell in all patients fully treated, and there was a striking clinical improvement in most patients. The blood urea was usually unchanged or became nearer to normal, while the serum phosphate altered variably. Only two of the eight patients who were studied at necropsy had microscopical nephrocalcinosis; corneal calcification was evident in both before phosphate treatment was started.This oral inorganic phosphate (1 gramme thrice daily) is a safe and effective means of treating hypercalcaemia due to carcinoma. An intravenous infusion of 1 gramme over eight hours may sometimes be required initially for patients who are vomiting.
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PMID:Phosphate treatment of hypercalcaemia due to carcinoma. 417 70

18 French women with bone metastases of breast cancer were treated with norethisterone 60 mg per day (except 1 woman given 20 mg daily) for 2 months or until the end of the remission from 1969-1972. The patients ranged from 39-84 years (mean 57.7). In 16 breast cancer had 0een diagnosed 6 months to 16 years before (mean 43 months). Calcemia was less than 102 mg per 1; calcuria was above 250 mg per 24 hours in 3. The bone lesions were lytic in 13 and mixed in 5. Progestagens were the first treatment for bone metastases in 10; others had ovariectomy, androgens, cortisone, chemotherapy, adrenalectomy, and hypophysectomy. Since the response of these metastases is difficult to evaluate, the authors chose criteria of disappearance of pain and stabilization of radiographic lesions. In 6 patients pain was relieved within 2-4 weeks, and lesions stabilized or recalcified in 2. In 5 of the 6 erythrocyte sedimentation rate became normal in 2 months; calcemia normalized in 1; calcuria decreased in 4. Remission lasted 3-9 months (mean 5.6). After remission, androgens were effective in 3 or 4. In 6, norethisterone was stopped because it was ineffective. 6 others had to stop for intolerance: vomiting in 1, jaundice in 2, hypercalcemia in 3.
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PMID:[Treatment of bone metastases of breast cancer with progestogens]. 482 May 23


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