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)

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

In a consecutive series of 100 neck explorations for primary hyperparathyroidism, 42 patients were 60 years of age or older; in this group of elderly patients the surgical cure rate was 100%. These patients were reviewed retrospectively by means of a structure interview. Twenty-one patients had had preoperative neuromuscular symptoms that ranged from coma to subjective muscular weakness. These patients had significantly-higher preoperative serum calcium and parathyroid hormone levels than did 21 patients without neuromuscular symptoms (P = 0.003 and P = 0.046, respectively). Most of the neuromuscular symptoms improved in the postoperative period. In particular, 15 of 17 patients with muscle weakness reported a significant improvement, while 14 of 15 patients who suffered from fatigue and lethargy reported an improvement. An improvement also occurred in the level of day-to-day function in eight patients. While surgery for primary hyperparathyroidism generally is undertaken for a specific indication, such as severe hypercalcaemia or renal stones, it appears from this study that neuromuscular symptoms also may improve, particularly in elderly patients.
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PMID:Neuromuscular symptoms in elderly patients with hyperparathyroidism: improvement with parathyroid surgery. 339 14

Eight patients with sarcoidosis seen at the Royal Children's Hospital, Melbourne, during the past 10 years were reviewed. Five of the eight patients came from non-metropolitan areas. The major presenting symptoms were cough, fatigue and weight loss; peripheral lymphadenopathy and hepatomegaly were common. None of the patients had eye or central nervous system involvement. Seven patients had bilateral hilar adenopathy on chest radiograph and six had parenchymal lung changes. Angiotensin converting enzyme was measured in six patients and was elevated in all, while hypercalcaemia was present in three patients. Five patients had a tissue biopsy showing the characteristic non-caseating granulomas. Corticosteroid therapy was used for four patients and was given for hypercalcaemia in three patients and for severe restrictive lung disease in one patient.
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PMID:Sarcoidosis in children. 356 75

A 74-year-old woman was hospitalized because of decreased appetite, fatigue, and weight loss. The laboratory examination revealed hypercalcemia, a slightly increased serum creatinine level, and a markedly elevated serum level of 1,25-dihydroxyvitamin D3. The most important finding the physical examination revealed was enlarged inguinal lymph nodes. A biopsy disclosed lymphocyte-depleted Hodgkin's disease. After steroids, but not after calcitonin, both the elevated calcitriol concentration and serum calcium normalized. In spite of intensive chemotherapy, a further episode with hypercalcemia occurred and increased 1,25-dihydroxyvitamin D3 serum levels were observed. According to the available evidence it seems probable that the humoral hypercalcemia in this patient resulted from production of 1,25-dihydroxyvitamin D3 in the tumor.
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PMID:Hypercalcemia and elevated serum 1,25-dihydroxyvitamin D3 in a patient with Hodgkin's lymphoma. 375 25

A 58-year-old man was initially seen with fatigue and weight loss. Laboratory examination detected hypercalcemia, elevated 1,25-dihydroxycholecalciferol levels, low parathyroid hormone (PTH) concentrations, and subperiosteal bone resorption. The patient underwent subtotal parathyroidectomy for presumed hyperparathyroidism, but serum calcium and 1,25-dihydroxycholecalciferol levels remained elevated following surgery. Search for another cause of the hypercalcemia disclosed enlarged para-aortic lymph nodes, biopsy specimens of which demonstrated Hodgkin's disease. After treatment of the patient with two cycles of chemotherapy with mechlorethamine hydrochloride, vincristine sulfate, procarbazine hydrochloride, and prednisone, serum calcium, 1,25-dihydroxycholecalciferol, and PTH levels normalized. We speculate that the humoral hypercalcemia in this patient resulted from tumor production of 1,25-dihydroxycholecalciferol.
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PMID:Humoral hypercalcemia in Hodgkin's disease. Association with elevated 1,25-dihydroxycholecalciferol levels and subperiosteal bone resorption. 383 28

There is an increasing use and variety of beta-adrenoceptor blocking agents (beta-blockers) available for the treatment of hyperthyroidism. Recent comparative studies suggest that atenolol (200mg daily), metoprolol (200mg daily); acebutolol (400mg daily), oxprenolol ( 160mg daily), nadolol ( 80mg daily) and timolol (20mg daily) produce a beneficial clinical response equal to that seen with propranolol ( 160mg daily). Most beta-blockers reduce resting heart rate by approximately 25 to 30 beats/min, although a lesser reduction is seen with those possessing intrinsic sympathomimetic activity such as oxprenolol and pindolol. While earlier studies employing large doses of intravenous propranolol concluded that beta-blockade reduced myocardial contractility, more recent non-invasive studies suggest that the predominant cardiac effect is on heart rate. In patients with cardiac failure, beta-blockers may, however, produce a profound fall in cardiac output. Nevertheless, in combination with digoxin they may be useful in controlling the atrial fibrillation of thyrocardiac disease. beta-Blockers improve nervousness and tremor (although to a lesser extent with cardioselective agents) and severe myopathy, and they also reduce the frequency of paralysis in patients with thyrotoxic periodic paralysis. There is often subjective improvement in sweating but usually no major effect on eye signs. Recent studies show a 10% reduction in oxygen consumption/basal metabolic rate with long term oral use of selective or nonselective beta-blockers. In addition, many agents (propranolol, metoprolol, nadolol and sotalol but not acebutolol, atenolol or oxprenolol) reduce circulating tri-iodothyronine (T3) concentration by between 10 and 40%, although the clinical significance of this effect (if any) is not established. beta-Blockers may also have endocrinological effects on gastrin, cyclic AMP, catecholamines and other hormone levels. Given in adequate dosage, propranolol has been shown to control thyrotoxic hypercalcaemia. Minor side effects (nausea, headaches, tiredness, etc.) are quite common but overall beta-blockers are well tolerated by the thyrotoxic patient. The major use of these drugs is in symptomatic control while awaiting definitive diagnosis or treatment. As an adjunct to antithyroid drugs or radioactive iodine, beta-blockers will produce a satisfactory clinical response in the weeks to months before these forms of therapy produce a euthyroid state. beta-Blockers are more convenient than antithyroid drugs in the control of patients receiving therapeutic radioiodine, in that continuous therapy and assessment of biochemical response is possible.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of beta-adrenoceptor blocking drugs in hyperthyroidism. 614 1

A cervical lymph node enlarged since 3 weeks was to be removed in a 12-year-old boy, whose only complaint was slight fatigue. Routine screening revealed hypercalcemia of 7.3-8.1 mval/l. This rose to 9.2 mval/l despite furosemide-induced high fluid turnover and prednisone while diagnostic evaluation proceeded. Serum phosphate was low consistently. Malignancy, vitamin D-intoxication, immobilisation and familial conditions could be ruled out as causes. Highly elevated serum-parathormone levels inspite of hypercalcemia, and ultrasonography of the neck were the most helpful evidence of a parathyroid adenoma. Calcitonin was effective in lowering serum-calcium to 6-7 mval/l preoperatively.
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PMID:[Asymptomatic, excessive hypercalcemia n a 12-year-old boy]. 685 83

An unusual clinical presentation of moderate hypercalcemia as a result of primary hyperparathyroidism is described. The patient complained of fatigue, depression, thirst, polyuria, and focal neurologic symptoms including amaurosis fugax, anomia, right upper-extremity dysesthesias, and a left cerebral transient ischemic attack. No structural central nervous system abnormality could be documented. Signs and symptoms disappeared when serum calcium levels were reduced from 13.2 to 9.8 mg/100 ml. They have not recurred in 30 months of follow-up. The association of focal neurologic disease and hypercalcemia is uncommon. Although the precise pathophysiologic mechanism is unclear, this patient's symptoms suggest a vascular etiology.
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PMID:Focal neurologic symptoms in hypercalcemia. 718 1

The Southwest Oncology Group (SWOG) studied the response rate and toxicity of merbarone (1,000 mg/m2 IV continuous infusion days 1-5, q 21 days) in patients with advanced metastatic renal cell carcinoma. Among 36 eligible patients, there was one partial response for a response rate of 3% (95% C.I. 0.1-15%). There were no mixed responses. There were no treatment related deaths or adverse drug reactions. Significant anemia, diarrhea, and hypercalcemia were observed. Mild to moderate degrees of malaise/fatigue/lethargy, dizziness/vertigo, hyperglycemia, creatinine increase, nausea, vomiting, weight loss, pedal edema, dyspnea, and granulocytopenia were noted. Merbarone does not have significant activity as a single agent in advanced renal cell carcinoma.
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PMID:Phase II evaluation of merbarone in renal cell carcinoma. 786 Feb 33

It could be advantageous for the parathyroids to be able to sense not only the absolute concentration of extracellular Ca2+, but also the rate and direction of change of Ca2+, thereby allowing the parathyroids to respond earlier to threats to Ca2+ homeostasis. By using high and low Ca2+ dialysis in a single session, we examined the parathyroid response to direction of change of Ca2+ during acute Ca2+ perturbation in nine hemodialysis patients. Separate PTH/ionized calcium (PTH/iCa) response curves were generated for rising Ca2+ and falling Ca2+. Significant directional hysteresis (higher PTH level during falling than during rising Ca2+) was found. During hypercalcemia, PTH levels were between 2.2 and 1.6 times higher at iCa concentrations of between 0 and +0.1 mM above the baseline iCa, when Ca2+ was falling than when it was rising. During the phase of induced hypocalcemia, parathyroid fatigue was seen in six of the nine patients. Fatigue patients tended to have higher basal PTH (1-84) levels than those not showing fatigue. The existence of fatigue provides an explanation for directional hysteresis during hypocalcemia, and therefore parathyroid sensing of the direction of change of Ca2+ could not be assessed during hypocalcemia. These studies demonstrate a capacity of the parathyroids to sense the direction of movement of Ca2+ during hypercalcemia.
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PMID:Parathyroid sensing of the direction of change of calcium in uremia. 851 Mar 89


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