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

A case of watery diarrhea, hypokalemia and hypercalcemia associated with an islet cell tumor was described. A 62-year old man exhibited frequent watery diarrhea and hypokalemia for two years. He had no peptic ulcer and serum gastrin level was normal. His serum calcium was abnormally high and serum phosphate was lowered. He had secretin-like activity in his plasma. Autopsy revealed a small islet cell tumor in the pancreas and several metastatic masses in the liver. Microscopic examination revealed the tumor cell was not beta, alpha nor D cells. By electron microscopy the secretion granules of the tumor cell resembled those of S, M and T cells. It was not possible to decide which of the tree cell types was responsible for the pancreatic cholera.
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PMID:A case of watery diarrhea, hypokalemia and hypercalcemia associated with nonulcerogenic islet cell tumor of the pancreas. 17 23

A 60-year-old man with a history of excessive ingestion of calcium carbonate presented with azotemia, hypercalcemia and hyperphosphatemia. His acid-base status was initially normal. Following the cessation of calcium carbonate treatment, the hypercalcemia and azotemia disappeared, and the patient was found to be in metabolic acidosis with blunted acid excretion and a urine pH of 6.1. Kidney biopsy showed focal tubular calcification; the tubular damage was apparently caused by hypercalcemia and had resulted in renal tubular acidosis. During the three months of observation since that time there has been a tendecy for spontaneous remission of the renal tubular acidosis. Impaired renal hydrogen ion excretion prevented the development of metabolic alkalosis despite ingestion of alkali initially, and was later responsible for the metabolic acidosis. Renal tubular acidosis occurring as a sequel to the milk-alkali syndrome may aggravate the danger of nephrocalcinosis in this syndrome.
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PMID:Renal tubular acidosis due to the milk-alkali syndrome. 88 14

Rats fed abnormally composed isocaloric diets during 21 days (low magnesium, atherogenous, high in proteins or carbohydrates) develop a mean increase in total number of pancreatic A cells, a significant increase of A/B ratio (atherogenous), and hyperglucagonemia in most of the groups under study. Histologic examination reveals calcification most marked in animals under low magnesium and atherogenous diets. They are only scarce following high protein diet; a normal or carbohydrate rich diet nullifies this phenomenon. Independent of the morphologic and functional state of the islets, supplementation by argining and histidine of normal chow is followed by a certain degree of renal calcification. Lowered urinary magnesium and calcium and elevated urinary sodium and phosphate together with a tendency toward hypercalcemia point to stimulation of parathyroids during malnutrition. Absolute or relative hyperglucagonemia must be considered the main causstive factor.
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PMID:[Pancreatic islets, plasma glucagon and renal calcification in rats fed various diets. Results of a pilot study (author's transl)]. 110 41

We describe an adult patient who developed persistent hypercalcemia while bedridden for more than three months with pancreatitis and sepsis. On the basis of hypercalciuria, suppressed serum intact PTH, suppressed serum 1,25-dihydroxy vitamin D3 and no clinical evidence of malignancy, the diagnosis of immobilization hypercalcemia was established His hypercalcemia improved during treatment with saline, calcitonin and/or etidronate. With active mobilization and weight-bearing exercises, serum calcium finally normalized. We discuss clinical and laboratory features as well as current modalities of treatment of this rare form of hypercalcemia in adults.
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PMID:Immobilization hypercalcemia in an adult patient with pancreatitis and sepsis: case report. 148 89

Severe cardiac arrhythmias (Lown class IVa), rapid loss of physical capacity and dyspnoea on the slightest exertion occurred in a 55-year-old man with idiopathic dilated cardiomyopathy. In the preceding year he had recurrent diarrhoea and lost 23 kg in weight. He was found to have hypercalcaemia (3-3.2 mmol/l). The heart failure significantly improved under treatment with twice daily 12.5 mg captopril, 100 mg spironolactone daily, furosemide 40 mg twice daily, and digitoxin 0.07 mg daily. The arrhythmia responded to verapamil 80 mg and quinidine 160 mg, both drugs three times daily. Primary hyperparathyroidism was found to be the cause of the hypercalcaemia (parathormone 84 pmol/l). After the parathyroid adenoma had been removed the patient's condition again improved markedly. There were only rare monotopic extrasystoles, cardiac size regressed, and diuretics were no longer necessary. His medication at present is verapamil (80 mg three times daily), captopril (12.5 mg three times daily) and digitoxin (0.07 mg daily). It is concluded that the hypercalcaemia influenced the severity of the cardiomyopathy. It would seem that both intra- and extracellular calcium homoeostasis is of great importance in dilated cardiomyopathy.
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PMID:[The coincidence of rapidly progressing dilated cardiomyopathy and primary hyperparathyroidism. The course before and after the removal of a parathyroid adenoma]. 173 86

A 35-year old man presented with a 4-year history of impotence. His past history was significant for hypercalcaemia, bilateral pyelolithotomies for renal calculi and parathyroidectomy for hyperparathyroidism. He had an episode of haemetemesis and malaena a year before being seen here. Endocrine investigations revealed hyperprolactinemia, hypergastrinemia and increased basal acid output. Magnetic resonance imaging of the brain was indicative of a pituitary microadenoma. Computed tomographic scan of the abdomen revealed a bulky pancreas which was suggestive of a gastrin-secreting islet cell tumour. This case illustrates an unusual presentation of multiple endocrine neoplasia type 1 (MEN-1) with impotence and hyperprolactinemia. A short review of the literature was done.
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PMID:Multiple endocrine neoplasia type 1--presenting with impotence. 197 61

Severe hypercalcemia is a medical emergency requiring urgent treatment. It most commonly is caused by malignant tumors, as in the case study, but can also be caused by advanced hyperparathyroidism or high serum levels of vitamin D. The patient described in the case study shows clinical evidence of volume contraction due to hypercalcemia-related anorexia and vomiting. His elevated serum concentrations of urea nitrogen and creatinine reflect intravascular volume depletion and hypercalcemia-induced reduction of renal perfusion. He is also likely to have irreversible renal damage as a result of nephrocalcinosis. His central nervous system depression is most likely a result of hypercalcemia, but other central nervous system disorders such as cerebral metastases should be considered. Appropriate treatment would include intravenous fluids to correct volume depletion, dilute extracellular fluid calcium, and promote renal calcium excretion. Before waiting for the effects of volume expansion, the first dose of an inhibitor of bone resorption should be given. The agent of choice now (this may change when second-generation bisphosphonates become available) is plicamycin. Etidronate is a reasonable second choice. Because both drugs require at least 48 hours before their hypocalcemic action is manifest, calcitonin could be used to accelerate the rate of decline of the serum calcium. As the patient becomes more alert, weight-bearing and ambulation should be encouraged. With this combination of therapeutic modalities, this patient's serum calcium level should be corrected within 3 to 5 days. Intermittent injections of mithramycin or etidronate could be given on an outpatient basis approximately once a week in order to maintain the serum calcium within the normal range. One of the most important aspects of treatment in hypercalcemic patients is eradication of the underlying disease, which usually calls for specific antitumor therapy, including chemotherapy, radiation therapy, or surgery. Most of the agents currently available for the correction of hypercalcemia have cumulative toxicities or are only transiently effective and, therefore, their use should be considered a temporizing measure until specific treatment directed at the primary disease takes effect.
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PMID:Management of severe hypercalcemia. 200 13

Congenital laryngeal atresia is a rare cause of upper airway obstruction that leads to death unless a surgical airway is immediately established. We were able to resuscitate a baby boy with laryngeal atresia by the placement of an 18-gauge plastic intravenous cannula into the trachea, connected in turn to a 3-mL syringe without the plunger, and then to the connector to a 7.0-mm endotracheal tube. This arrangement allowed hand ventilation and sufficient gas exchange until a formal tracheotomy was established minutes later. The baby boy had deficient abdominal musculature (without cryptorchidism or obstructive uropathy), bilateral inguinal hernias, and idiopathic hypercalcemia (since spontaneously resolved), but no other major anomalies. His survival allowed measurements of pulmonary function in lungs distal to an obstructed upper airway, an arrangement that mimics experiments that examine the influence of lung fluid volume and pressure on developing lungs. The baby's lungs had a forced vital capacity (FVC) in the upper limits of normal (not grossly enlarged lungs seen in newborn animals undergoing ligation of the trachea in utero). Maximal expiratory flow at 25% of FVC from residual volume (MEF25) was decreased, indicating airway obstruction involving smaller airways. Although direct laryngoscopy failed to find a opening in the larynx, some communication probably existed during development to allow some drainage of lung fluid. This opening, in the form of a persistent pharyngoglottic duct, prevented gross distention of the developing lung, but provided an insufficient airway at birth.
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PMID:Pulmonary function studies in a newborn with congenital laryngeal atresia. 202 87

Kidney involvement by Non-Hodgkin's lymphoma is very common microscopically but rarely a cause of uraemia even when the parenchymatous involvement is considerable. Renal failure in cases of lymphoma is secondary to ureteral obstruction, hypercalcaemia, urate nephropathy, gammopathy or immunologically mediated nephrosis. This is a case where the patient presented to the ophthalmic O.P.D. with blurring of vision and admitted with full blown uraemia. He could not be saved and at autopsy, a gastrointestinal lymphoma was found in the caecum. His uraemia was due to massive parenchymatous involvement of the kidney, there being no ureteral obstruction, hypercalcaemia, urate or immunologically mediated nephropathy. Very few cases are reported in literature with such a presentation.
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PMID:Uraemia--a rare presentation of non-Hodgkin's lymphoma. 209 May 77

Discussed is the case of a 50-year-old man with a well advanced esophageal carcinoma who, during his final clinical course, suddenly developed hypercalcemia (max: 15.0 mg/ml). His serum parathyroid hormone level, however, remained within normal limits. On autopsy, an extensive metastasis to many organs and lymph nodes was noted but no evidence of a bone metastasis. Nude mice bearing the same tumoral tissue were found, on autopsy, to have similarly developed hypercalcemia and cells that were cultured were found to produce an excessive amount of Prostaglandin E2 (PGE2). These findings suggest that this humoral hypercalcemia of malignancy (HHM) was caused by excessive PGE2 produced by the tumor cells, although other possible factors should be investigated.
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PMID:[Esophageal carcinoma with hypercalcemia that appeared to be caused by prostaglandin E2 produced by the tumor cells]. 225 Mar 67


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