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

A retrospective study of 22 hypertensive patients who were treated with thiazide diuretics for 2 to 12 yr revealed that 36% developed transient, self-limited asymptomatic elevations of serum calcium which occurred at varying periods of therapy and returned to normal within 2 to 4 wk despite continued administration of thiazides. These episodes of hypercalcemia correlated positively with increases in total protein, albumin, and globulin. The same phenomenon of intermittent hypercalcemia occurred in a prospective study of 11 patients but not in control subjects. The mean serum total calcium of the prospectively studied hydrochlorothiazide-treated patients was found to be higher than the nonthiazide control group. This difference was due to increased protein-bound calcium. The total proteins, serum albumin, and serum beta globulins of the treated group were higher, probably due to depletion of extracellular fluid. The presence of slightly elevated serum calcium in a patient treated with thiazides appears to be a common phenomenon and, unless it is marked, should not necessarily be construed as indicating covert hyperparathyroidism.
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PMID:Effect of thiazides on serum calcium. 46 32

Hypercalcemia is most commonly seen in normal infants as the result of normal rapid bone growth. The most common causative diseases are malignant disease and hyperparathyroidism. A variety of pharmacologic agents, especially vitamin D and its metabolites and thiazide diuretics, can elevate serum calcium levels. Hypersensitivity to vitamin D appears to be a cause of hypercalcemia in infants and in patients with granulomatous disease, such as sarcoidosis. Ingestion of escessive amounts of calcium, especially with alkali, may also cause hypercalcemia, as may prolonged immobilization, particularly under conditions of rapid bone turnover.
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PMID:Causes of hypercalcemia. 48 79

When correction was made for hypoalbuminaemia, 23 of 50 ambulant patients with definite or classical rheumatoid arthritis were found to have hypercalcaemia. When these 23 patients were studied 6 months later, 7 had hypercalcaemia as defined by the correction factor for a low serum albumin level, and 6 of these patients had raised serum ionised calcium concentrations. Biochemical studies in the 23 patients indicated evidence of hyperparathyroidism, namely, hypophosphataemia, increased serum alkaline phosphatase, hyperchloraemia, and reduced tubular reabsorption of calcium. However, serum immunoreactive parathyroid hormone concentrations were normal. Only one patient had an abnormally low serum 25-hydroxy-vitamin D result: this patient had a high level of urinary D-glucaric acid and was receiving phenobarbitone for treatment of epilepsy. The biochemical features suggestive of parathyroid overactivity were particularly found in patients with raised serum calcium levels. The cause of hypercalcaemia in rheumatoid arthritis remains to be explained.
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PMID:Hypercalcaemia in rheumatoid arthritis: investigation of its causes and implications. 51 39

A case of hyperparathyroidism, who presented with unusual complex neurological symptomatology is reported. Mental confusion, asterixis and elevated cerebrospinal fluid protein with marked pleocytosis dominated the neurological picture. All these findings subsided upon correction of hypercalcemia, suggesting direct relationship between cerebrospinal fluid abnormalities, asterixis and this metabolic disturbance.
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PMID:Hyperparathyroidism presenting with unusual neurological features. 52 9

A leiomyoma of the small bowel produced laboratory features of hyperparathyroidism which disappeared promptly after tumour resection. Hypercalcaemia, hypophosphatemia, hyperchloremia, elevated chloride/phosphorus ratio, increased urinary cyclic AMP, and blood levels of immunoreactive parathormone were present. Electron microscopy showed dense round granules in the tumour cells.
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PMID:[Leiomyoma of the small bowel with hypercalcaemia: presence of a substance with parathormone activity (author's transl)]. 53 84

Twenty of ninety patients with hyperparathyroidism had associated pathology of the thyroid gland. Three carcinomas of the thyroid were found incidentally at the time of surgery for hyperparathyroidism. The association of thyroid lesions and hyperparathyroidism was frequently reported and explained previously on the basis of hypercalcemia acting as a goitrogen. Current evidence, however, suggests radiation as a strong probable factor in the production of this association. Attention should be given to the thyroid gland and of dominant nodules inspected. Concomitant management of those nodules according to the degree of suspicion they arouse, should be undertaken at the time of neck exploration for hyperparathyroidism.
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PMID:Thyroid lesions in patients with hyperparathyroidism. 53 65

A 66-year-old woman presented with hypercalcemia and a past history of external radiation to the neck. Hyperparathyroidism in this patient was caused by a parathyroid adenoma. The literature associating hyerparathyroidism with prior radiation of the head and neck was reviewed and analyzed. Current evidence supports a relationship between external radiation of the head or neck and the development of hyperparathyroidism as a late complication. Analysis of data available suggests that radiation-association hyperparathyroidsim develops after an average latent period of 38 years. Parathyroid adenoma occurred more often than did hyperplasia. Parathyroid carcinoma has not been reported in irradiated patients with hyperparathyroidsim. Neither age at radiation exposure, age at diagnosis of hyperparathyroidsim, nor interval between exposure and diagnosis was associated with a specific histologic diagnosis (adenoma or hyperplasis).
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PMID:Hyperparathyroidism after radiation of the head and neck: a case report and review of the literature. 53

Forty-six renal hypercalciuric normocalcaemic patients were treated with hydrochlorothiazide (50mg/day) and amiloride (5 mg/day), both to reduce new stone formation and to suppress parathyroid hyperfunction. A reduction of hypercalciuria and suppression of parathyroid hyperactivity were observed in 41 patients, while in the other five patients no evidence of parathyroid suppression was found and hypercalcaemia developed. Four of five patients underwent parathyroidectomy which was followed by a normalisation of biochemical signs of hyperparathyroidism. These results suggest that the appearance of hypercalcaemia in renal hypercalciuric patients during hydrochlorothiazide/amiloride treatment may be of diagnostic value in unmasking pharmacologically non-suppressible normocalcaemic hyperparathyroidism.
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PMID:Thiazide diuretics in renal hypercalciuria. 54 1

In order to investigate the frequency of fasting hypergastrinaemia in primary hyperparathyroidism (A) and in chronic hypercalcaemia (B), in 40 and 16 patients respectively gastrin, parathyroid hormone (PTH) and serum calcium levels were measured and compared with those of a control group (40 subjects) with similar distribution of sex and age. Moreover, possible linear relationships between these parameters were investigated. Notwithstanding significant differences in calcium and PTH levels between the three groups (A: high PTH, high Ca++; B: low PTH, high Ca++; C: normal PTH and Ca++ levels), no significant difference in gastrin levels were found. However, in the first group, a marked increase of gastrin was observed in one patient, very probably affected by a gastrin-secreting tumor (positive secretin test). While no linear relationship between PTH and gastrin values was present in all the three groups, a significant correlation between serum calcium and fasting gastrin was detectable in the group A, ruling-out the above mentioned patient. Present data suggest that PTH does not modify gastrin levels and that chronic moderate hypercalcaemia does not raise serum fasting gastrin, at least in clinical conditions. Moreover, the frequency of hypergastrinaemia in hyperparathyroidism is very low and it seems to be present only in patients with gastrin-secreting tumors.
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PMID:Fasting serum gastrin in primary hyperparathyroidism and in chronic hypercalcemia. 54 29

Reversible hypertension occurred in a patient during episodes of hypercalcemia caused by hyperparathyroidism, vitamin D toxicity, and an infusion of calcium during an 11-year period of observation. It is suggested that normal renal function may be required for the hypertension of hyperparathyroidism to be reversible and that the hypertension may be directly related to the hypercalcemia in some patients. Early surgery is suggested for otherwise asymptomatic, mildly hypercalcemia hyperparathyroidism that is accompanied by hypertension.
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PMID:Reversible hypertension. Caused by the hypercalcemia of hyperparathyroidism, vitamin D toxicity, and calcium infusion. 57 60


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