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

The clinical utility of the urinary cyclic AMP:creatinine ratio in assessing parathyroid function was evaluated in 33 hypercalcemic patients and compared this with the determination of the renal component of urinary cyclic AMP. We found the discriminatory value of urinary cyclic AMP:creatinine ratio to be slightly superior and to have additional advantages. Not only did the urinary cyclic AMP:creatinine ratio show empirically somewhat better discrimination between normals and patients with primary hyperparathyroidism, but it is technically simpler than the determination of the nephrogenous cyclic AMP. Our urinary cyclic AMP excretion data show 90% discrimination of primary hyperparathyroid subjects from normals. Among all hypercalcemic patients studied who had both elevated urinary cyclic AMP and elevated parathyroid hormone (PTH) levels by radioimmunoassay (RIA), 77% had primary hyperparathyroidism, and 23% had malignancy-associated hypercalcemia. Of those patients with malignant tumors and hypercalcemia, half had elevated urinary cyclic AMP and two thirds had elevated PTH by RIA. These data suggest that these tests have little discriminatory value in differentiating primary hyperparathyroidism from malignancy-associated hypercalcemia. No hypercalcemic patient who had both serum PTH and urine cyclic AMP in the normal range was found to have primary hyperparathyroidism. This suggests that further observation and evaluation is indicated in such patients before exploratory surgery is undertaken.
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PMID:Urinary cyclic AMP:creatinine ratio and nephrogenous cyclic AMP as indicators parathyroid functional status. 300 73

The effects of alternate and simultaneous administrations of calcium (Ca) and phosphorus (P) on Ca metabolism in children receiving total parenteral nutrition (TPN) were examined. Eight children, aged 2 to 36 months, were studied. The following three solutions were administered: solution 1 contains Ca (533 mg/liter); solution 2 contains P (413 mg/liter); and solution 3 contains Ca (267 mg/liter) and P (207 mg/liter). Solutions 1 and 2 were administered alternately for 24-hr periods. (Results) I. During administration of solution 1, significant hypophosphatemia (4.39 +/- 0.26 mg/dl) and hypercalcemia (9.96 +/- 0.15 mg/dl) were observed and, conversely, during administration of solution 2, significant hypocalcemia (8.36 +/- 0.18 mg/dl) and hyperphosphatemia (6.16 +/- 0.27 mg/dl) were observed. During administration of solution 3, the serum levels of both minerals were maintained within the normal ranges (Ca 9.46 +/- 0.12 mg/dl, P 5.65 +/- 0.21 mg/dl). II. The urinary excretion of cyclic AMP was significantly lower during administration of solution 1 (6.67 +/- 0.45 nmol/mg creatinine (Cr] as compared with solution 3 (7.50 +/- 0.61 nmol/mg of Cr). On the other hand, the excretion was significantly higher during administration of solution 2 (11.55 +/- 1.58 nmol/mg of Cr) as compared with solution 3, indicating the existence of secondary hyperparathyroidism. III. The Ca and P retention rates were significantly higher with solution 3 (Ca 79.0 +/- 5.5%, P 73.2 +/- 7.2% of the intake) than with solutions 1 and 2 alternately (Ca 62.7 +/- 4.5%, P 49.2 +/- 9.3%). (Conclusions) Simultaneous administrations of Ca and P are preferable to their alternate administrations for Ca metabolism in children receiving TPN.
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PMID:Effects of alternate and simultaneous administrations of calcium and phosphorus on calcium metabolism in children receiving total parenteral nutrition. 302 Feb 67

The diagnostic work-up of a patient with (familial) hypocalciuric hypercalcemia (FHH) is discussed. The patient showed no clinical signs of hypercalcemia. There were no indications of vitamin D intoxication. In the first degree family members no hypercalcemia was found. Physical examination was normal. In contrast to hyperparathyroidism, FHH is usually symptomless. Furthermore, FHH is characterized by a normal chloride/phosphate ratio, a normal, but relatively high, serum parathyroid hormone level, a relatively low urinary calcium excretion, a calcium-creatinine clearance ratio less than 0.01 and a normal cyclic AMP excretion.
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PMID:[Hypercalcemia in childhood. A boy with asymptomatic hypocalciuric hypercalcemia]. 302 63

In primary hyperparathyroidism, an operation is indicated when the calcemia exceeds 115 mg/l and phosphoremia is low in several successive instances, regardless of the symptoms, even if PTH levels and cervical ultrasonography are normal. In case of calcemia under 110 mg/l, the diagnosis must be confirmed by titration of the nephrogenic cyclic AMP and symptomatic patients must be operated upon as well as asymptomatic patients with a life expectancy exceeding 10 years. In case of acute hypercalcemia, the procedure must be performed as a semi-emergency without waiting for a definite diagnosis, since the course may rapidly be fatal in spite of all medical treatments. Ultrasonography mostly presents the advantage of detecting intrathyroid parathyroids glands. The experience of the surgeon is essential for the mandatory locating of 4 glands, and the choice of the surgical strategy. In front of a secondary indication for failure or recurrence, one must take into consideration what was seen and done during the first procedure, the calcemia levels and clinical, radiological or biological consequences. Finally, in case of cancer (2 p. cent), the best prognosis rests in wide excision of the thyroid compartment and nodes areas, since medical treatments and radiation therapy are ineffective.
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PMID:[Surgery of primary hyperparathyroidism in 1988. Strategies during primary operations, in case of failure and in case of cancer]. 305 11

Tumors causing humoral hypercalcemia of malignancy (HHM) were implanted to athymic nude rats. In one of these rat models transplanted with uterine cancer (UCC), a complete reproduction of human HHM syndrome was achieved: hypercalcemia, hypophosphatemia with increased urinary phosphate and cyclic AMP excretion, and suppressed serum 1,25-dihydroxy-vitamin D (1,25(OH)2D) level. In another hypercalcemic nude rat model implanted with oral cavity cancer (OCC), all the features were similar except for markedly elevated serum 1,25(OH)2D. Hypercalcemia disappeared by surgical removal of the tumors in both models, confirming the humoral mechanisms for causing these features. Furthermore, in UCC tumor-bearing rats, hypophosphatemia, increased renal phosphate excretion, and reduced serum 1,25(OH)2D concentration were already present when these rats were only marginally hypercalcemic. These results raise the possibility that the changes in renal tubular phosphate handling and vitamin D metabolism in HHM are not secondary to hypercalcemia but are due to direct effects of the humoral factor(s) that cause this syndrome. Extracts of both tumors exhibited stimulation of cyclic AMP production in osteoblastlike cells, UMR 106, which could be almost completely inhibited by parathyroid hormone (PTH) antagonist, human PTH(3-34). By comparing the nature and characteristics of humoral factor(s) from UCC and OCC models, mechanisms responsible for causing these abnormalities can be explored. Thus, these nude rat models can be useful for elucidating the underlying mechanism of the development of HHM.
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PMID:A hypercalcemic nude rat model that completely mimics human syndrome of humoral hypercalcemia of malignancy. 314 74

A 38-year-old woman with megakaryoblastic chronic myelocytic leukemia (CML) crisis developed recurrent episodes of severe hypercalcemia, manifested by nausea and vomiting and later by dyspnea and hypoxia. The levels of serum parathyroid hormone and serum and urine cyclic AMP were normal. Autopsy revealed widespread metastatic calcifications in various organs, including the lungs. The case suggests that hypercalcemia complicating blast crisis of CML is not related to blast cell phenotype, can cause severe pulmonary malfunction, and is a terminal event. The hypercalcemia most probably resulted from bone resorption, either directly by the megakaryoblasts or by secretion of osteolytic substances.
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PMID:Hypercalcemia complicating a megakaryoblastic crisis of chronic myelocytic leukemia. 316 88

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

A synthetic peptide corresponding to the first 34 amino acids of the parathyroid hormone-related protein (PTH-rP) produced by a human tumor associated with hypercalcemia was examined for skeletal and renal effects on calcium metabolism in vivo and in vitro. These effects were compared with those of human parathyroid hormone (1-34), hPTH (1-34). Equal doses of PTH-rP(1-34) and hPTH(1-34) produced equivalent stimulation of adenylate cyclase in vitro in bone cells and kidney cells and tubules. Subcutaneous injection of PTH-rP(1-34) in mice caused a significant dose-related increase in blood ionized calcium similar to that seen with hPTH(1-34) at equivalent doses. Repeated injections of equal doses of both peptides caused sustained hypercalcemia which was significantly greater in PTH-rP(1-34)-treated mice, although each induced comparable increases in histomorphometric indices of osteoclastic bone resorption. PTH-rP(1-34) and hPTH(1-34) also caused similar increases in bone resorption when incubated with fetal rat long bones in organ culture. Infusion of either peptide into thyroparathyroidectomized rats suppressed urinary calcium excretion and increased urinary excretion of cyclic AMP. PTH-rP appears to have similar effects to those of PTH on the skeleton, the kidney, and overall calcium homeostasis.
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PMID:Effects of a synthetic peptide of a parathyroid hormone-related protein on calcium homeostasis, renal tubular calcium reabsorption, and bone metabolism in vivo and in vitro in rodents. 334 49

Routine estimation of plasma calcium has made the finding of asymptomatic hypercalcaemia a frequent occurrence. A high index of suspicion for familial hypocalciuric hypercalcaemia (FHH) will lead to accurate diagnosis and avoidance of unnecessary parathyroid surgery. Four FHH kindreds with 16 hypercalcaemic members were found in an unselected referral population over 3 years. Differentiation from primary hyperparathyroidism (42 patients in the same period) was facilitated by analysis of fasting blood and urine for renal handling of calcium, phosphate and cyclic AMP. We found that a plot of serum PTH against fasting calcium excretion separated all cases of each disorder. The discriminatory power of these two variables was confirmed by multivariate discriminant function analysis. An elevated plasma chloride was found to be common to both diseases and of no value in differentiation.
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PMID:Fasting calcium excretion and parathyroid hormone together distinguish familial hypocalciuric hypercalcaemia from primary hyperparathyroidism. 345 Apr 51

The relation between circulating 1,25-dihydroxyvitamin D (1,25(OH)2D) levels and intestinal calcium absorption--as determined by an oral calcium load test--was studied in 16 patients with hypercalcaemia of malignancy (HM) and 16 with hypercalcaemic primary parathyroidism (HPT). In the HPT group serum calcium rose significantly after the oral calcium load and the increment correlated significantly with 1,25(OH)2D levels. While 1,25(OH)2D levels were raised to within the hyperparathyroid range in a number of HM patients, there was no correlation between change in serum calcium and 1,25(OH)2D level in the HM group and serum calcium did not rise significantly after the oral calcium load. HM patients with detectable or raised 1,25(OH)2D levels typically had few, or no, bone metastases in association with squamous lung cancers. A high proportion of these patients exhibited other aspects of hyperparathyroid-like activity such as increased renal tubular calcium reabsorption, depressed renal tubular phosphate reabsorption and elevated urinary cyclic AMP excretion. Conversely, HM patients with undetectable 1,25(OH)2D levels typically had extensive metastatic bone disease in association with breast carcinoma and were less likely to exhibit other hyperparathyroid-like features. It is postulated that in the former, the 'inappropriately' detectable or raised 1,25(OH)2D levels may have been due to enhanced renal 1 alpha-hydroxylase activity stimulated by the parathyroid hormone (PTH)-like effect of a non-PTH ectopic humoral mediator. In the latter the suppressed 1,25(OH)2D levels would be the predicted result of a non-humorally mediated hypercalcaemia. It is currently unclear why intestinal calcium absorption was depressed in all HM patients when 1,25(OH)2D levels were normal or raised in some cases. It is possible, however, that in HM there is 'end organ' resistance to the effects of 1,25(OH)2D due to a generalized malabsorptive process.
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PMID:Comparison of intestinal calcium absorption and circulating 1,25-dihydroxyvitamin D levels in malignancy-associated hypercalcaemia and primary hyperparathyroidism. 365 75


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