Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of hypercalcemia in patients with known cancers may be due to the cancers themselves, or to co-existing primary hyperparathyroidism. The differentiation of primary hyperparathyroidism from the hypercalcemia of malignancy is important since the relief of distressing symptoms and prevention of hypercalcemic crises and renal failure can be accomplished relatively easily by parathyroid surgery in the former condition, and only with difficulty, at times, with fluids and drugs in the latter condition. The histories of three recent patients are presented, which demonstrate the difficulties inherent in the differentiation of these conditions. These patients were ultimately found at operation to have primary hyperparathyroidism in addition to malignancies of the cervix, adrenal gland and kidney. In our experience the following have been helpful in establishing a diagnosis; history of hypercalcemia prior to development of cancer, the type of cancer itself, the effect of cancer therapy on the hypercalcemia, and selective venous sampling with radioimmunoassay for parathyroid hormone.
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PMID:The differentiation of primary hyperparathyroidism from the hypercalcemia of malignancy. 111 56

Primary hyperparathyroidism and malignancy are responsible for the majority of reported cases of hypercalcemia. Suspected hypercalcemia should be documented on more than one occasion, preferably with the measurement of ionized calcium. Determination of intact parathyroid hormone with a modern two-site immunoassay is the single most important laboratory analysis in the differential diagnosis of hypercalcemia. Intact parathyroid hormone is increased or inappropriately high in primary hyperparathyroidism and suppressed or low normal in hypercalcemia of malignancy. Midregion and carboxylterminal radioimmunoassays are less effective in separating parathyroid and nonparathyroid hypercalcemia. In malignancy, hypercalcemia may result from local osteolysis or humoral factors. Although ectopic parathyroid hormone is produced rarely and certain lymphomas secrete 1,25-dihydroxyvitamin D, parathyroid hormone-related protein is elevated in the majority of patients with humoral hypercalcemia of malignancy. Recent developments in the measurement of parathyroid hormone-related protein should help to define the physiologic function of parathyroid hormone-related protein and its role in the differential diagnosis and therapy of hypercalcemia.
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PMID:Hypercalcemia and parathyroid disorders. 159 19

The two most frequent causes for hypercalcemia are primary hyperparathyroidism and hypercalcemia associated with malignancy. Elevated or inappropriately high PTH serum levels are the hallmark of hyperparathyroidism. Sensitive immunometric assays for the secreted, biologically active, intact parathyroid hormone molecule, PTH-(1-84), employ two populations of region-specific antibodies, take advantage of saturation kinetics rather than competitive binding, and have many technical advantages over conventional radioimmunoassay. Approximately 90% of patients with primary hyperparathyroidism have elevated serum levels of PTH-(1-84) by immunometric assay; the remainder have inappropriately elevated values of PTH for the serum calcium concentration. Clinical correlation studies comparing measurements of PTH using antisera that recognize the carboxyl, midregion, or amino terminus of PTH with PTH levels determined by immunometric assays demonstrate elevated values in equivalent numbers of hyperparathyroid individuals. Immunometric assays for PTH-(1-84) have their greatest value in separating patients with hyperparathyroidism from those with hypercalcemia of malignancy. In earlier studies using region-specific antisera, there was virtually always an overlap of serum PTH levels in hyperparathyroidism and hypercalcemia associated with malignancy. In contrast, analysis of results using PTH-(1-84) immunometric assays in several hundred reported patients shows a complete separation of PTH values. Clinical judgment, combined with measurement of PTH in the setting of hypercalcemia, can lead to the diagnosis of hyperparathyroidism with confidence in essentially all patients.
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PMID:Immunoassays for parathyroid hormone 1-84 in the diagnosis of hyperparathyroidism. 172 83

Parathyroid hormone-related protein (PTHrP) is a recently described hormone, that was isolated from malignant tumors. It shows many properties of parathyroid hormone (PTH) and is related to the pathogenesis of humoral hypercalcemia of malignancy. Therefore, we analyzed PTHrP in the sera of 30 patients with hypercalcemia of malignancy and compared the values with those obtained in patients with primary hyperparathyroidism, Paget's disease of bone, and normal subjects. PTHrP was quantitated with radioimmunoassay (RIA) using aminoterminal antibodies without and with chromatographical sample purification applying SEP-PAK C18 cartridges. Measurements of PTHrP without sample purification yielded high values in all patient groups. There was no differentiation between patient groups. However, quantitation of PTHrP after SEP-PAK C18 purification of the samples resulted in values above the normal range only in tumour patients. In 30 normal subjects PTHrP levels were 110 +/- 75 pg-eq/ml. Eight out of 30 patients with malignant tumours displayed PTHrP-concentrations above 335 pg-eq/ml. PTHrP levels in patients with primary hyperparathyroidism or Paget's disease of bone were within the normal range. PTHrP concentrations were not affected from renal function. We conclude, that determination of PTHrP after sample purification may contribute to the differential diagnosis of malignant disease.
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PMID:[PTH-related protein (PTHrP) in serum of patients with tumor hypercalcemia]. 205 82

Hypercalcemia is one of the most serious metabolic disorders associated with cancer. The incidence and clinical circumstances associated with hypercalcemia vary in different types of cancer. Hypercalcemia is the most frequent metabolic complication of breast cancer and is usually related to widespread osteolytic metastases; however, local and systemic humoral factors mediating bone resorption have been described. In some patients with breast cancer, hypercalcemia results from treatment with estrogens, antiestrogens, androgens, or progestins. Coexisting primary hyperparathyroidism rarely confounds the diagnosis. In patients with lung cancer, the incidence of hypercalcemia varies with histology and is often unrelated to bone metastases. Hypercalcemia may occur either late or early in the disease but is seldom a presenting symptom. In patients with cancers of the head and neck region, hypercalcemia is most often associated with advanced recurrent and terminal disease, presumably humorally mediated. In renal cell carcinoma, hypercalcemia is also an adverse prognostic indicator, commonly mediated by humoral factors. On the other hand, almost all patients with multiple myeloma have extensive osteolytic bone destruction and hypercalcemia is frequently a presenting symptom. Hypercalcemia is uncommon in most lymphomas; however, it is usually a prominent feature of adult T-cell lymphomas and also occurs in some large cell, diffuse B-cell lymphomas. Awareness of the setting in which hypercalcemia of malignancy occurs will lead to its prompt diagnosis and institution of appropriate therapy.
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PMID:Overview of cancer-related hypercalcemia: epidemiology and etiology. 218 51

We report results for adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood from 183 patients with disorders of calcium metabolism (primary hyperparathyroidism, secondary hyperparathyroidism of malabsorption, primary hypoparathyroidism, Paget's disease, acromegaly, hypercalcemia of malignancy, osteoporosis, sarcoidosis, idiopathic hypercalciuria, and familial hypocalciuric hypercalcemia). The correlation and the equation for the linear regression between adjusted ionized calcium (y) and actual ionized calcium (x) were y = 1.011x + 0.005 mmol/L, r = 0.992, Sy,x = 0.021 mmol/L. Results were similar within each diagnostic group. Consistent agreement between adjusted and ionized calcium was observed in 96.7% of patients representing a variety of the most frequently encountered disorders of calcium metabolism. Thus we find adjusted ionized calcium to be as useful as actual ionized calcium for evaluation of patients with such disorders. Adjusted ionized calcium may therefore also be a logical choice for establishing agreement between laboratories for reference intervals in healthy adults.
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PMID:Adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood compared for clinical evaluation of patients with disorders of calcium metabolism. 231 Dec 30

We have examined circulating concentrations of a parathyroid hormone-like peptide (PLP) in patients with malignancies and in patients with hyperparathyroidism. The radioimmunoassay employed reacts with synthetic amino-terminal fragments of PLP but not with parathyroid hormone. Elevated plasma PLP concentrations were observed in 50% of patients with malignancy and hypercalcemia and in 15% of normocalcemic cancer patients, mean values being higher in the former group. Detectable plasma PLP concentrations were found in 2 of 39 control subjects. In 2 patients with breast cancer plasma PLP declined concomitantly with a reduction in tumor burden. Adenocarcinoma of the breast and squamous cell carcinomas were most frequently associated with high plasma PLP levels although a variety of histologic types were represented. The presence of metastases on bone scans did not correlate with either the severity of hypercalcemia or the extent of PLP elevation. Increased concentrations of plasma PLP were also observed in 4 of 20 patients with primary hyperparathyroidism and in 5 of 16 patients with chronic renal failure and secondary hyperparathyroidism. Gel filtration analysis of immunoreactive PLP in plasma from 2 hypercalcemic breast cancer patients revealed heterogeneity, with, in each case, both large (greater than 15 kD) and small (6-7 kD) molecular weight amino-terminal moieties. The results document the presence of PLP in the circulation of patients with cancer and are consistent with a pathogenetic role for PLP in the hypercalcemia of malignancy irrespective of whether skeletal metastases have occurred. PLP may also contribute to the skeletal and/or renal manifestations of hyperparathyroid states.
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PMID:Circulating concentrations of parathyroid hormone-like peptide in malignancy and in hyperparathyroidism. 231 98

Serum bone GLA-protein, a modern and sensitive marker of bone turnover, was measured in 15 patients with primary hyperparathyroidism, 18 patients with hypercalcemia of malignancy, 41 patients with bone metastasis without hypercalcemia, and 29 healthy subjects. Serum bone GLA-protein was increased in primary hyperparathyroidism (17.6 +/- 3.9 ng/ml) and normal in hypercalcemia of malignancy (5.2 +/- 2.8 ng/ml; p less than 0.001 vs hyperparathyroidism) and in normocalcemic patients with bone metastases. In primary hyperparathyroidism parathyroid hormone correlated positively with urinary calcium excretion (p less than 0.05) and with urinary hydroxyproline excretion (p less than 0.001). The sensitivity of serum bone GLA-protein measurements in differentiating between primary hyperparathyroidism and hypercalcemia of malignancy was 91% and the specificity 84%. Thus this marker appears to be a useful tool for the differential diagnosis of hypercalcemias.
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PMID:Serum bone GLA-protein in hypercalcemia of primary hyperparathyroidism and malignancy. 232 Dec 72

TSH serum levels and thyroid function in 32 patients with primary hyperparathyroidism and hypercalcemia were compared to those of 30 age and sex-matched normal subjects. Serum T3 and T4 concentrations in hyperparathyroidism were not different from normal. However, basal serum TSH concentrations measured with an ultrasensitive immunoradiometric assay were significantly lower than normal (1.09 +/- 0.49 vs 2.06 +/- 0.85 mU/l, p less than 0.001). In hyperparathyroidism, TSH, but not T4 or T3, was negatively correlated with serum calcium, not with iPTH. The increase in TSH (delta TSH) 30 min after the iv injection of TRH was also significantly blunted in patients with primary hyperparathyroidism; delta TSH was highly correlated with basal TSH in hypercalcemic patients. The basal TSH concentration was higher and no longer different from normal (1.70 +/- 1.2 mU/l) 2 to 12 months after removal of the parathyroid adenoma, when serum calcium was normalized, whereas T3 and T4 did not change. A low basal TSH with normal T4 and low T3 was found in 13 patients with hypercalcemia of malignancy. In these patients, TSH increased after treatment of hypercalcemia with 3-amino-l,hydroxypropylidene-1, 1-bisphosphonate, whereas T4 did not change. The results suggest that the set point of pituitary thyroid feedback control could be decreased in chronic hypercalcemia and that hypercalcemia could render the thyroid more sensitive to TSH.
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PMID:Low basal thyrotropin with normal thyroid function in primary hyperparathyroidism. 251 13

This article covers considerations in the etiologies and therapy of hypercalcemia. The differential diagnosis of hypercalcemia is discussed, with particular emphasis on primary hyperparathyroidism and the hypercalcemia of malignancy. Clinical features of hypercalcemia are also discussed. Therapy of hypercalcemia is considered from the point of view of principles and general and specific measures, with emphasis on a pathophysiologic rationale for therapy.
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PMID:Etiologies and therapy of hypercalcemia. 266 80


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