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)

A prospective screen for hypercalcaemia in 58,053 hospital in-patients was conducted over 12 months. The incidence of hypercalcaemia was 0.6%, being transient in 19.2% of patients and sustained in the remainder. The most common causes in the sustained group were malignancy (45%) and primary hyperparathyroidism (16.5%). The incidence of primary hyperparathyroidism was 78/100,000 hospital in-patients, and its discovery was directly attributable to the survey in over half the cases.
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PMID:The incidence and causes of hypercalcaemia. 344 97

Serum bone gamma-carboxyglutamic acid-containing (Gla) protein (sBGP), a sensitive and specific marker of bone turnover, was measured in 25 patients with primary hyperparathyroidism and in 24 patients with bone metastases with or without hypercalcemia. Despite similar levels of hypercalcemia, sBGP was increased in primary hyperparathyroidism (14.2 +/- 9.6 ng/ml, P less than 0.001), was decreased in malignant hypercalcemia (3.1 +/- 2.8 ng/ml, P less than 0.001), and was normal in patients with bone metastases without hypercalcemia (6.6 +/- 2.7 ng/ml). In primary hyperparathyroidism, sBGP was correlated with serum immuno-reactive parathyroid hormone (r = 0.90), calcium (r = 0.73), and with the adenoma weight (r = 0.79). After parathyroidectomy, sBGP slowly returned to normal values within 2-6 mo, suggesting that sBGP reflects increased bone turnover rather than a direct effect of parathyroid hormone on BGP synthesis at the cell level. An iliac crest biopsy was performed in 11 patients with primary hyperparathyroidism and in 9 cancer patients in a noninvaded area. sBGP was significantly correlated with all parameters reflecting bone formation but not with bone resorption. Patients with bone metastases were analyzed according to the presence or the absence of hypercalcemia. In contrast to normocalcemic patients who had normal sBGP, hypercalcemic patients had decreased sBGP (P less than 0.001) and a lower bone formation at the cellular level (P less than 0.05). Thus, biochemical and histological data suggest that an unknown humoral factor might be responsible for this uncoupling between increased resorption and decreased formation. This uncoupling, rather than local release of calcium by the metastatic process, might be responsible for hypercalcemia in patients with bone metastases.
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PMID:Serum bone gamma carboxyglutamic acid-containing protein in primary hyperparathyroidism and in malignant hypercalcemia. Comparison with bone histomorphometry. 348 13

Osteocalcin (serum bone-Gla protein, sBGP), serum alkaline phosphatase (sAP) and urinary hydroxyproline/creatinine ratio (uOH-Prol/creatinine) have been measured in 21 patients with primary hyperparathyroidism (PHPT) and in nine patients with hypercalcaemia of malignancy (HM). A positive linear correlation between sBGP and uOH-Prol/creatinine ratio (y = 0.023 + 0.0025x; r = 0.705; p less than 0.01) and between sBGP and sAP (y = 35.6 + 2.14x; r = 0.430, p less than 0.05), have been observed in the PHPT patients. No correlation was found in the HM patients. PHPT patients have been grouped according to their uOH-Prol/creatinine ratio (group A: uOH-Prol/creatinine greater than 0.034; group B: uOH-Prol/creatinine less than or equal to 0.034). Group A presented sBGP higher than the control group (11.06 +/- 5.7 vs. 4.2 +/- 1.2 ng/ml; p less than 0.001) (mean +/- SD). Group B presented sBGP similar to the control group (4.4 +/- 1.96 ng/ml) (mean +/- SD). Group A presented serum calcium (sCa) higher than group B (3.11 +/- 0.28 vs. 2.78 +/- 0.09 mmol/l; p less than 0.01) (mean +/- SD). In HM patients uOH-Prol/creatinine ratio was elevated as compared with the control group (0.074 +/- 0.036 vs. 0.024 +/- 0.004; p less than 0.001) (mean +/- SD), but sBGP was normal or low (range: indetectable-5.1 ng/ml). The simultaneous estimations of sBGP and uOH-Prol/creatinine ratio improve the differential diagnosis between these two forms of hypercalcaemia: high uOH-Prol/creatinine ratio with concomitant high sBGP point to the presence of PHPT. Elevated uOH-Prol/creatinine ratio with normal or low sBGP suggest the existence of HM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Osteocalcin and urinary hydroxyproline/creatinine ratio in the differential diagnosis of primary hyperparathyroidism and hypercalcaemia of malignancy. 349 57

There are a variety of water and electrolyte disorders in patients with cancer. These disorders occur during the growth of tumors, generally as a consequence of inadequate intake and absorption of electrolytes, renal failure secondary to tumor or rapid tumor destruction and production of metabolically active substances by the tumor. In this paper, the electrolyte abnormalities associated with cancer were reviewed. Hyponatremia is one of the most common clinical electrolyte abnormalities in advanced cancer. Some patients may have hyponatremia, in spite of increased total body sodium and absence of a defect in water diuresis. This status is designated as "sick cell syndrome" or "essential hyponatremia". In addition, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in association with various tumors has been described. This syndrome is principally due to water retention, but can also be due to continuous urinary loss of sodium, and hypo-osmolality. Hypercalcemia is associated with coexistent primary hyperparathyroidism, prostaglandin (PGE2) or osteoclast-activating factor. It now seems likely that ectopic PTH is rarely the cause of hypercalcemia in nonparathyroid cancer. There are no data supporting the ectopic production of vitamin D-like substance as an important factor in the hypercalcemia of cancer. There are three general categories in which patients with hypercalcemia and cancer may be placed: those with bone metastases, those without bone metastases of solid tumors and those with hematologic malignancies. Hypokalemia is associated with ectopic ACTH- and insulin--producing tumors, and is often found in patients with mucin-secreting, potassium-losing adenocarcinoma of the colon.
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PMID:[Electrolyte abnormalities associated with cancer: a review]. 352 93

In this study, we compared serum parathyrin radioimmunoassay values obtained with three commercially available kits in a series of normal subjects, patients on dialysis, patients with primary hyperparathyroidism and with hypercalcemia due to malignancy. The calcium of these subjects was simultaneously evaluated. Two of these three kits measure two different C-terminal portions of the molecule and the third the mid region of PTH. The Behring and Byk kits were most efficient in that the results were obtained rapidly. The mid region assay is not more contributive than the C-terminal assays. Among these, the Behringer kit seems to produce the best diagnostic discrimination when the PTH and calcium are coupled. As far as the diagnostic specificity is considered, the latter kit seems however less efficient than the two others.
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PMID:[Comparative study of the diagnostic contribution of C-terminal and medio-regional determination of parathyroid hormone in man]. 355 Jun 22

A unique case of familial hyperparathyroidism associated with carcinoma of the colon is presented. Two brothers presented initially with colonic carcinoma and years later both were found to have primary hyperparathyroidism on the basis of parathyroid hyperplasia. This raises the issue of associated malignancies in patients with hyperparathyroidism, especially if they are found to be familial. One member of the family developed severe, recurrent hypercalcemia with bone disease, and thus the need for continued follow-up is emphasized.
Cancer 1987 Aug 01
PMID:Familial hyperparathyroidism in association with colonic carcinoma. 359 82

Thirty-five women with breast cancer and primary hyperparathyroidism (1 degree HPT) were admitted to Memorial Hospital during a 25-year period. The incidence of primary hyperparathyroidism in the breast cancer patients was similar to the incidence in the total patient population at Memorial Sloan-Kettering Cancer Center (0.15% and 0.14%, respectively). The patients with 1 degree HPT disease had clinical findings which distinguished them from those patients with cancer-related hypercalcemia. Eighty percent of the breast cancer patients with primary hyperparathyroidism had earlier stage disease (Stage 0, Stage 1, Stage 2); whereas 97% of the patients with breast cancer and hypercalcemia (not due to 1 degree HPT) had advanced disease. There appeared to be a trend towards improved survival in the breast cancer patients with primary hyperparathyroidism when compared to patients of similar stage of disease who did not have parathyroid disease.
Cancer 1987 Oct 01
PMID:Distinguishing features of primary hyperparathyroidism in patients with breast cancer. 362 Nov 32

A direct immunoassay for circulating intact human PTH (hPTH) is described. The method relies on the formation of an immune complex of labeled antiamino-terminal PTH antibody, intact hPTH, and solid phase antimidregion PTH antibody. A chemiluminescent aryl acridinium ester is used as label. Serum samples (100 microL) are incubated with labeled antibody, and subsequently the bound fraction is separated by the addition of solid phase antibody. The bound luminescence is quantitated in an automatic luminometer. Luminescence intensity is directly proportional to the amount of intact PTH present in the sample. Only intact PTH was found to react in this system; there was no significant interference from PTH fragments. The assay detection limit of 0.8 pmol/L hPTH-(1-84) allowed detection of intact PTH in the serum of all normal subjects tested. A clear distinction was found between hypercalcemic individuals subsequently proven to have primary hyperparathyroidism and those with malignancies. The assay offers several advantages over previously described PTH immunoassays with regard to specificity, rapidity, and reagent stability. It, thus, provides a valuable means of investigating parathyroid physiology and clinical disorders of extracellular calcium metabolism.
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PMID:Circulating intact parathyroid hormone measured by a two-site immunochemiluminometric assay. 362 8

Hypercalcaemia in squamous cancer of head and neck is not uncommon. Atypical symptoms make the diagnosis difficult. Immediate therapeutic intervention is necessary to prevent life-threatening complications. The causes include dietary calcium excess, vitamin-D-intoxication, bone metastasis and primary hyperparathyroidism. The paraneoplastic syndrome of ectopic hyperparathyroidism leading to the hypercalcaemia syndrome is induced by several different hormones. Ectopic production of parathyroid hormone or similar substances, increased synthesis of prostaglandins and vitamin-D-like steroids are proposed. Two typical cases are demonstrated.
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PMID:[Tumor-associated hypercalcemia syndrome in patients with squamous cell carcinomas of the head and neck. Differential diagnosis of a paraneoplastic syndrome]. 370 Jan 42

The relation between urinary sodium excretion (NaE) and renal tubular calcium reabsorption (TmCa/GFR) was assessed in patients with hypercalcaemia associated with malignancy and primary hyperparathyroidism. On acute saline loading of seven normally hydrated patients with primary hyperparathyroidism and five patients with malignancy, raised values of TmCa/GFR were reduced to normal in most cases, in association with increases in NaE. The reduction in TmCa/GFR, which occurred, may have been due to a reduction in proximal tubular calcium reabsorption associated with sodium: this would have obscured the effect of humorally mediated increases in distal tubular calcium reabsorption, which are stimulated either by parathyroid hormone or by a putative humoral mediator in hypercalcaemia of malignancy. In patients who were normally hydrated NaE and TmCa/GFR were not significantly correlated. When data were included from patients who were dehydrated and from those undergoing acute saline loading, significant inverse correlations between NaE and TmCa/GFR were observed both in primary hyperparathyroidism (r = -0.49; p less than 0.02) and malignancy (r = -0.60; p less than 0.001). In clinical practice changes in TmCa/GFR associated with sodium seem to be of minor importance under normal circumstances, but they become evident at the upper and lower extremes of urinary sodium excretion. In clinical studies of renal calcium handling urinary sodium excretion must also be assessed, as interpreting TmCa/GFR data is difficult in states of excessive sodium loading or depletion.
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PMID:Influence of urinary sodium excretion on the clinical assessment of renal tubular calcium reabsorption in hypercalcaemic man. 372 17


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