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)

We investigated the possible involvement of parathyroid hormone-related protein (PTHrP) in 2 cases of metastatic pancreatic neuro-endocrine tumors associated with severe hypercalcemia. Both patients displayed biochemical alterations in renal tubular reabsorption of calcium and phosphate, as well as in urinary cAMP excretion, similar to those encountered in primary hyperparathyroidism, although plasma levels of parathyroid hormone were within the normal range. Tumor protein extracts stimulated cAMP production, which was inhibited by the PTH-antagonist (8,18 Nle, 34 Tyr)bPTH-(3-34)amide, in the PTH-responsive osteoblastic cell line UMR-106. Northern blot analysis of tumor extracts revealed the presence of PTHrP mRNA transcripts, while PTH mRNA was undetectable. In contrast, neither PTHrP mRNA(s) nor cAMP-stimulating activity was detectable in other neuroendocrine tumors not accompanied by hypercalcemia. These results demonstrate that certain pancreatic neuroendocrine tumors associated with hypercalcemia can synthesize and release PTHrP.
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PMID:Parathyroid hormone-related protein and hypercalcemia in pancreatic neuro-endocrine tumors. 239 7

1. The serum concentrations of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were measured in 44 patients with primary hyperparathyroidism. 2. In 14 patients the serum concentration of 1,25-dihydroxyvitamin D was greater than normal (142-337 pmol/l). One patient had a subnormal concentration of 1,25-dihydroxyvitamin D (36 pmol/l) but no other evidence of vitamin D deficiency. 3. The possible biological determinants of the serum concentration of 1,25-dihydroxyvitamin D were sought by multivariate analysis of relevant variables. The serum concentration of 1,25-dihydroxyvitamin D was found to be significantly and positively correlated with the serum concentrations of 25-hydroxyvitamin D (P less than 0.001) and parathyroid hormone (P less than 0.003), and with the glomerular filtration rate (P less than 0.03), and negatively correlated with the serum concentrations of calcium (P less than 0.02) and phosphate (P = 0.055) (multiple R = 0.638, P less than 0.002). 4. In primary hyperparathyroidism the major determinant of serum 1,25-dihydroxyvitamin D is the availability of precursor 25-hydroxyvitamin D. 5. The finding that serum 1,25-dihydroxyvitamin D is commonly normal in patients with primary hyperparathyroidism despite an adequate state of vitamin D nutrition, can be explained in terms of the constraining influences of hypercalcaemia and variable degrees of renal dysfunction on the biosynthesis of 1,25-dihydroxyvitamin D.
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PMID:Determinants of the serum concentration of 1,25-dihydroxyvitamin D in primary hyperparathyroidism. 253 4

Certain patients with malignant hypercalcemia display enhanced bone resorption and changes in renal tubular handling of calcium and phosphate similar to those encountered in primary hyperparathyroidism. A tumoral protein probably responsible for this syndrome has recently been described. Produced by a gene other than that of parathyroid hormone, it shows an aminoterminal homology with the physiological hormone. In some respect both proteins exert similar effects. This parathyroid hormone-analogue may also be involved in physiological regulatory functions.
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PMID:[PTH-like tumor peptide and malignant hypercalcemia]. 255 73

Parathyroid hormone radioimmunoassay (RIA), specific for mid-region of the PTH molecule, has been proven to be extremely useful for the differential diagnosis of abnormal calcium metabolism. Recently, we developed a highly sensitive RIA for PTH, consisting of PTH antiserum (CH9), 125I labelled Tyr42 hPTH (43-68) and synthetic hPTH (1-84) as standard. This RIA cross-reacted with mid-region and carboxyl terminals of PTH. The within-assay and between-assay coefficients of variation were less than 4.6% and less than 8.6%, respectively. The limit of detection was 50pg/ml. The levels of serum calcium, serum phosphate, serum creatinine, Tmpo4/GFR and creatinine clearance (Ccr) in normal healthy volunteers aged 20 to 50 years remained almost constant and showed 9.24 +/- 0.34mg/dl (mean +/- SD, n = 242), 3.34 +/- 0.38mg/dl (n = 242), 0.870 +/- 0.121mg/dl (n = 242), 3.20 +/- 0.54mg/dl GF (n = 189) and 103 +/- 17ml/min (n = 137), respectively. All healthy volunteers (n = 326) had measurements of PTH in the blood. From 20 to 50 years, normal PTH mean was 374 +/- 97pg/ml (+/- SD, n = 237) and ranged from 180-568pg/ml, and from 60 to 80 years it was 471 +/- 133pg/ml (n = 34) and ranged from 205-737pg/ml. Since we found that PTH was markedly elevated above normal when Ccr was below 40ml/min, and PTH was very significantly correlated with the reciprocal of Ccr (r = 0.8996, P less than 0.001) using a multivariate analysis, all of the patients whose Ccr was higher than 40ml/min were selected and examined in the following studies. Serum PTH values completely separated patients with surgically proven primary hyperparathyroidism (1 degree HPT) from malignant associated hypercalcemia (MAH), and patients with idiopathic hypoparathyroidism (IHP) from pseudohypoparathyroidism (PHP), both of which were diagnosed by Ellsworth-Howard test. PTH values in all of the patients with 1 degree HPT (n = 23) were above normal, but those with MAH (n = 6) were below the normal or lower normal range. PTH values in patients with PHP (n = 7) showed above normal, while those with IHP (n = 5) were below the normal range. PTH was normalized in post operative status in all patients after parathyroidectomy (n = 6). These results indicate that this PTH RIA is extremely useful for the differential diagnosis in diseases with calcium abnormalities.
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PMID:[Clinical studies using a highly sensitive radioimmunoassay for mid-region and carboxy terminus of parathyroid hormone in normal, hypo- and hypercalcemic states]. 255 7

A protein responsible for the biochemical syndrome similar to primary hyperparathyroidism associated with certain tumors has been recently characterized and its effects at the level of bone and kidney reported. However, the relative role of tubular reabsorption of calcium (Ca) and bone resorption in the pathogenesis of hypercalcemia induced by this factor is still debated. We investigated the effects of a synthetic amino-terminal fragment of parathyroid hormone-related protein [PTHrP-(1-34)] administered chronically by intraperitoneal osmotic minipumps in thyroparathyroidectomized (TPTX) rats. Clearance studies performed on day 6 of treatment after a 24 h fast revealed an increase in renal tubular reabsorption of Ca and a decrease in renal tubular reabsorption of phosphate (Pi), accompanied by an increase in cAMP excretion. PTHrP-(1-34) (90 pmol/h) stimulated bone resorption as evaluated by an increment in fasting urinary Ca excretion. Although the bone resorption inhibitor aminopropylidene diphosphonate fully corrected urinary Ca excretion and reduced plasma Ca from 3.04 +/- 0.07 to 2.44 +/- 0.21 mM (p less than 0.05), this latter value remained considerably higher than in TPTX control rats (1.54 +/- 0.12 mM, p less than 0.01). In contrast, when the agent WR-2721, which is known to decrease the renal tubular reabsorption of Ca by a PTH-independent mechanism, was given, a further drop in plasma Ca and an increase in urinary Ca excretion were observed. These findings are similar to those found in animals implanted with the hypercalcemic Leydig cell tumor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of bone and kidney in parathyroid hormone-related peptide-induced hypercalcemia in rats. 255 91

In order to obtain a useful screening index for primary hyperparathyroidism (PHPT), seven patients with PHPT and fifty-one patients with nonparathyroid hypercalcemia (NPHC) were studied retrospectively. Serum calcium, inorganic phosphate (IP), alkaline phosphatase, albumin (Alb), chloride (Cl), total protein, urea nitrogen and creatinine (Cre) were analyzed at the same time. Discriminant analysis using a stepwise variable select method was applied to these patients. A discriminant function (F 1) was derived from three laboratory tests; F 1 = -0.660 x [IP] + 0.142 x [Cl] + 0.564 x [Alb] - 14.4 (PHPT: F 1 greater than 0.641). F 1 had sensitivity of 100% and specificity of 72.5% (14 false positives) in diagnosing PHPT. Next, another discriminant function (F 2) was derived from PHPT and the false positive patients; F 2 = -2.61 x [IP] + 0.286 x [Cl] - 4.24 x [Cre] - 19.3 (PHPT: F 2 greater than 0.412). When F 2 was applied to positive patients by F 1, final sensitivity was 100% and specificity was 98%. This screening method was tested prospectively in fifty-six consecutive samples of hypercalcemia (PHPT 4, NPHC 52), resulting in sensitivity of 100% and specificity of 98%. It was proved that our screening method using two step discriminant functions was very useful to diagnose PHPT.
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PMID:[A screening index for primary hyperparathyroidism using discriminant functions]. 260 57

A 67-year-old woman was admitted to our department because of 5 years' duration of proximal muscle weakness. Serum CK was high, and EMG showed myogenic pattern, and muscle biopsy revealed remarkable inflammatory cells infiltrating around the destroyed muscle fibers. Her muscle weakness and hyperCKemia markedly improved by corticosteroid therapy, suggesting that the diagnosis was compatible with polymyositis (PM). In addition, serum calcium was high and phosphate was low. Serum parathormone level significantly elevated. The findings of diagnostic imaging procedures including echography, scintigraphy, and computed tomography of the parathyroid glands suggested presence of parathyroid adenoma with cystic degeneration in the thyroid tissue. There was only one case report of PM associated with primary hyperparathyroidism (PHP) as the literature referred. In this case, we could not prove direct relationship between PM and PHP. The association might have been coincidental. However, PHP might have played some role in the pathogenesis of muscular involvement, or there might be a similar immunological mechanism as seen between PM and malignancy. It is possible that association of PM and PHP is more frequent than generally considered. It may be necessary to pay more attention to find out the association of PM and PHP.
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PMID:[A case with polymyositis associated with primary hyperparathyroidism]. 261 6

A 12-year-old girl was admitted to our hospital with signs of an acute abdomen with paralytic ileus. The previous and family history were without abnormalities. Abdominal pain and vomiting had started two days earlier. On palpation the swollen abdomen was painful and there was an increased tension in the left upper part. The clinical diagnosis of acute pancreatitis was confirmed by an increased serum level of lipase (4480 U/l). Clinical chemical investigations further revealed a permanent hypercalcemia in the range of 6.4 to 8.3 mval/l. This, together with concomitantly reduced levels of serum phosphate and a threefold increased level of parathyroid hormone (343 pg/ml, upper limit of reference = 100 pg/ml) were consistent with a hyperparathyroidism. In fact, sonography of the cervical organs revealed a solitary adenoma of the parathyroid glands. After surgery serum levels of calcium returned to normal. Hypercalcemia as a consequence of primary hyperparathyroidism has to be included in the differential diagnosis of acute pancreatitis in childhood.
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PMID:[Acute pancreatitis as an initial manifestation of hypercalcemia in primary hyperparathyroidism in childhood]. 265 77

In a chance observation, a 74-year-old woman was found to have hypercalcaemia (3.0 mmol/l) and multiple skeletal osteolyses. A diagnosis of multiple myeloma was made after the demonstration of paraproteins in serum (IgG-kappa) and a 10% proportion of plasma cells in a pelvic crest biopsy. Oral chemotherapy with melphalan and prednisone failed to alter the calcium level. Simultaneous increase in alkaline phosphatase and reduction in serum phosphate concentration led to further tests: determination of peripheral venous parathormone concentration, ultrasound examination of the neck, thallium-technetium subtraction scintigraphy and selective venous parathormone measurements. The results demonstrated the coexistence of primary hyperparathyroidism. The calcium level became normal after surgical removal of a parathyroid adenoma.
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PMID:[Hypercalcemia in coexistent parathyroid adenoma and multiple myeloma. Problems of differential diagnosis]. 266 81

In normal individuals, 1,25-dihydroxyvitamin D (1,25-D) levels regulate calcium (Ca) absorption according to Ca intake; its synthesis is stimulated by low Ca intake, probably via increased parathyroid hormone (PTH) secretion, to increase Ca absorption, and suppressed during high intake to reduce Ca absorption. The body also adapts Ca absorption in response to renal Ca excretion, and phosphate absorption in response to phosphate intake. These adaptations may fail or be impaired in certain diseases. In disorders of overadaptation, the intestinal tract absorbs excessive amounts of Ca due to overproduction of 1,25-D, as in absorptive hypercalciuria, sarcoidosis, primary hyperparathyroidism, and tumoral calcinosis. Intestinal hyperabsorption and hypercalciuria may occur on both low- and high-Ca diets. Primary hyperparathyroidism and hypoparathyroidism are bihormonal, related to over- and underproduction, respectively, of both 1,25-D and PTH. Underadaptation disorders are typically related to low 1,25-D synthesis or resistance to this metabolite; examples include postmenopausal osteoporosis, chronic renal failure, and osteomalacia. Many of these adaptational disorders can be relieved or improved by manipulating Ca, phosphate, sodium, or protein intake or by administering exogenous 1,25-D. Overabsorption of Ca and other substances, such as oxalate, may be responsible for Ca nephrolithiasis. Hypocitraturia (which may be a complication of certain diseases or the result of unbalanced diet or excessive exercise), diets high in readily metabolizable sugars and purine-rich proteins (meat, poultry, and fish), and low fluid intake can all contribute to stone formation. Various regimens may reduce the risk of Ca nephrolithiasis.
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PMID:Calcium metabolism. 268 27


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