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)

Calcium, phosphate and alcaline phosphatase levels were determined in the serum of 29 patients with suspected primary hyperparathyroidism. Phosphate clearance according to Kyle, 24 hours urine hydroxyproline excretion during collagen free diet, the excretion of cAMP in the 24 h urine during calcium restricted diet were examined with regard to the diagnostic value and relevance as compared to the consumption of laboratory and staff time. The elevation of the serum calcium levels are not specific and only of minor diagnostic value. It has been found that the highest diagnostic value is given by the Kyle-test using 15 mg Ca ions/kg body weight. No false positive results were recorded. The excretion of hydroxyproline and calcium are only of limited value. Serum alcaline phosphatase and cAMP excretion have no diagnostic significance whereas concentration of serum phosphate may have some value.
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PMID:[Value and relevance of metabolic function tests in the diagnosis of primary hyperparathyroidism (author's transl)]. 17 61

Phosphate concentration was found to be significantly elevated in the saliva of uremic patients (dialyzed and non-dialyzed) when compared to normal subjects and to dialysis patients after parathyroidectomy. Salivary calcium concentrations were similar in all groups examined. As increased salivary phosphate was found also in primary hyperparathyroidism, we attribute our findings to the secondary hyperparathyroidism of the uremic state.
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PMID:Salivary phosphate and calcium concentrations in uremia. 50 92

A patient with primary hyperparathyroidism whose bone scan showed signs of extensive pulmonary and gastric calcifications is described. The patient also had renal insufficiency. A review of the literature and of data of 13 patients with primary hyperparathyroidism who were seen in the Department of Internal Medicine at the University Hospital of Maastricht, led to the conclusion that only in patients with renal insufficiency could ectopic calcifications be expected to occur. Phosphate retention, rather than the hyperphosphaturia that occurs in that particular situation, is cited as the cause.
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PMID:A patient with primary hyperparathyroidism and an abnormal bone scan. 302 69

Phosphate indices (serum phosphate, tubular reabsorption of phosphate, renal threshold phosphate concentration (TmP/GFR) and index of phosphate excretion) were studied in 88 hypercalcaemic subjects: 64 with primary hyperparathyroidism (HPT) and 24 with hypercalcaemia from other causes, predominantly malignant disease. HPT patients as a group could easily be separated from normal subjects (n = 16) and patients with functional hypoparathyroidism (n = 7) by use of the phosphate variables but these indices were of little discriminating value for the differential diagnosis between HPT and hypercalcaemia from other causes. There was no difference in the urinary cyclic adenosine monophosphate (cAMP) excretion between the two hypercalcaemic patient groups, but HPT patients had clearly elevated serum parathyroid hormone (PTH) levels compared with normal PTH concentrations in patients with other causes of hypercalcaemia. A positive correlation between cAMP and serum calcium and an inverse relationship between cAMP and TmP/GFR were found in patients with hypercalcaemic malignant disease. These findings suggest the existence of a humoral factor with PTH-like effects in malignant disease. Since PTH levels were low, the physiological actions were apparently not mediated by circulating PTH. No difference in the values for phosphate variables, PTH, cAMP or serum calcium was found between renal stone-forming and stone-free patients with HPT.
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PMID:Clinical studies on phosphate handling in hypercalcaemia. 629 62

Recent studies have emphasized the pathophysiological importance of circulating 1,25-dihydroxyvitamin D ((1,25-(OH)2D] in the pathogenesis of hypercalciuria and renal stone formation in primary hyperparathyroidism. Reasoning that phosphate administration might be capable of reducing the plasma concentration of 1,25-(OH)2D in patients with a prominent 1,25-(OH)2D-mediated absorptive component to their disease, 10 carefully selected patients were treated with oral phosphate (1500 mg elemental phosphorus daily) for 1 yr. Phosphate treatment significantly reduced circulating 1,25-(OH)2D levels (84 to 56 pg/ml), the calciuric response to an oral calcium tolerance test (0.30 to 0.21 delta mg calcium/dl GF), and calcium excretion on an unrestricted calcium diet (438-269 mg/day), in essence reversing the absorptive pattern of abnormalities observed before treatment. This response, however, was accompanied by an increase in biochemical hyperparathyroidism, as assessed by circulating immunoreactive PTH and nephrogenous cAMP excretion. In patients with biochemical evidence of an increase in bone resorption before therapy, histomorphometric, radiographic, and biochemical data revealed a trend toward a reduction in bone turnover during phosphorus therapy, with an apparent maintenance of coupled bone resorption and bone formation. This trend, however, was of marginal statistical significance in the patient group as a whole. It is concluded 1) that phosphate therapy represents a viable medical alternative in selected patients with primary hyperparathyroidism, 2) that the net response in treated patients is multifaceted and complex, and 3) that the efficacy of phosphate therapy will ultimately depend upon its long term effects on skeletal homeostasis.
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PMID:A detailed evaluation of oral phosphate therapy in selected patients with primary hyperparathyroidism. 630 Jan 78

Phosphate stones are divided in two groups: I. Infection stones = triple phosphate stones (struvite and carbonate apatite). II. Calcium phosphate stones = Hydroxy apatite. Ad I. For the formation of this stone, infection with urease-producing bacteria is essential. It is important to look for factors that cause infection and for metabolic abnormalities. Three possibilities for treatment are discussed: Acidifying the urine: orally with NH4NO3 or NH4Cl; dosage is possible up to 12 g a day (metabolic acidosis!). Irrigation for instance with Renacidin ; when using a nephrostomy-tube, one can start 5 days after the operation. It is important to look for fever and flank pain. Especially useful in cases with small residual stones. Reduction of phosphate excretion in urine ( Shorr -regimen). Some aluminium combinations reduce the intestinal phosphate absorption as a result of the formation of a nonabsorbable aluminium-phosphate combination. This can be combined with a low calcium- and phosphate diet. In several publications good results are shown. Also when using a less rigid regimen, satisfactory results are seen: decrease of the phosphate excretion from 30 to 17 mmol/24 h (own investigation). Urease-inhibitors result in a lower urine-pH and a decrease of the ammonium-concentration. there are only a few publications with results, but AHA seems able to reduce the stone size in 24% of the patients. Ad II. This stone is concerning formation and treatment much like the calcium oxalate stone. In case of an alkaline urine one must look for primary hyperparathyroidism and renal tubular acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Conservative therapy of phosphate calculi]. 653 26

A radioimmunoassay for human parathyrin has been developed and characterized with whole-molecule (residues 1-84) human parathyrin and with the 1-34, 44-68, and 53-84 amino acid residue fragments of it. The antiserum used reacted with the whole molecule and with the 44-68 and 53-84 fragments, but not with the 1-34 fragment. Parathyrin concentrations in the serum of 118 normal subjects and of 112 patients with surgically proved primary hyperparathyroidism were determined with this assay. The mean results were 39 (SD 13) microL-Eq/mL for the normals and 111 (SD 77) microL-Eq/mL for the patients with primary hyperparathyroidism (p less than 0.0005). The upper 95% confidence limit of the normal range was 60 microL-Eq/mL. For 54 patients with primary hyperparathyroidism, the preoperative values for serum parathyrin, calcium, and phosphate--but not creatinine--were statistically different from the postoperative values (paired t-test, p less than 0.0005). Normal subjects showed significant (p less than 0.0005) differences in serum calcium concentrations but not in parathyrin concentrations, compared with concentrations found in cancer patients and patients who had thiazide-induced hypercalcemia. Phosphate concentration in serum, although not a specific indicator of disease, is a valuable clue to the diagnosis of primary hyperparathyroidism.
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PMID:Development and validation of a new radioimmunoassay for parathyrin (PTH). 705 38

Fibroblast growth factor-23 (FGF-23) is a circulating factor regulating phosphate and vitamin D homeostasis. Phosphate intake and an administration of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) increase circulating FGF-23 levels, and elevated FGF-23 prevents hyperphosphatemia and vitamin D toxicity by hyperphosphaturia and suppression of circulating 1,25(OH)(2)D level, comprising a feedback loop to maintain phosphate and vitamin D homeostasis. Excess secretion of parathyroid hormone (PTH), another phosphaturic factor, elevates the serum calcium level in primary hyperparathyroidism. PTH also elevates circulating FGF-23 level, which cooperatively enhances the phosphaturia, resulting in hypophosphatemia. The circulating FGF-23 level increases as renal function declines in chronic kidney disease (CKD), and it exhibits significant and positive correlations with serum phosphate, calcium, and PTH in CKD patients on maintenance hemodialysis, suggesting that these parameters regulate circulating FGF-23 level. Tight associations between circulating FGF-23 and calcium levels were observed both in patients with primary hyperparathyroidism and in CKD patients on maintenance hemodialysis, suggesting the role of serum calcium on FGF-23 regulatory mechanisms. FGF-23 may have a physiological role in preventing tissue damage such as ectopic calcifications, partly via suppressing the serum calcium x phosphate product by accelerating urinary phosphate excretion and suppressing vitamin D activation.
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PMID:Regulatory mechanisms of circulating fibroblast growth factor 23 in parathyroid diseases. 1797 83

Hypophosphatemia is defined as a serum phosphate level of less than 2.5 mg/dL (0.8 mmol/L). Hypophosphatemia is caused by inadequate intake, decreased intestinal absorption, excessive urinary excretion, or a shift of phosphate from the extracellular to the intracellular compartments. Renal phosphate wasting can result from genetic or acquired renal disorders. Acquired renal phosphate wasting syndromes can result from vitamin D deficiency hyperparathyroidism, oncogenic osteomalecia, and Fanconi syndrome. Genetic disorders of renal hypophosphatemic disorders generally manifest in infancy and are usually transmitted as an X-linked hypophosphatemic rickets. Symptoms of hypophosphatemia are nonspecific and most patients are asymptomatic. Severe hypophosphatemia may cause skeletal muscle weakness, myocardial dysfunction, rhabdomyolysis, and altered mental status. The diagnostic approach to hypophosphatemia should begin with the measurement of fractional phosphate excretion; if greater than 15% in the presence of hypophosphatemia, the diagnosis of renal phosphate wasting is confirmed. Renal phosphate wasting can be divided into 3 types based upon serum calcium levels: primary hyperparathyroidism (high serum calcium level), secondary hyperparathyroidism (low serum calcium level), and primary renal phosphate wasting (normal serum calcium level). Phosphate supplementations are indicated in patients who are symptomatic or who have a renal tubular defect leading to chronic phosphate wasting. Oral phosphate supplements in combination with calcitriol are the mainstay of treatment. Parenteral phosphate supplementation is generally reserved for patient with life-threatening hypophosphatemia (serum phosphate < 2.0 mg/dL). Intravenous phosphate (0.16 mmol/kg) is administered at a rate of 1 mmol/h to 3 mmol/h until a level of 2 mg/dL is reached.
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PMID:Hypophosphatemia: an evidence-based problem-solving approach to clinical cases. 2062 6