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)

Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess. Charts of 100 inpatients with hypophosphatemia were reviewed and the patients divided into five groups on the basis of serum phosphate level: 18, 2.1 to 2.4 mg/dL; 49, 1.6 to 2.0 mg/dL; 20, 1.1 to 1.5 mg/dL; 12, 0.6 to 1.0 mg/dL; 1, 0.1 to 0.5 mg/dL. The effect of glucose ingestion on serum phosphate level was shown in one normal patient. Whenever carbohydrate was administered intravenously (45 cases), this was considered the primary cause of the hypophosphatemia. Other causes were as follows: diuretics, hyperalimentation, alcoholism, respiratory alkalosis, dialysis, insulin, corticosteroids, diabetic ketoacidosis, vomiting, phosphate-binding antacid, Gram-negative sepsis, primary hyperparathyroidism, saline, epinephrine, gastrointestinal malabsorption, and unknown. Hypophosphatemia in hospitalized patients may have multiple causes.
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PMID:Hypophosphatemia in hospitalized patients. 44 90

We have studied 83 patients with recurrent calcium stone formation in an attempt to determine an approximate incidence of metabolic disturbances associated with stone disease. Male veterans (n = 42), male non-veterans (n = 13), and women (n = 28) composed the group. We divided the groups in such fashion because they represented generally two distinct socioeconomic groups. Primary hyperparathyroidism was present in 19 per cent of the subjects; a marked predominance of women (15/16) was noted. Hypercalciuria of renal or intestinal origin was present in 23 per cent of the group. Of interest was a group of male veterans (17/83) in whom normocalciuria, normocalcemia, and normal serum phosphate were associated with high values of immunoreactive parathyroid hormone. These subjects had low urine phosphate. This set of findings indicates that these patients may be a new subgroup of stone-forming patients. Metabolic abnormalities could not be detected in 38 per cent of the patients. Classification of stone subjects is essential for rational management.
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PMID:Some characteristics of recurrent calcium stone formers in Puerto Rico. 45 11

1. In primary hyperparathyroidism an increased bone turnover is seen, accompanied by osteitis fibrosa (= fibroosteoclasia, FO) in severe forms of the disease. Both types of bone reaction may be detected by microradioscopy X-rays of the hand, extensive striation of metacarpal cortical bone indicating increased bone turnover and subperiosteal resorption of phalanges pointing to FO. 2. In the present study 65 patients with proven PHPT were evaluated before and 39 after operation. Microradioscopy was combined with biochemical assessment of hyperparathyroidism including alkaline serum phosphatase (aPh) as an index of osteoblastic activity, hydroxyprolin excretion (HyPro) reflecting bone turnover, immunoreactive parathyroid hormone levels (PTH), serum calcium (SCa), urinary calcium (UCa), serum inorganic phosphorus (SP) and clearance of phosphate (Cp). A comparison was made with the incidence of renal stone disease and the degrees of metacarpal striation (StG) and subperiosteal resorption (UG) were followed after operation. 3. Preoperative X-rays of 60% of the PHPT subjects showed increased StG and/or UG, and in 41,5% the diagnosis of PHPT was possible from the X-ray findings only. There existed a significant correlation between StG and UG on one hand and aPh, HyPro and PTH on the other. No correlation, either positive or negative, was seen between FO and the incidence of renal stones. After surgery, subperiosteal bone lesions disappeared in all patients, while intracortical striations persisted in half of the subjects despite the normalised bone turnover. Thus, primary hyperparathyroidism may not only lead to endosteal bone loss but to an irreversible intracortical bone deficit as well.
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PMID:[Primary hyperparathyroidism--bone turnover and osteitis fibrosa assessed by x-ray (author's transl)]. 45 67

Malignant disease and primary hyperparathyroidism are the most common causes of hypercalcemia, but there are many minor causes. Mechanical or humoral factors, or both, may underlie the increase in bone resorption. Parathyroid hormone (PTH) is a major mediator of bone resorption, but many other humoral agents have the same effect, eg, prostaglandin, osteoclast-activating factor, and thyroid hormone. Serial determination of total calcium concentration is the most important laboratory test in hypercalcemia. Other useful tests include the determination of serum and urinary phosphorus concentration, chloride/phosphate ratio, urinary cyclic adenosine 3',5'-monophosphate (cAMP) level; carboxyl-terminal PTH assay; corticosteroid challenge; and appropriate radiologic studies. Nephrogenous cAMP and urinary prostaglandin determinations are research tools that hold great promise in the future. Differentiation between PTH- and non-PTH-mediated hypercalcemia determines subsequent steps in diagnosis and treatment.
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PMID:Differential diagnosis of hypercalcemia: a mechanistic approach. 48 78

The serum levels of total calcium and anorganic phosphate have been the leading parameters in the diagnosis of primary hyperparathyroidism. In addition to these, it is now possible to measure ionized calcium (Ca++) by an ion-selective electrode and parathormone (PTH) by C- and N-terminal radioimmunoassays (RIA). Whereas Ca++ determination and C-terminal PTH RIA represent a diagnostic progress, this can not be claimed for the N-terminal PTH RIA in peripheral venous blood especially in border-line cases.
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PMID:[New diagnostic examinations in patients with urinary calculi, taking into consideration primary hyperparathyroidism]. 48 11

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

Serum chloride and phosphate concentrations were measured in 79 hypercalcemic patients. The chloride values were higher (mean 106.7 mEq/l) and phosphate lower (mean 2.08 mg/100 ml) in the 53 hyperparathyroid patients, where as the chloride concentrations were lower (mean 99.3 mEq/l) and phosphate higher (mean 4.07 mg/100 ml) in the 26 patients with hypercalcemia from other causes. The chloride phosphate ratio ranged from 19 to 32 in the subjects with hypercalcemia from other causes with 90 per cent of values less than 30. In patients with primary hyperparathyroidism we found 96 per cent of the values more than 34. From our experience with chloride phosphate ratio it seems to us that this ratio is a very useful and simple preliminary test for distinguishing patients with primary hyperparathyroidism from patients with hypercalcemia from other causes, with normal renal functions.
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PMID:The chloride phosphate ratio as the screening test for primary hyperparathyroidism. 52 Oct 12

Scintiscanning to detect the uptake of bone-seeking radioactive isotopes by soft tissue is a promising technique for the in vivo study of visceral calcification. Visceral uptake of such radioisotopes was studied in 40 patients: 22 undergoing long-term dialysis, 9 with malignant disease and hypercalcemia and 9 with primary hyperparathyroidism and hypercalcemia.Fifteen patients, 11 undergoing dialysis and 4 with malignant disease, had radioisotope uptake in the lungs, and 5, 3 undergoing dialysis and 2 with malignant disease, had uptake in the stomach. None of the patients with primary hyperparathyroidism had visceral uptake, nor did the patients with uptake have radiologic evidence of pulmonary or gastric calcification. The dialysis patients with visceral uptake had a mean calcium x phosphate product of 84.3 +/- 23.7 (standard deviation), which was significantly greater (P < 0.001) than that of patients without such uptake (59.2 +/- 14.0). Similarly, in patients with malignant disease and visceral uptake the Ca x P product was 72.2 +/- 6.4 - significantly greater (P < 0.005) than that of patients without such uptake (49.3 +/- 6.7).These findings indicate that scintiscanning for the visceral uptake of a bone-seeking radioisotope is a simple and effective technique for the in vivo study of visceral calcification. An elevation in the Ca x P product seems to be the single most important factor in the production of visceral calcification.
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PMID:Detection and pathogenesis of visceral calcification in dialysis patients and patients with malignant disease. 62 Mar 83

The influence of hypercalcemia on renal function was studied retrospectively in 13 patients suffering from primary hyperparathyroidism, sarcoidosis, vitamin D intoxication, malignant lymphoma or chronic lymphatic leucemia. Different kinds of treatment, depending upon the primary disease, often induced a rapid fall in the serum calcium concentration. The serum creatinine concentration always fell simultaneously. The serum phosphate concentration fell in all but two patients. Changes in serum calcium and serum creatinine correlated significantly (p less than 0.001), as did changes in serum calcium and serum phosphate concentrations (p less than 0.05). Serum calcium/serum creatinine and serum calcium/serum phosphate ratios were significantly higher in patients with primary hyperparathyroidism than in patients with hypercalcemia of non-hyperparathyroid origin (p less than 0.01, p less than 0.001). This suggests a different effect of calcium on the glomerular filtration rate in hyperparathyroid and non-hyperparathyroid patients, the latter group being more sensitive to the influence of hypercalcemia. Possible explanations for this difference, such as a protective effect of PTH on the glomerular filtration, are discussed.
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PMID:Reversible renal failure caused by hypercalcemia. A retrospective study. 64 44

Linear discriminant analysis, a multivariate statistical procedure, applied to serum calcium, phosphate, alkaline phosphatase, bicarbonate, chloride, creatinine and tubular reabsorption of phosphate, proved to be effective in distinguishing patients with Primary Hyperparathyroidism from other hypercalcaemic patients in eithy-four retrospective cases. The application of the model to thirty-four prospective cases enabled us to separate correctly, hyperparathyroid patients from non-parathyroid hypercalcaemic patients.
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PMID:Discriminant analysis in the differential diagnosis of hypercalcaemia. 64 88


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