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)

Sixty-one consecutive patients were examined to determine the current mode of presentation of primary hyperparathyroidism (pHPT). Of these patients, 37.7% were asymptomatic, and the initial indication of pHPT was hypercalcemia, which was found unexpectedly on biochemical screening of the serum in elderly patients. Hypertension was twice as common among patients with pHPT as in the general population (36.1%). The next most common presentations were urinary calculi (18%) and mental depression (18%). The most useful discriminant laboratory tests were serum calcium, phosphorus, chloride, and parathormone (PTH). The calculated coefficient of correlation of PTH to land weight was high (r = 0.571, p less than 0.001). There was very significant correlation between PTH and seriousness of bone disease (r = 0.620, p less than 0.001). After parathyroidectomy, 3.3% of patients remained hypercalcemic, 93% were normocalcemic, and 1.6% were hypocalcemic.
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PMID:Clinical and biochemical features in primary hyperparathyroidism. 291 78

Twenty-two patients, all with surgically proven primary hyperparathyroidism, were studied by TI-201 thallous chloride and Tc-99m pertechnetate subtraction imaging. Fifteen parathyroid adenomata and one hyperplastic gland between 0.33 and 14.8 g were correctly localized in 16 patients. Two adenomata and seven hyperplastic or histologically normal parathyroids between 0.1 g and 1.4 g in seven patients were not localized. One patient had a correctly localized 13.0-g adenoma with a nonlocalized 0.3 g hyperplastic parathyroid gland and there were two false positive localizations. Sensitivity was 64% (glands), and 73% (patients). There was only fair correlation with parathormone (PTH) levels, but these were elevated in all but four of the patients with correctly localized parathyroids. The authors conclude that the imaging procedure is useful but its sensitivity is limited by difficulty in localizing correctly small glands, particularly those of less than 0.5 g, which comprised 29% of those excised.
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PMID:Localization of enlarged parathyroid glands by thallium-201 and technetium-99m subtraction imaging. Gland mass and parathormone levels in primary hyperparathyroidism. 298 88

Baseline levels and increases in urinary cyclic AMP excretion (UcAMP) and immunoreactive parathormone (iPTH) were studied before and during infusion of EDTA in euparathyroid patients with renal stones (n=11), patients with primary hyperparathyroidism (PHP; n=14) and patients with vitamin D deficiency (n = 12). In all three groups, EDTA evoked a significant rise in iPTH and UcAMP. In patients with PHP and in those with vitamin D deficiency, there was a sufficiently close relationship between increments in iPTH (delta iPTH) and in UcAMP (delta UcAMP) (r = 0.90, P less than 0.001 and r = 0.67, P less than 0.02, respectively) to use this model to assess renal sensitivity for changes to endogenous PTH levels. We quantified sensitivity of the kidney for PTH, by calculating the ratio delta UcAMP/delta TPTH for the three studied groups. The ratio was comparable in patients with renal stones (16.7 +/- 10.3) and PHP (13.8 +/- 4.9, P greater than 0.10), but was significantly increased in patients with vitamin D deficiency (33.2 +/- 17.9; P less than 0.01 versus patients with renal stones and P less than 0.01 versus patients with PHP). Within the group of patients with PHP there was no correlation between baseline serum calcium concentrations and the ratio delta UcAMP/delta TPTH. It is concluded that in patients with vitamin D deficiency, renal sensitivity to PTH is increased compared with patients with PHP and euparathyroid patients with renal stones, perhaps an expression of a teleological useful adaptation of end organ sensitivity.
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PMID:The renal sensitivity for endogenous parathormone in patients with primary hyperparathyroidism, vitamin D deficiency and renal stones. 301 31

A 63-year-old woman was treated medically for primary hyperparathyroidism because of a recent myocardial infarction. She received propranolol alone or combined with either cimetidine, calcitonin or disodium etidronate (EHDP). The treatment did not affect the elevated serum parathormone or urinary cyclic AMP levels, nor did it correct the elevated serum 1,25(OH)2D and the decreased serum 24,25(OH)2D levels in this patient. Propranolol combined with either cimetidine or with EHDP (600 mg/day) caused a mild decrease in the serum calcium level which, however, remained within the hypercalcemic range. Following surgery all parameters returned to normal. We conclude that the above medical regimens were incapable of correcting the hyperparathyroid condition in this patient.
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PMID:Medical treatment of primary hyperparathyroidism: effects on parathormone and vitamin D metabolites. 312 29

We measured parathyrin (PTH) in peripheral venous blood samples and in thyroid veins (both homolateral and contralateral to the lesion) in 13 patients with surgically confirmed parathyroid adenomas. Two different RIAs were used, one specific to the mid-region of the molecule (44-68, M-PTH), the other specific to the carboxy-terminal region (65-84, C-PTH). With the M-PTH assay we established a statistically significant multiple correlation (P less than 0.05) between the PTH concentrations in blood from the peripheral and thyroid veins; no significant correlation was found when we used the C-PTH assay. Our results confirm the superiority of the M-PTH RIA over the C-PTH RIA for study of hormonal secretion in primary hyperparathyroidism.
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PMID:Measurement of parathyrin in blood from thyroid veins: two radioimmunoassays compared in patients with primary hyperparathyroidism. 316 34

The management of autonomous (primary or tertiary) hyperparathyroidism is controversial for two important reasons: (1) Diagnosis of primary or tertiary hyperparathyroidism (as distinct from reactive or secondary hyperparathyroidism) has been revolutionized in the past 20 years as a result of routine inclusion of serum calcium concentration assays in serum multiautomated analysis, now obtained routinely for both hospitalized as well as ambulatory patients. The prevalence of primary hyperparathyroidism in the general population has appeared to rise as a consequence of this assay and the enhanced detection of this disease. This situation has confused the management of hyperparathyroidism since most patients now present with asymptomatic disease, and the need for surgical treatment is controversial in asymptomatic individuals. (2) Primary hyperparathyroidism usually is caused by hypersecretion of parathyroid hormone by an autonomously functioning parathyroid adenoma. In a small percentage of cases, multigland hyperplasia is present. In experienced hands, surgical removal of an adenoma within the thyroid bed cures the hyperparathyroidism 90% to 95% of the time, without performance of a preoperative procedure to localize the adenoma. Approximately 10% of parathyroid tissue is ectopic in location, however. Furthermore, approximately two thirds of "missed" adenomas are within the thyroid bed. Reexploration in the event of a failed operation therefore is not an uncommon occurrence. Parathyroid localization procedures clearly are indicated in patients with primary hyperparathyroidism who have evidence of persistent disease after a failed attempt at surgical cure. In patients first presenting with primary hyperparathyroidism, the need for a localization procedure is less clear, since surgery appears to be successful much of the time without it. Regardless of the nature of the above controversies, surgery for autonomous hyperparathyroidism continues, and localization procedures become more popular. Preoperative localization procedures such as angiography and venography with venous sampling for parathormone are cumbersome and invasive. Noninvasive tests to localize the parathyroid glands have emerged in the past 10 years, including dual tracer radionuclide scintigraphy with 201-thallous chloride and 99m-technetium pertechnetate, high-resolution computer tomography, and fine parts ultrasonography. Dual tracer scintigraphy with thallium and technetium is reported to have a localization sensitivity of 70%-90%. False-negative studies occur primarily in patients with small adenomatous or hyperplastic glands.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Parathyroid imaging: its current status and future role. 331 48

Urate metabolism was studied in 53 patients with primary hyperparathyroidism. They had compared to controls significantly higher serum urate and reduction of the clearance of urate. In 14 of the tested patients with primary hyperparathyroidism serum urate was increased above normal limits. Six months after parathyroidectomy serum urate fell significantly from 365.3 +/- 75.7 mumol/l to 265.7 +/- 48.3 mumol/l, in 26 patients where urate measurements were available before as well as after surgery. Serum urate levels in our patients with primary hyperparathyroidism did not correlate with clearance of urate. Levels of serum urate cannot be entirely explained by the decrease in renal clearance of urate. Serum urate levels did not correlate with severity of skeletal changes expressed by serum B-ALP and urinary excretion of hydroxyproline. These results suggest that parathormone does not increase the part of the urate pool coming from the nucleic acids of the increased bone metabolism.
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PMID:Primary hyperparathyroidism and hyperuricaemia are associated but not correlated with indicators of bone turnover. 343 54

Hyperparathyroid crisis secondary to primary hyperparathyroidism has variously been described as hypercalcemic crisis, parathyroid storm, and parathyroid intoxication as well as other equally descriptive terms. Whatever the nomenclature, all emphasize the seriousness and urgency of the condition. Although fewer than 200 cases have been described since the first report by Hanes in 1939, it is generally agreed that hyperparathyroid crisis is more prevalent than commonly appreciated. The signs and symptoms of the syndrome are believed due not only to the presence of hypercalcemia, but to the toxic effects of parathormone as well. Its wide, but nonspecific clinical spectrum makes it easily confused with other causes of rapidly fatal cardiovascular or renal disease. The mortality in untreated cases is essentially 100 per cent. With combined medical-surgical treatment, it is still reported as high as 60 per cent. Three patients with severe hyperparathyroid syndrome are reported. Effective control of both hypercalcemia and the toxic effects of acute hyperparathyroid crisis was achieved with the use of parenteral cimetidine. Definitive surgical removal of a solitary parathyroid adenoma was performed in all three patients. The intimate relationship of the bioavailability of cimetidine and its effect in primary hyperparathyroidism is clearly demonstrated. An analogy to the use of cimetidine in Zollinger-Ellison syndrome is made. Both are endocrinopathies that require doses of cimetidine in excess of that normally considered therapeutic for peptic ulcer disease. The signs and symptoms of hyperparathyroid crisis as well as current modalities of treatment are reviewed. It is concluded that parenteral cimetidine is an important aid in the management of acute hyperparathyroid syndromes secondary to primary hyperparathyroidism.
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PMID:Hyperparathyroid crisis reviewed: a role for parenteral cimetidine? 352 23

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

Since Sherwood's report in 1979, contradictory findings have been published with regarding the treatment of primary hyperparathyroidism with Cimetidine. We studied 16 patients with primary hyperparathyroidism treated with 1,200 mg of Cimetidine and followed-up clinically and biochemically. A decrease in serum calcium and urinary CAMP was observed after the fourth week of Cimetidine therapy with no significant change in parathormone levels. In none of the cases did Cimetidine seem to provide a treatment of hyperparathyroidism, a condition which remains curable with surgery.
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PMID:[Cimetidine treatment of primary hyperparathyroidism]. 360 67


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