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)

Vitamin D metabolites in serum and calcitriol receptor concentration in parathyroid tissue were examined in 52 patients operated on for primary hyperparathyroidism. The calcitriol receptor levels were not different in parathyroid adenomas (mean 224 fmol/mg of protein, range 29-509, N = 43), normal parathyroid tissue (mean 245, range 31-690, N = 20), and primary parathyroid hyperplasia (mean 172, range 46-477, N = 9). Preoperative serum levels of calcitriol concentration correlated inversely to the calcitriol receptor in normal parathyroid tissue in patients with adenoma (r = -0.57, N = 17, p = 0.017), but no such correlation was found in the corresponding adenomas (r = 0.14, p = 0.59). In 31 patients in whom both pre- and postoperative vitamin D metabolite analyses were carried out, 23 had lower calcitriol postoperative concentrations compared to preoperative values (p = 0.012, sign test). No change was found in the other vitamin D metabolites postoperatively. By multiple regression analysis calcitriol concentration in serum was inversely correlated to the serum concentration of urea and phosphate (p = 0.003). We conclude that calcitriol may influence calcitriol receptor expression in normal parathyroid tissue, but not in adenomatous parathyroid gland. Furthermore, serum calcitriol was correlated to the renal function, and phosphate level, and in most patients the calcitriol concentration was lower after the operation.
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PMID:Serum vitamin D metabolites and calcitriol receptor concentration in parathyroid tissue in primary hyperparathyroidism. 133

Controversy exists concerning indications for primary hyperparathyroidism surgery, tests to localize parathyroid tumors, pathologic criteria for adenoma and hyperplasia, and unilateral versus bilateral surgery for hyperparathyroidism. Seventy cases were reviewed. Results of localization tests, sites of aberrant tumors, symptoms, complications, and ratio of adenoma to hyperplasia will be presented. The foreseeable trends are continued improvement in localization techniques, earlier intervention in the disease spectrum, unilateral exploration for adenoma and bilateral surgery for hyperplasia, and acceptance of primary nodular hyperplasia and normal size with hypercellularity as pathologic entities in primary parathyroid hyperplasia.
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PMID:Trends in primary hyperparathyroidism surgery. 155 92

Hypertension in primary hyperparathyroidism (HPT) was previously attributed to hypercalcemia per se or to impaired kidney function. Of 441 consecutive patients operated on for HPT over 24 years, 57% were hypertensive. Preoperative blood pressure remained fairly constant during the study period, despite otherwise markedly changing clinical picture with, latterly, more asymptomatic patients. The preoperative systolic blood pressure (SBP) was significantly correlated to both serum calcium (p less than 0.001) and serum creatinine (p less than 0.05), but not when the influence of age was taken into account in a multiple regression analysis. Other pathogenetic factors in hypertension were therefore probable. When the statistical analysis was adjusted for differences in age and serum calcium, blood pressure was lower in the HPT patients with parathyroid hyperplasia than in those with adenoma (153 +/- 31/90 +/- 14 vs. 163 +/- 29/91 +/- 14 mmHg, p less than 0.01 for SBP). The concept that parathyroid hyperplasia represents a mild (early) form of HPT that may precede adenoma formation is corroborated by our observations, which also indicate that there is no simple cause-and-effect relationship accounting for hypertension in primary HPT.
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PMID:Hypertension in primary hyperparathyroidism in relation to histopathology. 168 31

Multiple gland parathyroid disease is the pathological finding in primary hyperparathyroidism (HPT) in about 10% to 20% of all patients and in approximately a third of all patients with persistent or recurrent disease. The variability of multiple gland disease spans from 2 adenomas to diffuse hyperplasia in patients with multiple endocrine neoplasia type 1. This variability calls into question the proposed common pathophysiologic background in all of these cases. As primary treatment of multiple gland primary HPT, subtotal parathyroidectomy and thymectomy or total parathyroidectomy and heterotopic autotransplantation including thymectomy can be equally advocated. Recurrent hyperparathyroidism frequently occurs in cases of diffuse parathyroid hyperplasia. This must be considered especially in patient follow up and before each surgical procedure. Thus, a defined but adaptable therapeutic regimen might prevent permanent hypoparathyroidism and persistent hyperparathyroidism.
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PMID:Management of primary hyperparathyroidism caused by multiple gland disease. 168 44

Primary hyperparathyroidism (PHPT) is increasing in incidence and detection, primarily because of the aging of our population and the widespread use of automated serum calcium determination. As a result, a substantial number of "early" cases or "biochemical" PHPT are being detected. The indications for parathyroidectomy in such early cases of PHPT are currently under debate, primarily because of economic issues. These factors underscore the importance of research into the basic mechanisms and natural history of PHPT. We investigated an animal model of diet-induced PHPT that retains two crucial aspects of PHPT: elevation of endogenously produced parathyroid hormone (PTH), accompanied by gross and microscopic changes in the native parathyroid glands. Female Long-Evans rats were divided into six groups of 15 each and fed a control diet (Ca/P of 1:2) or a high-phosphate diet (Ca/P of 1:7) for 1-, 2-, or 3-month intervals. Compared with the control animals, serum PTH levels were elevated at all three time intervals in the experimental group, whereas serum calcium levels were decreased at all time intervals. Serum creatine levels were also elevated at all time intervals, whereas serum phosphorus levels did not change. Parathyroid histopathologic studies demonstrated no change at 1 month, whereas nine of 15 experimental animals showed mild hyperplasia at 2 months and 13 of 14 showed mild to moderate hyperplasia with gland enlargement at 3 months compared with control animals. Histopathologic examination of the kidneys showed no change at 1 month but focal parenchymal inflammation with calcium deposition at 2 and 3 months in the experimental groups. In conclusion, the high-phosphate diet successfully induced the earliest changes of PHPT: elevated PTH levels and parathyroid hyperplasia. However, because renal function was mildly compromised early on, some element of early secondary (renal) hyperparathyroidism may have supervened quickly. Because this model is simple, it may be useful to investigate this complex syndrome further, as well as its natural history and the complications it produces in other organs such as the kidneys.
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PMID:High phosphate diet-induced primary hyperparathyroidism: an animal model. 174 75

The surgical management of patients with persistent or recurrent primary hyperparathyroidism is reviewed. The several factors allowing the surgeon to formulate a correct working diagnosis and to successfully remove all abnormal parathyroid tissue are individually discussed and recent results of re-operative parathyroid surgery are presented. In particular, direct surgical exploration based on aggressive pre-operative localization studies, the use of intra-operative ultrasound to facilitate intra-operative dissection, cryopreservation of excised parathyroid tissue with potential for delayed autograft to avoid permanent hypoparathyroidism, and the use of intra-operative monitoring of urinary cyclic adenosine monophosphate levels in patients with parathyroid hyperplasia in whom the surgeon is uncertain whether all abnormal parathyroid tissue has been removed, each contribute to a high rate of successful management (greater than 95%) for patients with the difficult problem of persistent or recurrent primary hyperparathyroidism.
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PMID:Management of patients with persistent or recurrent primary hyperparathyroidism. 176 37

The efficiency of preoperative radioactive toluidine blue (RTB) scintigraphy for the localization of parathyroid pathology was evaluated prospectively in 69 patients (age range, 15 to 81 years; mean, 56 years) with primary hyperparathyroidism. Four patients have previously undergone negative exploratory surgery. Patients underwent preoperative dual radionuclide parathyroid-RTB/technetium 99m (Tc 99m)-thyroid scintigraphies with a computer-interfaced gamma-camera with a pinhole collimator. Computer-acquired scintigraphic data were analyzed for parathyroid localizations by an RTB-parathyroid/thyroid superposition technique. At surgery, parathyroid adenomas were found in 64 patients (single adenomas in 60 patients; two adenomas in four patients), nine of these adenomas were mediastinal. Four patients had parathyroid hyperplasia. One patient had no parathyroid pathology (negative exploratory surgery). Correlation between the surgical-pathologic findings and the scintigraphic RTB localization studies disclosed a sensitivity of 87%, with a specificity of 94%, and an overall accuracy of 92%. The routine use of preoperative scintigraphic parathyroid-RTB/Tc 99m-thyroid localization has proved to be highly effective, enabling detection of small hyperfunctioning parathyroid glands in normal and ectopic locations in a wide range of weights. In this series a success rate of 98% was achieved on initial and reexploratory surgery for primary hyperparathyroidism.
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PMID:The use of radioiodinated toluidine blue for preoperative localization of parathyroid pathology. 194 52

Chromogranin-A (CgA), also termed secretory protein-I, is an acidic glycoprotein that is synthesized and secreted by cells of the diffuse endocrine and neuroendocrine system. Several previous studies had suggested that plasma levels of CgA were elevated in patients with primary hyperparathyroidism. In the present study we sought to examine expression of the CgA gene in human parathyroid tissue from patients with primary hyperparathyroidism. We characterized the mRNAs coding for CgA and beta-actin in parathyroid tissue fragments obtained from 12 patients with parathyroid adenomas, 11 patients with familial multiple endocrine neoplasia type I (FMEN I) with parathyroid hyperplasia, and 11 normal subjects. The mRNAs were detected and analyzed by dot and Northern blot hybridization using cDNA probes. CgA mRNA transcripts of 2.1 kilobases were detected in normal and pathological parathyroids. Similarly, beta-actin mRNA species of 2.1 kilobases was present in all tissues. The relative level of parathyroid tissue CgA mRNA, calculated as the CgA/beta-actin mRNA ratio, was 73 +/- 18 in parathyroid adenoma, 73 +/- 20 in FMEN I, and 100 +/- 9 in controls (mean +/- SE; expressed as a percentage of the control reference group value). There were no significant differences among the steady state levels of CgA mRNA levels in these three groups (F = 0.98; P = 0.39). These results demonstrate that expression of CgA mRNA is qualitatively and quantitatively normal in parathyroid tumors from patients with FMEN I and parathyroid adenoma.
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PMID:Expression of chromogranin-A messenger ribonucleic acid in parathyroid tissue from patients with primary hyperparathyroidism. 234

We sought an explanation for prior findings of high plasma chromogranin-A (Chr-A) in primary hyperparathyroidism. Chr-A was measured in plasma samples from 55 controls and 73 patients with primary hyperparathyroidism caused by adenoma (n = 14), sporadic or familial hyperplasia (n = 10), or familial multiple endocrine neoplasia type 1 (FMEN1; n = 49). Serum or plasma samples were also tested for calcium, PTH, gastrin, pancreatic polypeptide, CG alpha, and PRL. Plasma Chr-A was 34 +/- 10 in parathyroid adenoma, 55 +/- 33 in parathyroid hyperplasia without FMEN1, 63 +/- 88 in FMEN1, and 25 +/- 8 in controls (mean +/- SD; nanograms per ml; FMEN1 or parathyroid hyperplasia vs. control, P less than 0.05). Plasma Chr-A did not correlate with other hormonal variables in controls. Plasma Chr-A correlated with log serum gastrin (r = 0.43; P = 0.003) and plasma PTH (r = 0.52; P less than 0.05) only in FMEN1. In FMEN1, plasma Chr-A was highest in subjects with Zollinger-Ellison syndrome (ZES, 120 +/- 127; no ZES, 30 +/- 33 (P less than 0.0001). Parathyroidectomy did not decrease plasma Chr-A in patients with parathyroid adenoma or parathyroid hyperplasia. For FMEN1 patients with available pre- and postparathyroidectomy samples, Chr-A decreased postoperatively in four of five patients with ZES compared to none of six patients without ZES (P less than 0.05). Elevated plasma Chr-A is not a general feature of primary hyperparathyroidism. Elevated plasma Chr-A in primary hyperparathyroidism was restricted principally to patients who also had ZES. Primary hyperparathyroidism may influence the level of Chr-A by an effect of hypercalcemia or elevated PTH on Chr-A secretion from pancreatic islet tissue.
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PMID:Plasma chromogranin-A in primary hyperparathyroidism. 257 19

A 9-year-old boy, who had been admitted to the Pediatric Department for the examination of IgA nephropathy, was transferred to our urological clinic on Aug. 6, 1985, because of parathyroid crisis. Before urological consultation, he had been complaining of bilateral knee and calcaneal pain, anorexia and abdominal pain, which had persisted for several days. Laboratory data indicated serum Ca of 17.6 mg/dl, iP of 2.3 mg/dl and iPTH of 0.77 ng/ml. Roentgenographic examination such as chest, extremities and neck computed tomography showed no abnormal findings. The final diagnosis was parathyroid crisis caused by primary hyperparathyroidism and neck exploration was carried out on August. 10. Left upper parathyroid gland, which was 1 cm in diameter, was surgically removed. The other three glands were normal in size. Histological examination of the resected parathyroid gland revealed chief cell adenoma. In the post-operative course, serum Ca level was soon reduced to the normal range and bone pain disappeared rapidly. During the follow up period of 2.5 years, the patient was clinically free of recurrence. Only 23 cases of primary hyperparathyroidism in children have been reported in the Japanese literature. The clinical characteristics of these specific cases are that primary hyperparathyroidism in children shows a low incidence of renal lesion, but the complicated bone disease is of higher incidence compared with the adult cases. Histopathologically, parathyroid adenoma was frequently observed (14/19), and the other 5 cases were parathyroid hyperplasia.
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PMID:[Primary hyperparathyroidism in a child with parathyroid crisis--review of 24 cases reported in Japan]. 266 May 5


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