Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parathyroid storm in patients with primary hyperparathyroidism has previously been described as hyperparathyroid crisis, parathyroid intoxication or acute hyperparathyroidism. Whatever the nomenclature, all emphasize the severity and urgency of this disease entity. Although fewer than 200 cases have been described since the first report by Dawson in 1932, it is generally agreed that parathyroid storm is more prevalent than commonly appreciated. The symptoms and signs of the syndrome are not only due to the hypercalcemia, but also to the toxic effects of the parathyroid hormone (PTH). Its wide, but nonspecific clinical presentations make it easily confused with other cardiovascular or renal diseases. The mortality rate in untreated cases of parathyroid storm is essentially 100%. With combined medical-surgical treatment, it is still reported to be as high as 40%. Two patients with parathyroid storm were encountered at our institute recently, they both presented with severe hypercalcemia, consciousness disturbance and acute renal failure. The serum level of the intact form of PTH (iPTH) in both patients was greater than 1,000 pg/mL. Case 1, a 63-year-old female, presented with hypercalcemic crisis. Initially, good responsiveness to a saline infusion, steroids and furosemide administration was noted. Unfortunately, she became comatous after fine-needle aspiration of the parathyroid tumor. The recurrent storm was refractory to medical therapy, but was treated successfully by surgical removal of the single adenoma. This is a rare reported case regarding a hyperparathyroid storm after fine-needle aspiration of a parathyroid adenoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Parathyroid storm: report of two cases]. 136 14

Various functioning and non-functioning tumors arise from endocrine glands in both the sporadic and familial forms and pathophysiology of the tumors is variable due to differences in the sort of tumor-bearing endocrine organs and in the amount of hormones released. In this paper, gene abnormalities in growth hormone (GH)-secreting pituitary adenoma, ectopic GHRH-producing tumor, multiple endocrine neoplasia (MEN) and ectopic parathyroid hormone (PTH)-producing tumor are documented in relation to etiology and pathophysiology. GH-secreting pituitary adenoma is heterogeneous in clinical features, pathological findings and GH responses to various secretagogues. A point mutation of codon 201 of Gs alpha gene was observed in 2 out of 45 GH-secreting pituitary adenomas (4.4%), but no point mutation of Gi2 alpha gene was found. Pituitary tumors may occur at any stage of differentiation from the totipotent cells to mature anterior pituitary cells, and the mutations of Gs alpha and H-ras genes as well as loss of heterozygosity (LOH) found on chromosome 11 in some adenomas must be involved in their tumorigeneses. Since 1959, 34 patients with ectopic GHRH-producing tumor associated with acromegaly have been reported. In our case of MEN type 1, the paradoxical rise of plasma GH after TRH or glucose administration disappeared after resection of the tumor. The tumor cells showed neither rearrangement nor amplification of GHRH gene and 20 oncogenes including ras, myc, and erb. Only LOHs of HRAS1 and D11S151 were detected in this tumor, but no point mutation was found in HRAS1 gene. Therefore, a kind of tumor suppressor gene may be involved in the tumorigenesis of the tumor in addition to inactivation of MEN-1 locus. In MEN-1 patients, we reported LOH on chromosomes 1, 9, 11 and 16, while we reported point mutation as being present only in Gs alpha gene on chromosome 20. This point mutation was found specifically in GH-secreting pituitary adenoma but not in hyperplastic parathyroid and pancreas adenoma. These data suggest that in MEN-1 patients tumorigenesis occurs and advances from hyperplasia and adenoma to cancer during multistep changes of genes such as inactivation of MEN-1 gene and other tumor suppressor genes and activation of oncogenes. Ectopic PTH-producing tumor was first reported by us in 1989, and this was followed by 2 papers. These patients showed a disturbance of consciousness and high levels of serum calcium and plasma PTH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathophysiology and gene abnormalities of endocrine tumors]. 136 16

Fine needle aspiration (FNA) biopsy in conjunction with ultrasonic definition of nonpalpable masses in the neck region is being used more frequently. Currently available preoperative localization tests have failed, in many instances, to delineate adequately the location of missed adenomas of the parathyroid gland. We describe herein the use of ultrasonically guided FNA of parathyroid tissue with immunoperoxidase confirmation for precise localization of the diseased gland. Three patients with persistent hypercalcemia after exploration of the neck were referred to Ochsner Clinic, New Orleans. In two of these patients, a parathyroid adenoma had been removed, while in one patient no adenoma was found. All patients had elevated calcium (range 10.9 to 11.6 milligrams per deciliter), low phosphorous and elevated parathyroid levels. Preoperative ultrasonography to localize the suspected parathyroid glands was performed, with FNA and immunohistochemical confirmation. Smears confirmed adequate cellular material. Alcohol fixed, Papanicolaou stained and air dried, Wright's and Giemsa stained smears were evaluated for the presence of parathyroid cells by conventional cytologic examination. The Papanicolaou-stained slides were then decolorized in 1 percent hydrochloric acid in 70 percent ethanol. After decolorization, the smears were stained for parathyroid hormone (PTH) in an avidin-biotin complex (ABC) system, using a commercially available ABC kit (Vector Laboratories Inc.). The primary antibody is a polyclonal antiserum generated in rabbits against a synthetic human PTH. Negative controls were obtained from normal thyroid glands. In all three patients, the diseased gland was localized by ultrasound with cytologic and immunohistochemical confirmation, one on the right side and two on the left side. At surgical excision, the adenomas weighed 0.8 and 0.75 gram and the carcinoma, 0.75 gram. In two, intraoperative identification of the diseased gland was aided by ultrasound directed methylene blue injection into the adenoma. During a follow-up evaluation of eight to 24 months, serum calcium had remained normal in two patients, and one patient had become hypocalcemic and required calcium supplements. The preoperative localization allowed a direct surgical approach to the side in question in all patients. Ultrasonically guided FNA in an immunoperoxidase system can be a valuable preoperative localization technique for patients with recurrent hyperparathyroidism, thus avoiding extensive exploration of the neck with the subsequent complications.
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PMID:Immunoperoxidase confirmation of ultrasonically guided fine needle aspirates in patients with recurrent hyperparathyroidism. 144 38

A 59-year-old woman with primary hyperparathyroidism was found to have a parathyroid adenoma behind the left clavicle. Preoperatively, it appeared as a hypoechoic mass on ultrasonography, as a hot nodule on thallium scintigraphy, and as a high signal on T2-weighted magnetic resonance imaging. Histological, immunohistochemical and ultrastructural studies of the surgically resected tumor revealed a parathyroid adenoma composed mainly of oxyphil cells with production of a parathyroid hormone. Moreover, a multilocular lesion of lymphangiectasia was contained. Hypercalcemia was alleviated postoperatively. These observations corroborated a functioning parathyroid oxyphil cell adenoma. This is the first case report of functioning oxyphil cell adenoma of the parathyroid gland with lymphangiectasia in Japan.
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PMID:A case of primary hyperparathyroidism due to an oxyphil cell adenoma. 147 90

PRAD1 (parathyroid adenoma 1) gene at chromosome 11q13 has been cloned from parathyroid adenomas as a putative oncogene, activated by translocation with the parathyroid hormone gene. 4.5 kb and 1.7 kb mRNA are transcribed and both have the same open reading frame of 885 bp encoding 34 kd protein of a cyclin gene family, cyclin D1. Recently, overexpression of PRAD1 gene has been reported to be correlated closely with the rearrangement of bcl-1 locus, particularly in centrocytic lymphoma. In our study, overexpression of PRAD1 gene was shown in five B cell lines with t(11;14)(q13;q32) including one centrocytic lymphoma line and 4 myeloma lines, when compared with other hematopoietic cell lines without translocation. One of the cell lines, SP-49, demonstrated a truncated mRNA of 3.4 kb, in addition to 1.7 kb of normal size. Southern blot analysis demonstrated a rearrangement with PRAD1 cDNA probe, suggesting that the gene is altered in this particular cell line. By cloning analysis, we confirmed that 1.8 kb deletion in 3' region of PRAD1 gene eliminating the destabilizing signal of PRAD1 mRNA, gave rise to the aberrant mRNA of 3.4 kb. These findings suggest that PRAD1 gene is most likely the candidate oncogene for bcl-1 activated by t(11; 14)(q13;q32) translocation. The gene alteration found in one cell line, SP-49, might also play an important role for deregulation of the gene.
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PMID:[Overexpression of PRAD1 gene in B-cell malignancy with t(11;14)(q13;q32) translocation]. 151 59

The relationship between preoperative serum levels of intact parathyroid hormone (PTH), serum calcium, and the weight of parathyroid adenoma has been investigated in 44 patients undergoing surgery for primary hyperparathyroidism due to single gland disease. There was no significant correlation between preoperative serum calcium and either intact PTH concentration or adenoma weight (r = 0.465 and 0.381, respectively). Although there was a significant correlation between PTH concentration and adenoma weight (r = 0.850, p less than 0.0005), this correlation was lost when two unusually heavy adenomas weighing 10.98 and 15.23 g were removed from the analysis. Clearly, a preoperative direct prediction of gland weight determined from PTH level was not possible. Patients with adenomata heavier than 750 mg had a significantly lower circulating PTH level per mg of adenoma than patients with glands lighter than 750 mg. PTH secretion in vitro in low calcium medium by adenoma cells from glands weighing less than 1 g was higher than secretion by cells from adenomas heavier than 1 g. Larger parathyroid adenomata appear to secrete less PTH per unit weight in vivo and per unit cell in vitro under conditions of maximal stimulation.
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PMID:The relationship between adenoma weight and intact (1-84) parathyroid hormone level in primary hyperparathyroidism. 153 63

Parathyroid hormone-related protein (PTHrP) was first identified in human malignant tumors associated with humoral hypercalcemia of malignancy. We immunohistochemically examined the distribution of PTHrP both in 7 normal parathyroid glands and in a 20 parathyroid adenomas. Sixty-five percent of parathyroid adenomas (13 cases) were positive for PTHrP, whereas only one normal parathyroid gland was positive for PTHrP in the area of transitional oxyphil cells. Many parathyroid adenomas (12 cases) were composed of both PTHrP-positive cells and--negative cells, and these two different type of cells showed a tendency to form nodules respectively in parathyroid adenoma. Although both chief cells and oxyphil or transitional oxyphil cells were positive for PTHrP in parathyroid adenoma, oxyphil or transitional oxyphil cells were more responsible for PTHrP production than chief cells. Chief cells are thought to produce parathyroid hormone mainly in parathyroid adenoma. On the other hand, little is known concerning the function and role of oxyphil or transitional oxyphil cells. Our results suggest that oxyphil or transitional oxyphil cells in parathyroid adenoma may have some functional roles different from those of chief cells through the production of PTHrP.
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PMID:The presence of immunoreactive parathyroid hormone-related protein in parathyroid adenoma cells. 155 86

A rare occurrence of the association of parathyroid adenoma in a case of thyroid papillary carcinoma is described. The patient was incidentally found to have parathyroid adenoma which was preoperatively diagnosed to be a metastatic lymph node. Analysis of her serum obtained before operation showed an elevation of serum parathyroid hormone (PTH) concentration without hypercalcemia. Since the association of hyperparathyroidism is high in patients with thyroid diseases, examination of not only serum levels of calcium and PTH but also careful interpretation of computed tomography (CT) and/or nuclear magnetic imaging (MRI) is necessary in the diagnosis of co-existing asymptomatic hyperparathyroidism.
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PMID:A case of papillary carcinoma of the thyroid associated with parathyroid adenoma without hyperparathyroidism. 163 47

Calmodulin has been identified in parathyroid cells and is thought to play an important role in the production or secretion of parathyroid hormone. However, a detailed investigation of calmodulin-binding proteins in parathyroid glands has not been conducted. In this study, we attempted to determine the presence of calmodulin-binding protein in human parathyroid adenoma by affinity chromatography. The eluted protein from a calmodulin-coupled Sepharose 4B column with EGTA was analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis which revealed a major protein band of Mr 50,000. A Ca2+/calmodulin-dependent protein kinase activity was detected at the protein peak using dephosphorylated casein as a substrate. The 50 kDa band was identified as calcium/calmodulin-dependent protein kinase II (CaM-kinase II) by immunoblotting. The substrate specificity, pH dependency and affinity for calmodulin of this enzyme were identical to those of CaM-kinase II from rat brain. Also, the kinase activity was sensitive to KN-62, a specific inhibitor of CaM-kinase II. In total, 0.48 mg of this kinase was purified from 3 g human parathyroid adenoma.
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PMID:Purification and characterization of calcium-calmodulin kinase II from human parathyroid glands. 166 May 13

Patients receiving lithium for the management of manic depressive disorders appear to be at increased risk for development of hypercalcemia. Some (but not all) clinical studies and several in vitro studies suggest that lithium alters release of parathyroid hormone. Because hypercalcemia may result from an increase in the mass of parathyroid tissue, we studied the in vitro effect of lithium on tritiated thymidine (3H-TdR) incorporation as a measure of DNA synthesis. Dispersed cells from previously cryopreserved tissue from 18 patients undergoing surgery for single-gland hyperparathyroidism (adenoma) and five patients with secondary hyperparathyroidism were incubated with graded concentrations of lithium chloride and, after a 5-day incubation, were pulsed with 3H-TdR. Adenoma cells exposed to 2.0 mmol/L lithium (therapeutic level is approximately 0.8 to 2.0 mmol/L) demonstrated increased 3H-TdR incorporation compared with cells not exposed to lithium (average increase 56%). Secondary hyperplasia cells exhibited a similar but less striking response. There was no lithium-induced 3H-TdR incorporation in four preparations with normal bovine parathyroid cells. We conclude that lithium in therapeutic doses increases 3H-TdR incorporation into adenoma cells, may serve as a mitogen for human parathyroid adenoma, and could promote or accelerate hyperparathyroidism.
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PMID:Lithium increases tritiated thymidine uptake by abnormal human parathyroid tissue. 166 Jun 26


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