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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tissue sections from 17 cases of parathyroid adenoma and ten cases of parathyroid hyperplasia were examined for mitotic activity. Mitoses were identified in 12 of the 17 cases of parathyroid adenoma and in eight of the ten cases of parathyroid hyperplasia. Clinical follow-up of all patients, even the four patients in whom numerous mitoses were present, showed no evidence of recurrent or aggressive disease. Mitotic activity alone is an unreliable indicator of aggressive potential in parathyroid disease.
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PMID:Mitotic activity in benign parathyroid disease. 721 56

The regulation of parathyroid hormone (PTH) secretion by calcium was studied in normal and abnormal parathyroid tissue from five patients with a parathyroid adenoma. Dispersed cells were prepared from the adenoma and from a portion of a normal parathyroid gland and were incubated for two hours with varying concentrations of calcium. PTH release as a function of the concentration of calcium was determined by radioimmunoassay (C-terminal). Cells from the normal glands showed a lower set-point for calcium (the concentration of calcium causing half of the maximal inhibition of PTH release) than those from the adenomas in four of five cases. Moreover, both set-point and maximal PTH release at low concentrations of calcium were significantly lower in normal glands from patients with an adenoma than in normal glands from patients with normal calcium homeostasis (0.77 +/- 0.04 [SEM] versus 0.99 +/- 0.03 mM calcium and 3.4 +/- 0.43 versus 10.1 +/- 0.78 ng/10(5) cells/hr, respectively). These observations may explain, in part, the transient hypocalcemia frequently seen in patients after removal of a parathyroid adenoma. In addition, they suggest that the set-point for calcium and maximal PTH release in normal parathyroid tissue may be altered by prior exposure to chronic hypercalcemia or other physiologic variables. Finally, the "normal" set-point that we have noted previously in parathyroid tissue from some patients with primary parathyroid hyperplasia may be inappropriately high for the hypercalcemia seen in those cases.
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PMID:Abnormal calcium-regulated PTH release in normal parathyroid tissue from patients with adenoma. 728 44

Eight of 23 patients undergoing total thyroidectomy for radiation-associated nodular thyroid disease were found to have unsuspected parathyroid hyperplasia or adenoma at operation. The total serum calcium level was normal preoperatively in each patient. Serum ionized calcium and parathyroid hormone levels were measured in five patients preoperatively and were normal in each case. These pathologic findings in normocalcemic patients may represent a preclinical form of hyperparathyroidism, which would be further evidence linking radiation to the pathogenesis of hyperparathyroidism. The parathyroid glands should be evaluated both pre-operatively and at operation in all patients who have a history of radiation and require thyroidectomy.
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PMID:Unexpected parathyroid disease discovered at thyroidectomy in irradiated patients. 728 27

Thirty-nine patients with primary hyperparathyroidism were studied four to eight years after their initial operation. In six patients, both the pathologist and surgeon agreed on the diagnosis of solitary adenoma; in 16 patients, the surgeon diagnosed solitary adenoma and the pathologist parathyroid hyperplasia (microscopic hyperplasia). In 16 patients, primary chief cell hyperplasia was agreed upon by the pathologist and surgeon. In the 16 patients with microscopic hyperplasia, there have been no long-term recurrences of hypercalcemia, but, in two patients, plasma parathyroid hormone levels are high. Parathyroid hormone--total calcium regression curves demonstrate significant preoperative correlation in solitary adenoma, p less than 0.01, and primary chief cell hyperplasia, p less than 0.05. After operation, significant correlations were not found between parathyroid hormone and total calcium. T-testing slope differences of pre- and postoperative parathyroid hormone--total calcium regression curves demonstrates a significant (p less than 0.01) shift to the right of the microscopic hyperplasia patients after operation, moving them to a broader range of total calcium per picogram parathyroid hormone. We conclude that 1) in primary hyperparathyroidism, positive regulation of total calcium by autonomously released parathyroid hormone exists in patients with solitary adenoma and chief cell hyperplasia; 2) autonomously functioning parathyroid tissue has been removed by operation for solitary adenoma with coexistent microscopic parathyroid hyperplasia. In this four- to eight-year follow-up period, it is clear that microscopic parathyroid hyperplasia is not associated with recurrent hypercalcemia. Two functionally distinct forms of parathyroid suppression are suggested; positively regulated microscopic hyperplasia and negatively regulated pathologically suppressed glands.
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PMID:Primary hyperparathyroidism: four- to eight-year postoperative follow-up demonstrating persistent functional insignificance of microscopic parathyroid hyperplasia and decreased autonomy of parathyroid hormone release. 728 4

Parathyroid autografts were implanted in 11 patients at this institution. Four patients had total or subtotal parathyroidectomy and implantation for parathyroid hyperplasia or adenoma, while 7 had one or more parathyroids removed and implanted during total thyroidectomy for carcinoma of the thyroid. Hyperplastic parathyroid was implanted in 4 instances and normal parathyroid in 7. Recurrent hyperparathyroidism occurred in 1 patient with an implanted adenoma who was returned to a normocalcemic state by partial reexcision ("titration") of the implanted tissue. All implants were placed in muscle pockets, a single site being used for patients receiving normal parathyroid tissue, and multiple sites for patients receiving hyperplastic glands. Those patients receiving forearm implants were followed up by serial parathyroid hormone determinations in venous blood drawn from both arms. In all cases, elevated levels were found on the implanted side, as compared to the contralateral control side.
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PMID:Autografts of normal and hyperplastic human parathyroid: experience in eleven patients with immunoassay monitoring of function in seven. 740 59

Parathyroid specimens removed from patients with clinical hyperparathyroidism were cultured in a two-layer soft-agar system. Four patients had parathyroid hyperplasia and one had a parathyroid adenoma. Colonies grew from single-cell suspensions of each specimen. Plating efficiency ranged from 0.001 to 0.05%. No colonies grew from normal bovine parathyroid specimens. Parathormone was detected in 0.9% NaCl solution incubated with the culture plates of three of the four human specimens tested. Parathormone levels determined by radioimmunoassay ranged from 10.4 < 100 ng/ml. Plates tested serially showed a progressive rise in parathormone levels with time and an increase in colony size and number. Microscopic evaluation of the cellular layer showed clusters of cells morphologically consistent with parathyroid origin. Colonies remained viable for approximately 3 weeks. These data confirm that malignancy of tissue in vivo is not necessary for colony formation in agar and that human parathyroid hyperplasia or adenoma cells produce and secrete parathormone in this system.
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PMID:Direct cloning of human parathyroid hyperplasia cells in soft-agar culture. 743 51

The parathyroids from ten consecutive cases of chronic renal failure coming to operation in a period of seven years were studied by light and electron microscopy. The clinical and biochemical data as well as the levels of immunoreactive parathormone (iPTH) were reviewed. For the sake of comparison adenomata from two cases of primary hyperparathyroidism were studied. In the cases of chronic ;renal failure there were six cases of tertiary hyperparathyroidism with adenoma formation, surrounded by dense fibrous tissue and compression of adjacent parathyroid cell amidst a background of hyperplasia. Two cases showed secondary parathyroid hyperplasia and the remaining two cases were adenomata which clinically affected only one gland. Neither the biochemical data nor levels of iPTH allowed the cases with secondary hyperplasia to be separated from those with tertiary hyperparathyroidism. Similarly electron microscopy showed no distinct differences between these two groups of adenomata from cases of primary hyperparathyroidism. The diagnosis of tertiary hyperparathyroidism is made on a combination of clinical, biochemical and histological features, the histological features being most important. It is concluded that tertiary hyperparathyroidism is part of a histological spectrum in response to chronic renal failure and autonomous glands are related to the mass of parathyroid tissue present.
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PMID:The parathyroid in chronic renal failure-- a light and electron microscopical study. 744 5

P-glycoprotein (Pgp), the multidrug resistance (mdr) gene product, has been described in normal tissues with diverse physiologic functions. A broad role as a transporter protein for toxins, hormones, and physiologic metabolites has been provisionally deduced, based on structural analysis and immunoanatomic localization. Recently, significant levels of Pgp have been demonstrated in endocrine and hormonally responsive tissues and tumors. We examined calcium-regulated, clonal parathyroid epithelial (PT-r) and endothelial cells (BPE-1) and frozen parathyroid tissue from normal human parathyroid, parathyroid hyperplasia, parathyroid adenoma, and parathyroid carcinoma for expression of the multidrug resistance gene (Mdr1) and Pgp utilizing Northern and Western analysis and immunohistochemistry. We also investigated the effect of extracellular calcium (eCa) on Pgp expression in PT-r cells at the molecular/cellular level. Immunohistochemistry, utilizing three murine monoclonal antibodies (MAbs)--C494, JSB-1, and C219--which recognize spatially distinct cytoplasmic epitopes of Pgp, revealed strong immunoreactivity in PT-r cells, normal parathyroid, and parathyroid hyperplasia, and weak immunostaining in parathyroid adenomas. BPE-1 cells, endothelial cells, and parathyroid carcinoma were negative. PT-r cells showed a single 130 kDa band (120 KDa after glycosidase treatment) on Western blot and a 4.6 kb transcript on Northern analysis, consistent with Pgp. Western and Northern blot analysis of PTr cells cultured in different eCa concentrations showed that eCa up-regulated Pgp expression.
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PMID:P-glycoprotein is expressed in parathyroid epithelium and is regulated by calcium. 773 28

The relationship between parathyroid hormone-related protein (PTHrP) release from parathyroid cells and extracellular calcium ion concentration was investigated in three cases of parathyroid hyperplasia secondary to chronic renal failure and in four cases of parathyroid adenoma. Amounts of PTHrP released from individual parathyroid cells dispersed from surgical specimens were estimated by cell immunoblot assay. Parathyroid cells from both hyperplasias and adenomas showed significant suppression in the release of PTHrP with increase in extracellular calcium ions, but the amounts of PTHrP released from adenoma cells were significantly larger than from hyperplasia cells. The maximal value for PTHrP released within 120 minutes from adenoma cells was 2.91 +/- 2.11 x 10(-2) fmol/cell ([Ca2+], 0.4 mmol/L), and the minimal value was 1.32 +/- 0.35 x 10(-2) fmol/cell ([Ca2+], 2.0 mmol/L). On the other hand, the maximal value for PTHrP released from hyperplasia cells was 1.79 +/- 1.56 x 10(-2) fmol/cell ([Ca2+], 0.4 mmol/L), and the minimal value was 0.32 +/- 0.19 x 10(-2) fmol/cell ([Ca2+], 2.0 mmol/L). These results demonstrate actual release of PTHrP from abnormal parathyroid tissues into the extracellular space with the response to extracellular calcium ions depending on the cell status. Given the lack of definite histological criteria to differentiate between hyperplasias and adenomas in the parathyroid gland, the presently demonstrated significant difference in the ability to release PTHrP is important in pointing to parathyroid hyperplasia secondary to chronic renal failure as a distinct pathological entity separate from parathyroid adenoma.
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PMID:Inhibition of parathyroid hormone-related protein release by extracellular calcium in dispersed cells from human parathyroid hyperplasia secondary to chronic renal failure and adenoma. 777 90

Technetium99m (99mTc)-Sestamibi/123I subtraction scanning was prospectively performed in 30 patients with primary hyperparathyroidism in an attempt to locate enlarged glands before first surgery. Imaging results were compared to surgical findings; the surgeon tried to identify all parathyroid glands. Twenty-seven patients were found to have a solitary adenoma during surgery, and 3 had multiglandular parathyroid hyperplasia. Twenty-six parathyroid adenomas (96%) were accurately located before surgery. The smallest gland detected weighted 125 mg. Preoperative detection of two mediastinal adenomas allowed them to be excised by median sternotomy during the initial operation. 99mTc-Sestamibi/123I subtraction scanning predicted multiglandular involvement in two patients with parathyroid hyperplasia, whereas it showed a solitary image in the third. Ten patients (33%) had associated nodular thyroid disease, hindering image analysis and leading to one false positive result. 99mTc-Sestamibi scanning seems to be better for locating enlarged parathyroid glands than other noninvasive imaging techniques. However, 1) difficulties associated with thyroid nodules call for complementary thyroid scanning; and 2) images showing a solitary enlarged parathyroid gland do not rule out multiglandular disease. This technique should help in detecting lesions, such as mediastinal glands, that are difficult to find at initial surgery.
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PMID:Primary hyperparathyroidism: is technetium 99m-Sestamibi/iodine-123 subtraction scanning the best procedure to locate enlarged glands before surgery? 782 31


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