A study of parathyroid hyperplasia in chronic renal failure

Yong, Jim; Vrga, Lubica; Warren, Bruce A.

doi:10.1080/00313029400169291

Cited by 6 publications

(3 citation statements)

References 27 publications

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“…The cause of this asymmetric involvement is obscure. Histologically, islands of oxyphils are often present, and hyperplastic cells may replace the fat (18,19).…”

Section: Histologymentioning

confidence: 99%

Medical and Surgical Treatment for Secondary and Tertiary Hyperparathyroidism

2004

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Prevention and treatment of secondary hyperparathyroidism (SHPT) in patients on chronic maintenance hemodialysis and of tertiary hyperparathyroidism (THPT) in patients after kidney transplantation is a challenge for the nephrologist and for the surgeon. Indication and results of medical and surgical therapy for SHPT and THPT have remained under discussion during the last decades. This review resumes the current medical and surgical strategies for patients with SHPT and THPT.

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“…The cause of this asymmetric involvement is obscure. Histologically, islands of oxyphils are often present, and hyperplastic cells may replace the fat (18,19).…”

Section: Histologymentioning

confidence: 99%

Medical and Surgical Treatment for Secondary and Tertiary Hyperparathyroidism

2004

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“…2 Hyperplasia is generally considered as a nonneoplastic condition, whereas adenomas are neoplasms. However, these two entities may not be distinctly different, and at least some adenomas might have their origin in antecedent parathyroid hyperplasia, and develop from the latter via a series of somatic mutations.…”

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confidence: 99%

Deletion of 11q23 and Cyclin D1 Overexpression Are Frequent Aberrations in Parathyroid Adenomas

Hemmer

Wasenius

Haglund

et al. 2001

The American Journal of Pathology

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Hyperparathyroidism may result from parathyroid hyperplasia or adenoma, or rarely from parathyroid carcinoma. Pericentromeric inversion of chromosome 11 that results in activation of the PRAD1/cyclin D1 gene and tumor suppressor gene loss have been described as genetic abnormalities in the evolution of parathyroid neoplasms. We studied tissue samples taken from primary parathyroid hyperplasia, parathyroid adenoma, and histologically normal parathyroid tissue by comparative genomic hybridization, fluorescent in situ hybridization, and immunohistochemistry for cyclin D1. DNA copy number changes were infrequent in primary hyperplasia (4 of 24, 17%), but common in adenomas (10 of 16, 63%; P ‫؍‬ 0.0059). The most common change was deletion of the entire chromosome 11 or a part of it, with a minimal common region at 11q23. This change was present in five (31%) adenomas and two (8%) primary hyperplasias. Fluorescent in situ hybridization confirmed the presence of both MEN1 alleles located at 11q13 despite deletion of 11q23 in all three cases studied. Cyclin D1 was overexpressed in six (40%) of the 15 adenomas studied, whereas none of the 27 hyperplasias (P ‫؍‬ 0.0010) nor the five histologically normal tissue samples overexpressed cyclin D1. Either DNA copy number loss or cyclin D1 overexpression was present in 13 (81%) of the 16 adenomas. We conclude that DNA copy number loss and cyclin D1 overexpression are common in parathyroid adenomas. The region 11q23 is frequently lost in parathyroid adenomas and occasionally in parathyroid hyperplasias, and this suggests the possibility that a tumor suppressor gene that is important in their pathogenesis is present on 11q23. Hyperparathyroidism may be caused by parathyroid gland hyperplasia or adenoma, or very rarely by parathyroid carcinoma. The clinical manifestations of hyperparathyroidism vary, but the patient may present with recurrent nephrolithiasis, mental changes, peptic ulcers, and sometimes with extensive bone resorption. The annual incidence is estimated to be 0.03% in patients older than 60, but the estimated prevalence including undiscovered asymptomatic patients is 1 to 2% or higher. The diagnosis is made primarily on clinical grounds and presence of elevated serum parathyroid hormone, which is usually associated with elevated serum calcium levels and urine calcium excretion. Primary hyperparathyroidism is usually caused by a single parathyroid adenoma, but multiglandular parathyroid hyperplasia accounts for ϳ10 to 15% of primary hyperparathyroidism.

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“…CGA is also the precursor of several bioactive peptides that inhibit stimulated release of PTH and costored CGA [3,6,7,22,34]. Reduced expression of both CGA and PTH has been described in the parathyroid tissue with primary or secondary hyperparathyroidism [23,28,33]. The lack of concordant downregulation of mRNA levels of PTH and CGA in parathyroid cells of hyperparathyroidism indicates that the alteration of secretory rather than the synthetic capacity is responsible for the decreased cellular content of CGA and PTH [16,29].…”

Section: Discussionmentioning

confidence: 95%

Normocalcemic primary hyperparathyroidism in patients with recurrent kidney stones: pathological analysis of parathyroid glands

et al. 2006

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The lack of overt elevation of serum calcium concentration in some patients suffering from primary hyperparathyroidism is an intriguing clinical phenomenon. Previous studies have substantiated abnormal parathyroid tissue in these patients, but the extent and mode of derangements remained largely undefined. The parathyroid tissues from patients of normocalcemic primary hyperparathyroidism (NCPHPT) and those having normal parathyroid glands, hypercalcemic primary hyperplasia, secondary hyperplasia, and adenoma were compared by undertaking quantitative immunohistochemistry analysis on tissue microarray. The statistic results suggested that the parathyroid tissue of NCPHPT approximates more to normal gland than to its counterpart in other groups of parathyroid proliferative diseases in terms of the lack of significant alterations of calcium-sensing receptor (CaSR), chromogranin A (CGA), parathyroid hormone (PTH), and proliferation index (Ki67). On the other hand, the depressed vitamin D receptor (VitDR) and elevated cyclin D1 (CyD1) of NCPHPT indicated the inherent functional abnormalities in parathyroid cells. Our results imply that inherent functional disengagement may exist between CaSR and CyD1 or between CaSR and VitDR or both in parathyroid cells of symptomatic NCPHPT. Lack of enhanced release of CGA and PTH and discordance between proliferative activity and CyD1 expression in parathyroid cells may further hinder the development of hypercalcemia.

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A study of parathyroid hyperplasia in chronic renal failure

Cited by 6 publications

References 27 publications

Medical and Surgical Treatment for Secondary and Tertiary Hyperparathyroidism

Medical and Surgical Treatment for Secondary and Tertiary Hyperparathyroidism

Deletion of 11q23 and Cyclin D1 Overexpression Are Frequent Aberrations in Parathyroid Adenomas

Normocalcemic primary hyperparathyroidism in patients with recurrent kidney stones: pathological analysis of parathyroid glands

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