Literature DB >> 9099983

Comparative analysis of clonality and pathology in primary and secondary hyperparathyroidism.

L Shan1, M Nakamura, Y Nakamura, D Inoue, S Morimoto, T Yokoi, K Kakudo.   

Abstract

Parathyroid adenoma and hyperplasia are the most common causes for hyperparathyroidism, and distinction between them is controversial based on the current criteria for pathological diagnosis. We studied the clonality of hyperparathyroidism and its correlation with the pathological features, analysing 39 female patients with hyperparathyroidism. Clonality was successfully detected in 12 heterozygous cases by PCR amplification of PGK-1 gene. The 12 cases yielded 14 hypercellular glands, 8 affected by primary and 6 by secondary hyperparathyroidism. The results revealed that 7 of the 8 glands with primary hyperparathyroidism showed monoclonal proliferation. Only 1 gland pathologically diagnosed as adenoma showed a polyclonal pattern. In the 4 cases with secondary hyperparathyroidism, at least one monoclonal tumour was detected in each case. Our data indicate that monoclonal tumours are more common than expected in both primary and secondary hyperparathyroidism. Monoclonal tumours and polyclonal hyperplasia can co-exist in the same patient. Comparative study of the clonality and the pathological features showed that the clonality was consistent with the diagnosis of parathyroid adenoma, whereas it was in conflict with the diagnosis of hyperplasia with multigland involvement. One of the reasons for this is that we are ignorant of the true natures of hyperparathyroidism with multigland involvement.

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Year:  1997        PMID: 9099983     DOI: 10.1007/bf01324809

Source DB:  PubMed          Journal:  Virchows Arch        ISSN: 0945-6317            Impact factor:   4.064


  21 in total

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Journal:  Hum Pathol       Date:  1994-03       Impact factor: 3.466

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Journal:  J Clin Invest       Date:  1995-05       Impact factor: 14.808

10.  Clonality and X-inactivation patterns in hematopoietic cell populations detected by the highly informative M27 beta DNA probe.

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  10 in total

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3.  Polyclonal origin of parathyroid tumors is common and is associated with multiple gland disease in primary hyperparathyroidism.

Authors:  Yuhong Shi; Pedram Azimzadeh; Sarada Jamingal; Shannon Wentworth; Janice Ferlitch; James Koh; Nariman Balenga; John A Olson
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Review 5.  Potential applications of molecular biology in neuroendocrine tumors.

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Review 6.  Hyperparathyroidism and malnutrition with severe vitamin D deficiency.

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7.  Parathyroid invasion, nodal recurrence, and lung metastasis by papillary carcinoma of the thyroid.

Authors:  K Kakudo; W Tang; Y Ito; Y Nakamura; H Yasuoka; S Morita; A Miyauchi
Journal:  J Clin Pathol       Date:  2004-03       Impact factor: 3.411

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Authors:  Xavier Sanjuan; Bonita R. Bryant; Mark E. Sobel; Maria I. Merino
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9.  Clonal emergence in uremic parathyroid hyperplasia is not related to MEN1 gene abnormality.

Authors:  L Shan; Y Nakamura; M Murakami; M Nakamura; A Naito; K Kawahara; H Utsunomiya; I Mori; K Kakudo
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10.  Calcium intake and risk of primary hyperparathyroidism in women: prospective cohort study.

Authors:  Julie M Paik; Gary C Curhan; Eric N Taylor
Journal:  BMJ       Date:  2012-10-17
  10 in total

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