Abstract
Clonal assessment suggests that most parathyroid adenomas and a subset of uremic parathyroid hyperplasia are monoclonal. A weakness that remains in the prior clonal studies is assessing the clonal status of the tissue fragments containing multiple nodules rather than a single nodule emerging in the uremic parathyroid hyperplasia. We applied the X chromosome-linked phosphoglycerate kinase (PGK) gene inactivation assay method for clonality to study individual nodules. Materials were obtained from 31 cases with parathyroid adenoma and 16 with uremic parathyroid hyperplasia. 17 cases were heterozygous in the PGK-1 locus. We were able to assess the clonality of 10 parathyroid adenomas and 7 hyperplastic glands. Monoclonality was demonstrable in 9 of the 10 parathyroid adenomas and in 4 of the 7 hyperplastic glands. Further analysis of 11 individual nodules microdissected from 3 monoclonal and 1 polyclonal hyperplastic glands revealed that 6 nodules were monoclonal and 5 were polyclonal. Nodules arising in a hyperplastic gland could be of monoclonal or polyclonal origin. Polyclonal and monoclonal nodules coexisted within single glands. Our findings indicate a progression from generalized hyperplasia to a monoclonal tumor in uremic parathyroid hyperplasia. Comparing clonality with the parathyroid hormone (PTH) immunoreactivity and histological features, we found that monoclonal nodules showed a homogeneous immunoreactivity against PTH antibody, whereas most of the polyclonal nodules showed a heterogeneous staining. Classic morphological criteria alone was inadequate to distinguish a monoclonal from a polyclonal nodule.
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Shan, L., Kakudo, K., Nakamura, M. et al. Clonality of the parathyroid nodules with uremic parathyroid hyperplasia. Pathol. Oncol. Res. 3, 198–203 (1997). https://doi.org/10.1007/BF02899921
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DOI: https://doi.org/10.1007/BF02899921