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The role of hyperplasia in multiple parathyroid adenomas
Author(s) -
Larian Babak,
Alavi Sassan,
Roesler John,
Namazie Ali,
Blackwell Keith,
Calcaterra Thomas C.,
Wang Marilene B.
Publication year - 2001
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/1097-0347(200102)23:2<134::aid-hed1008>3.0.co;2-j
Subject(s) - adenoma , parathyroid adenoma , hyperplasia , pathology , hyperparathyroidism , parathyroid neoplasm , immunohistochemistry , primary hyperparathyroidism , medicine , biology
Background Parathyroid adenoma is the most common cause of primary hyperparathyroidism (pHPT). Adenomas usually involve only a single gland, and the remaining glands are normal or suppressed. Multiple parathyroid adenomas have been reported to occur in as high as 11% of patients with pHPT. The significant incidence of multiple adenomas with histologic similarities to hyperplasia has raised the possibility that adenoma is a continuation of the hyperplasia state. To test this theory, we used molecular genetics to compare clonality and proliferative activity of parathyroid adenoma with its corresponding normal glandular tissue. Furthermore, we devised a scheme to definitively distinguish between the different parathyroid states on a molecular level, because histologic distinction is unreliable. Methods The study included three patients with a diagnosis of singular parathyroid adenoma and three with double parathyroid adenomas. Paraffin‐embedded surgical specimens of both adenomas and normal glands were retrieved from each patient. Clonal analysis of the phosphoglycerolkinase (PGK) gene has suggested that parathyroid adenomas are monoclonal. Clonality of parathyroid adenomas and normal parathyroid glands was studied by polymerase chain reaction–based restriction fragment length polymorphic analysis for the PGK gene. Proliferative activity of the specimens was also analyzed using the immunohistochemical markers PCNA and Ki‐67. Results All adenomas were monoclonal and all normal parathyroid glands were polyclonal for the PGK gene in both the single and double adenoma specimens. All adenomas stained positive for proliferative activity. In the three patients with singular adenoma, proliferative activity was not detected in the normal parathyroid tissue. However, in the double adenoma group, two of the three patients showed hyperproliferative activity in the normal glands. Conclusion Proliferative activity consistent with hyperplasia was present in some normal glands of multiple adenoma patients. Our observation supports the theory that multiple adenomas may be a continuation of the hyperplasia state. © 2001 John Wiley & Sons, Inc. Head Neck 23: 134–139, 2001.