PARATHYROID CARCINOMA
Parathyroid carcinoma is responsible for <1% of cases of primary hyperparathyroidism.1,4,17,22,23 Often, the tumors are larger than adenomas, with an average weight of 12 g. Microscopically, parathyroid carcinoma is characterized by a trabecular arrangement of tumor cells (the latter divided by thick, fibrous bands), capsular and blood vessel invasion, and the presence of mitotic figures.17,22,23 The mitotic figures must be found in tumor cells, not in stromal or endothelial elements22 (Fig. 48-7). Cellular atypia, frequently found in benign parathyroid tumors, is uncommon in parathyroid carcinoma.17,22 The mere presence of capsular invasion cannot be equated with malignancy in a parathyroid tumor because large parathyroid adenomas may have undergone prior hemorrhage, with subsequent fibrosis and trapping of tumor cells within the capsule. Similarly, vascular invasion is difficult to determine, except if seen outside the vicinity of the neoplasm. Grossly, the surgeon often notes that the gland is adherent to or invasive into neighboring tissues (e.g., nerve, esophagus). Metastases at the time of presentation are unusual, but they may be found in local or regional lymph nodes. Indeed, in some patients, the diagnosis
of parathyroid carcinoma may not be made until metastases appear. The loss of the retinoblastoma (Rb) tumor-suppressor gene formerly was considered to be a marker for parathyroid carcinoma.24 However, its loss in some adenomas and its retention in some carcinomas have diminished the diagnostic usefulness of testing for loss of Rb in parathyroid tumors.23
of parathyroid carcinoma may not be made until metastases appear. The loss of the retinoblastoma (Rb) tumor-suppressor gene formerly was considered to be a marker for parathyroid carcinoma.24 However, its loss in some adenomas and its retention in some carcinomas have diminished the diagnostic usefulness of testing for loss of Rb in parathyroid tumors.23

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