Primary hyperparathyroidism is the clinical result of
parathyroid adenoma or
hyperplasia, rarely of
carcinoma. Clinical, serologic, and radiologic data are unable to discriminate a single
parathyroid adenoma from an enlarged hyperplastic gland. Morphologic features also overlap in
adenoma and small hyperplastic gland. Studying immunohistochemical expression of
fatty acid synthase (FAS), p53, Ki67 and bcl-2, we found that among 21
adenomas 19 (90.5%) were positive for FAS, 12 (57.2%) for Ki67, 11 (52.4%) for p53, and 16 (76.2%) for bcl-2; among 12
hyperplasias, 12 (100%) were positive for FAS, 6 (50%) for KI67, 8 (66.7%) for p53, and 8 (66.7%) for bcl-2. Statistical analysis showed that FAS was associated with
parathormone (PTH) (P =.001), Ki67 (P =.01), and p53 (P =.01). Moreover, FAS was associated with hyperplastic (P =.0001) and adenomatous glands (P =.0001). Ki67 was associated with both adenomatous (P =.02) and hyperplastic glands (P =.005). P53
protein were associated only with hyperplastic glands (P =.01). The different occurrence of p53 in parathyroids
adenoma and
hyperplasia may enable a different management and follow-up of the patients with
primary hyperparathyroidism, stratifing them into two groups. The first, with a "false"
adenoma having a high risk of relapse, may necessitate exams like serum
calcium levels, PTH concentrations, urinary
calcium levels for 24 hours, kidney functional tests, and radiology and ultrasound every 3 to 6 months, whereas the second with "true"
adenoma, at low risk of relapse, may be checked less frequently with serum
calcium levels and PTH concentrations.