Clinicians may be able to distinguish between parathyroid adenomas and parathyroid proliferative lesions by virtue of increased angiogenesis in the former, Greek scientists believe.
"The pathological distinction between parathyroid neoplasms and hyperplasias remains difficult in several cases," the team writes in the European Journal of Endocrinology.
Studies have shown, however, that the proliferation-associated and hypoxia-inducible protein endoglin (CD105) is abundantly expressed in angiogenic endothelial cells. In turn, vascular endothelial growth factor (VEGF) induces angiogenesis, and VEGF-R2 is a tyrosine kinase receptor expressed early in development by endothelial cell precursors.
Thomas Papathomas and co-workers, from the National and Kapodistrian University of Athens, therefore investigated whether immunohistochemical expression of CD105, VEGF, and VEGF-R2 would be of use in distinguishing between parathyroid adenomas and parathyroid proliferative lesions.
They examined tissue samples from 38 patients with primary hyperparathyroidism (HPT), 17 of whom had adenomas and 21 who had primary hyperplasias, and 30 patients with secondary HPT.
Revealingly, samples from parathyroid adenomas showed significantly greater CD105 immunoreaction than primary and secondary hyperplasia specimens.
Moreover, VEGF immunoreaction was much more prevalent among adenoma samples than primary and secondary hyperplasia tissues.
Samples with secondary hyperplasia showed VEGF-R2 immunoreactivity that was positively and significantly linked with VEGF expression, as well as with the apoptotic index of parathyroid cells.
Finally, in secondary hyperplasia specimens, an inverse correlation between cyclin D1 immunoexpression and angiogenic indexes, such as CD105 and VEGF, was observed.
"This study shows increased angiogenesis in parathyroid adenomas compared with parathyroid proliferative lesions," Papathomas et al conclude.