Introduction: The growth of a tumour is limited by its neovascularisation. Angiogenesis is dependent on a dynamic balance between its activators and inhibitors. One of the most important antiangiogenic factors is endostatin. The aim of the study was to assess the usefulness of serum endostatin levels as a potential marker of metastases of well-differentiated thyroid cancer, and to estimate the effect of endogenous TSH stimulation on serum endostatin levels.
Material and methods: The study group consisted of 68 patients with differentiated thyroid cancer. We provided a cross-sectional analysis of the study group divided into patients with distant and/or locoregional metastases and patients with remission, and compared it with serum endostatin levels of healthy volunteers. Serum endostatin concentration was measured by ELISA kits (R & D Systems).
Results: Median endostatin concentration was significantly higher in patients with distant metastases than in patients with remission (141.95 v. 105.345 ng/ml, p < 0.05). This was not observed in patients with locoregional metastases. Serum endostatin levels were significantly higher in the study group, including patients with remission, than in the control group of healthy volunteers (remission v. healthy median 105.3 v. 88.1 ng/ml, p < 0.05). During endogenous TSH stimulation, endostatin levels significantly decreased (122.94 v. 93.60 ng/ml, p < 0.05).
Conclusions: The study indicates that endogenous TSH stimulation plays a role in the regulation of endostatin secretion. Although median serum endostatin levels are higher in patients with distant metastases than in patients with remission, its clinical usefulness is limited due to the overlapping data between the study groups. (Pol J Endocrinol 2010; 61 (1): 7-12).