Endocrine Abstracts

Tumor growth is limited by its neoangiogenesis, which is dependent on dynamic balance beetween it’s activators and inhibitors. One of the most important antiangiogenic factor is endostatin. Therefore we hypothesized, that serum endostatin concentration would differ between patients with metastatic and non-metastatic thyroid cancer, with multinodular goiter and healthy subjects. We also hypothesized that endogenous TSH stimulation would effect serum endostatin level.

The study group consisted of 64 (55 females, 9 men), aged 44. 9±12.3 year, with differentiated thyroid cancer, treated in our department in the years 2003–2006. All patients had undergone total or near total thyroidectomy and radioactive iodine treatment, that had resulted in remission in 52 patients and persistent/recurrent disease in 12 patients. The study included two control groups – 30 patients with non-toxic multinodular goiter and 30 healthy subjects.

Serum endostatin concentration was was significantly higher in patients with distant metastases than in patients with remission (141 95 vs 105 345 ng/ml, P<0.05). This was not observed in patients with locoregional metastases. During endogenous TSH stimulation, endostatin levels significantly decreased (122 94 vs 9360 ng/ml, P<0.05). Serum endostatin levels in patients with metastases correlated with Tg levels. This was not observed in patients with remission.

Serum endostatin levels might be used as an additional marker of thyroid cancer with distant metasases. Endogenous TSH stimulation decreases endostatin levels in patients either with and without thyroid tissue, suggesting its regulatory effects through receptors located outside the thyrocytes.