Endocrine Abstracts

Introduction: Oxidative stress has been implicated in the pathogenesis of many thyroid diseases, such as non-toxic nodular goiter and Hashimoto’s thyroiditis. Nitric oxide synthases are responsible for the synthesis of nitric oxide from L-arginine. There are three isoforms of nitric oxide synthase (NOS): neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). They have important functions in inflammation and vasoregulation but their role in thyroid diseases is not well understood.

Methods: Thirty-one patients with thyroid goiter were included in the study: 18 cases with non-toxic nodular goiter (NTNG) and 13 patients with Hashimoto’s thyroiditis (HT). Normal glands served as controls. Frozen sections were incubated with purified mouse monoclonal antihuman antibodies against iNOS and eNOS. The dilution of the primary antibodies was 1:100 and was verified in a series of pilot experiments. The immunohistological investigations were performed by the BrightVision method from ImmunoLogic. The number of positively stained cells were counted and expressed as a mean value of at least 10 high power fields (HPF, 400x).

Results: Hashimoto’s thyroiditis demonstrated higher expression of both iNOS and eNOS in comparison with non-toxic nodular goiter and healthy thyroid gland. Positive staining for iNOS was observed in 96% of HT (4.6 cells/high power field - HPF), whereas only 42% of NTNG (2.1 cells/HPF) and 30% (1.9 cells/HPF) of healthy tissue showed immunoreactivity. eNOS was expressed in 89% of HT (4.1 cells/HPF), 40% of NTNG (2.0 cells/HPF) and 19% of healthy gland (1.9/HPF)

Conclusions: Oxidative stress markers could become indicators of disease activity and immunological phenotype. Alterations in the process of oxidative stress are implicated in the pathogenesis of autoimmune thyroid diseases, such as Hashimoto’s thyroiditis. However, the role of oxidative stress in inflammation of thyroid is still not completely known and further studies in this matter should be continued.