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Endocrine Abstracts (2014) 35 P977 | DOI: 10.1530/endoabs.35.P977

1Department of Endocrinology, Diabetology and Internal Medicine, Medical University, Bialystok, Poland, 2Centre for Clinical Research, Medical University, Bialystok, Poland, 3Department of Human Anatomy, Medical University, Bialystok, Poland.


Aim: In Hashimoto thyroiditis (HT) thyroid cells show abnormalities in the intracellular iodine metabolism, associated with the changes in the expression of key proteins involved in the biosynthesis of: thyroid peroxidase (TPO), thyroglobulin (Tg), sodium iodide symporter (NIS) and pendrin. The aim of the present study was to compare the expression of thyroid-specific genes, such as NIS and Tg, as well as pro-inflammatory cytokines, such as tumor necrosis factor-α (TNFα) and interleukin 1β in patients with HT and healthy individuals.

Subjects and methods: Thyroid cell were obtained from 39 patients with HT and 15 controls by an ultrasound guided fine-needle aspiration biopsy. Gene expression was assessed by quantitative RT-PCR.

Results: The patients with HT had significantly lower Tg and NIS mRNA (P=0.002 and P=0.001 respectively), as well as higher TNFα mRNA expression (P=0.049) than the controls. In the HT group Tg mRNA expression correlated positively with NIS mRNA expression (R=0.739, P=0.0001) and thyroid volume (R=0.465, P=0.0005), as well as negatively with TNFα mRNA expression (R=−0.490, P=0.001) and anti-peroxidase antibodies (TPOAb) level (R=−0.482, P=0.0002), whereas NIS mRNA expression correlated positively with thyroid volume (R=0.319, P=0.02), as well as negatively with TNFα mRNA expression (R=−0.529, P=0.0006), TNFα serum concentration (R=−0.320, P=0.001) and TPOAb level (R=−0.422, P=0.001).

Conclusions: Our results suggest a decreased Tg and NIS expression in thyroid cells of the patients with HT, which may result in reduced active iodide transport and thyroid hormone biosynthesis, as well as reduced thyroid volume. We should also mention that higher TNFα mRNA expression and serum TNFα concentration in the patients with HT, as well as a positive association between TNF-α and TPOAb levels might confirm a contribution of this pro-inflammatory cytokine to the development of Hashimoto thyroiditis.

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