ECE2009 Poster Presentations Thyroid (117 abstracts)
The changes of the IL-2,IL-4,IL-12, TNF-α and IFN-γ levels with L-thyroxine treatment in patients with Hashimoto's throiditis
Feyzullah Güçlü 1 , Bilgin Özmen 2 , Cengiz Kirmaz 2 , Sabriye Kafesçiler 2 , Fatma Taneli 2 & Zeliha Hekimsoy 2
1Department of Endocrinology, Antakya Government Hospital, Antakya, Turkey; 2Department of Endocrinology, Celal Bayar University Faculty of Medicine, Manisa, Turkey.
Background: Hashimoto’s thyroiditis is a chronic autoimmune thyroiditis. It is the most common cause of primary hypothyroidism in adolescent period, via autoimmune thyroid tissue destruction and affecting 2% of the population. In this study we want to investigate the role of the cytokines such as IL-2, IL-12, TNF-α and IFN-γ in the pathogenesis of the disease and the changes of cytokine levels with the L-thyroxine treatment.
Methods: About 65 female patients, aged 18–73 years with Hashimoto’s thyroiditis referred to Celal Bayar University Medical Faculty Endocrinology polyclinic were included in this study. After a 10–12 weeks L-thyroxin therapy period, all of the patients were turn into euthyroidic state. There was a statistically significant decrease in the levels of TSH (P<0.0001) and increase in the levels of FT4 (P<0.0001) at the same time. Also, the levels of anti-Tg (P<0.01) and anti-TPO (P<0.001) were significantly lower than pre-trreatment period. After the L-thyroxine treatment, a statistically significant decrease was shown (P<0.001) for the IL-12 levels. But decreasing of the IFN-γ levels was not statistically significant (P=0.276). On the other hand, no changes were determined of the IL-2 and IL-4 levels.
Conclusion: In our study which took a 10–12 week treatment (therapy) period, although there was a statistically significant decrease in serum IL-12 level, the statistically insignificant decrease in IFN-γ level can be interpreted as the inflammatory process in Th 1 type was stopped or slowed down.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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