Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2015) 37 EP967 | DOI: 10.1530/endoabs.37.EP967

ECE2015 Eposter Presentations Thyroid (non-cancer) (160 abstracts)

Immunohistochemical expression of Claudin-1 in Hashimoto's thyroiditis and Graves' disease patients

Tatjana Zake 1 , Sandra Skuja 1 , Katrina Pekarska 1 , Valerija Groma 1 , Ilze Konrade 1 & Regina Kleina 2


1Riga Stradins University, Riga, Latvia; 2Riga Eastern Clinical University Hospital, Riga, Latvia.


Introduction: Autoimmune thyroid diseases, including Graves’ disease (GD) and Hashimoto’s thyroiditis (HT), are complex diseases combining genetic susceptibility and environmental encounters leading to the breakdown of immune tolerance. The relationship between thyroid cancer (TC) and HT has been proven (Guarino et al. 2010), and the antibody specific association has been demonstrated (Azizi et al. 2014). Overexpression of claudin-1 appears to be an early finding in TC.

Aim: To estimate expression of claudin-1 in the thyroid tissue of patients with HT and GD assessed by immunohistochemistry.

Materials and methods: Patients presenting 17 cases of HT, 7 of GD, and 11 cases of ordinary colloidal goiter with normal thyroid function were enrolled in this study. Immunohistochemical staining was performed using an anti-claudin-1 antibody. The expression levels were calculated semiquantitatively.

Results: Claudin-1 showed a circumferential membranous staining pattern in thyroid follicular epithelial cells. Positive claudin-1 expression (staining in >5% of the cells) was observed in 27 out of 35 cases (77.1%). The highest claudin-1 mean expression level was observed in HT patients, although six out of 17 cases showed negative claudin-1 expression. The mean claudin-1 expression level in HT and GD thyroid cells was calculated as 1.65±0.63 and 1.22±0.19 respectively, whereas, in control group it was estimated as 1.58±0.44. Only eight out of 35 cases (22.9%) showed claudin-1 positivity in >50% of the cells (score 4); six of which presented with HT and 2 – with colloidal goitre.

Conclusion: These results demonstrate that HT and GD patients display different junction protein expression patterns. The overexpression of claudin-1 in HT when compared to control tissues and GD patients may be interpreted similarly to overexpression of claudins in epithelial-derived cancers, including TC, however, molecular mechanisms by which claudins affect tumourigenesis remain largely unknown.

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