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DOI: 10.1055/s-0031-1271620
© Georg Thieme Verlag KG Stuttgart · New York
Influence of Methimazole and Radioactive Iodine Treatment in the Serum Levels of the Chemokine CXCL10 in Hyperthyroid Patients with Graves’ Disease
Publikationsverlauf
received 03.08.2010
accepted 14.12.2010
Publikationsdatum:
31. Januar 2011 (online)

Abstract
The chemokine CXCL10 plays an important role in Graves’ disease (GD); however, data regarding the effectiveness of therapy are contradictory. Serum CXCL10 levels in 31 hyperthyroid patients were measured before and after establishing euthyroidism: 16 newly diagnosed GD patients received methimazole (MMI), 15 relapsed GD patients were treated with radioactive iodine (RAI), and 18 healthy subjects served as a control group. Baseline serum CXCL10 levels were higher than in controls (MMI group 144.0±48.24, RAI group 156.3±71.81 and control 71.32±26.03 pg/ml;p<0.01). In the MMI group, serum CXCL10 levels decreased following euthyroidism at 6 months (76.51±22.06 pg/ml; p<0.01) and 12 (76.42±34.07 pg/ml; p<0.01). In the RAI group, serum CXCL10 levels decreased after 3, 6, 9, and 12 months of RAI administration (82.37±55.01, 66.35±48.62, 68.76±28.87, and 74.94±49.74 pg/ml, respectively; p<0.05). Elevated serum TRAb levels in the MMI group (33.15±30.84) decreased at 6 months (14.64±16.57 IU/l; p=0.0070), whereas in the RAI group (44.61±60.66 IU/l) they increased to a peak level at 6 months (66.40±104.2 IU/l; p=0.003), which was significantly higher than those of the MMI group, but were decreased at 12 months (28.91±35.13 IU/l). Serum CXCL10 levels correlated with FT3 (r=0.48, p<0.0001), FT4 (r=0.47, p<0.0001) and TRAb (r=0.37, p=0.0014). In conclusion, these data show a relationship between serum CXCL10 and GD activity and suggest that a more complex mechanism is involved in the generation of the thyroid auto-antibodies TPOAb and TRAb.
Key words
hyperthyroidism - autoimmunity - CXC chemokines - CXL10 - autoantibodies - TSH-receptor antibodies - antibodies to thyroperoxidase
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Correspondence
J. H. Romaldini
Endocrinology Division
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