Serum levels of the interferon‐γ‐inducible α chemokine CXCL10 in patients with active Graves’ disease, and modulation by methimazole therapy and thyroidectomy. BJS 2006; 93: 1226-1231.
Published: 13th July 2006
Authors: A. Antonelli, P. Fallahi, M. Rotondi, S. M. Ferrari, M. Serio, P. Miccoli et al.
The interferon‐γ‐inducible chemokine CXCL10 is highly expressed in infiltrating inflammatory cells, and in thyrocytes in patients with Graves' disease. The aim of this study was to measure serum levels of CXCL10 in relation to thyroid function and treatment.
Serum levels of CXCL10 were measured in 22 patients with Graves' disease when hyperthyroid, when euthyroid under methimazole therapy, and 3 days after near‐total thyroidectomy. They were compared with levels in three groups of age‐ and sex‐matched controls: 44 subjects with no thyroid disorder, 44 patients with euthyroid autoimmune thyroiditis and 20 with toxic nodular goitre.
Basal serum levels of CXCL10 in patients with Graves' disease were higher than levels in patients with toxic nodular goitre or no thyroid disorder, and similar to levels in patients with autoimmune thyroiditis (mean(s.d.) 167(121), 100(24), 78(46) and 142(107) pg/ml respectively; P < 0·010). Among patients with Graves' disease, serum levels of CXCL10 were significantly higher in those aged over 50 years (P = 0·010), with a hypoechoic pattern at thyroid ultrasonography (P < 0·001) or with hypervascularity (P = 0·001). CXCL10 levels in patients with Graves' disease decreased significantly when euthyroidism was achieved by methimazole therapy (P < 0·010), and a further decrease was observed after thyroidectomy (P < 0·010).
Serum levels of CXCL10 are higher in newly diagnosed hyperthyroid patients with Graves' disease than in those with toxic nodular goitre, and decrease when euthyroidism is achieved with antithyroid therapy. This high level may be related to the active inflammatory phase of Graves' disease. A further reduction of CXCL10 levels after thyroidectomy indicates that it is produced mainly in the thyroid in patients with autoimmune thyroid disease. Copyright © 2006 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.Full text