Use of cxcl10 levels to predict thyroid autoimmunity following ifn-α therapy


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Rotondi M _ et al_. (2007) Serum CXCL10 levels and occurrence of thyroid dysfunction in patients treated with interferon-α therapy for hepatitis C virus-related hepatitis. _Eur J Endocrinol_


156: 409–414 Interferon (IFN)-α therapy is standard for patients with chronic hepatitis C virus infection, although this treatment is associated with the development of thyroid


autoimmunity. The chemokine CXC ligand number 10 (CXCL10) is involved in the pathogenesis of several thyroid-related autoimmune diseases. Rotondi and colleagues investigated whether


pretreatment levels of CXCL10 predict thyroid autoimmunity development in patients who undergo IFN-α therapy. This retrospective study included 25 patients (18 males) with hepatitis C


virus-related chronic hepatitis, and 50 age- and sex-matched healthy controls. The patients were given recombinant IFN-α–2a three times per week for at least 6 months. Patients were assigned


to two groups: those patients who did not develop thyroid autoimmune dysfunction during treatment (Group I, _n_ = 15), and those who did (Group II, _n_ = 10). Levels of CXCL10 were measured


before IFN-α therapy, and then at 2, 4 and 6 months after the first treatment session. Patients in Group I had higher pretreatment serum CXCL10 levels than those in Group II (308.6 ± 130.7


pg/ml versus 191.1 ± 69.4 pg/ml, _P_ <0.05); this trend was consistent at all time points throughout treatment. A larger proportion of patients in Group II had a favorable response to


IFN-α therapy than in Group I (90% versus 33%). The authors conclude that pretreatment CXCL10 measurement can identify those patients more likely to respond well to IFN-α therapy and to


develop thyroid autoimmunity; these patients should be carefully monitored with thyroid surveillance throughout treatment. RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE


CITE THIS ARTICLE Use of CXCL10 levels to predict thyroid autoimmunity following IFN-α therapy. _Nat Rev Endocrinol_ 3, 502 (2007). https://doi.org/10.1038/ncpendmet0521 Download citation *


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