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Analysis reveals no rise in IL-6 levels in thyroid conditions post-rIFN-α therapy, suggesting limited diagnostic value.
Background Serum interleukin-6 (IL-6) concentrations are frequently elevated in inflammatory thyroid diseases, such as subacute thyroiditis and amiodarone induced thyroiditis. We and others have recently observed that recombinant interferon-alpha (rIFN-α) therapy for chronic, active viral hepatitis and malignant disorders may induce thyroid dysfunction, including thyrotoxicosis secondary to thyroiditis. Serum IL-6 and its soluble receptor (sIL-6R) have been measured for the first time in patients with chronic active hepatitis receiving rIFN-α therapy. Methods Studies were carried out in 37 patients treated with rIFN-α for chronic, active viral hepatitis. Thyroid function tests and serum IL-6 and sIL-6R were measured before and during rIFN-α therapy. Results Six patients developed inflammatory or destructive thyrotoxicosis confirmed by elevated serum free T4 or free T3 concentrations, suppressed serum thyroid-stimulating hormone (TSH) values, and a low thyroid radioactive iodine uptake. Serum IL-6 and sIL-6R concentrations were not elevated in these patients with rIFN-α-induced thyroiditis. Conclusions These results suggest that serum IL-6 concentrations are not useful in differentiating between inflammatory thyrotoxicosis and hyperthyroidism induced by rIFN-α therapy as is the case in amiodarone-induced thyrotoxicosis. It is possible that rIFN-α therapy could be associated with an inhibitory effect of rIFN-α on the release of IL-6 from damaged thyroid cells and not on the basal secretion of IL-6.
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Minelli et al. (1996) studied this question.
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