1. Lack of increased serum interleukin-6 and soluble IL-6 receptor concentrations in patients with thyroid diseases following recombinant human interferon alpha therapy.
- Author
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Minelli R, Girasole G, Pedrazzoni M, Giuliani N, Schianchi C, Giuberti T, Braverman LE, Salvi M, and Roti E
- Subjects
- Female, Hepatitis, Chronic therapy, Humans, Hyperthyroidism blood, Hyperthyroidism etiology, Interferon-alpha therapeutic use, Male, Receptors, Interleukin-6, Recombinant Proteins adverse effects, Recombinant Proteins therapeutic use, Thyroid Diseases blood, Thyrotoxicosis blood, Thyrotoxicosis etiology, Antigens, CD analysis, Interferon-alpha adverse effects, Interleukin-6 blood, Receptors, Interleukin analysis, Thyroid Diseases etiology
- Abstract
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-alpha) 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-alpha therapy., Methods: Studies were carried out in 37 patients treated with rIFN-alpha for chronic, active viral hepatitis. Thyroid function tests and serum IL-6 and sIL-6R were measured before and during rIFN-alpha 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-alpha-induced thyroiditis., Conclusions: These results suggest that serum IL-6 concentrations are not useful in differentiating between inflammatory thyrotoxicosis and hyperthyroidism induced by rIFN-alpha therapy as is the case in amiodarone-induced thyrotoxicosis. It is possible that rIFN-alpha therapy could be associated with an inhibitory effect of rIFN-alpha on the release of IL-6 from damaged thyroid cells and not on the basal secretion of IL-6.
- Published
- 1996