LACK OF INCREASED SERUM INTERLEUKIN-6 AND SOLUBLE IL-6 RECEPTOR CONCENTRATIONS IN PATIENTS WITH THYROID-DISEASES FOLLOWING RECOMBINANT HUMAN INTERFERON-ALPHA THERAPY

Citation
R. Minelli et al., LACK OF INCREASED SERUM INTERLEUKIN-6 AND SOLUBLE IL-6 RECEPTOR CONCENTRATIONS IN PATIENTS WITH THYROID-DISEASES FOLLOWING RECOMBINANT HUMAN INTERFERON-ALPHA THERAPY, Journal of investigative medicine, 44(6), 1996, pp. 370-374
Citations number
28
Categorie Soggetti
Medicine, Research & Experimental","Medicine, General & Internal
ISSN journal
10815589
Volume
44
Issue
6
Year of publication
1996
Pages
370 - 374
Database
ISI
SICI code
1081-5589(1996)44:6<370:LOISIA>2.0.ZU;2-Q
Abstract
Background: Serum interleukin-6 (IL-6) concentrations are frequently e levated in inflammatory thyroid diseases, such as subacute thyroiditis and amiodarone induced thyroiditis. We and others have recently obser ved that recombinant interferon-alpha (rIFN-alpha) therapy for chronic , active viral hepatitis and malignant disorders may induce thyroid dy sfunction, 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 th erapy. Methods: Studies were carried out in 37 patients treated with r IFN-alpha for chronic, active viral hepatitis. Thyroid function tests and serum IL-6 and sIL-6R were measured before and during rIFN-alpha t herapy. Results: Six patients developed inflammatory or destructive th yrotoxicosis confirmed by elevated serum free T4 or free T3 concentrat ions, suppressed serum thyroid-stimulating hormone (TSH) values, and a low thyroid radioactive iodine uptake. Serum IL-6 and sIL-6R concentr ations were not elevated in these patients with rIFN-alpha-induced thy roiditis. Conclusions: These results suggest that serum IL-6 concentra tions are not useful in differentiating between inflammatory thyrotoxi cosis 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 s ecretion of IL-6.