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