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.

Lack of increased serum interleukin 6 and soluble IL6 receptor concentrations in patients with thyroid diseases following recombinant human interferon a therapy / Minelli, Roberta; Girasole, G; Pedrazzoni, Mario; Giuliani, Nicola; Schianchi, C; Giuberti, T; Braverman, L. E.; Salvi, M; Roti, E.. - In: JOURNAL OF INVESTIGATIVE MEDICINE. - ISSN 1081-5589. - 44:(1996), pp. 370-374.

Lack of increased serum interleukin 6 and soluble IL6 receptor concentrations in patients with thyroid diseases following recombinant human interferon a therapy.

MINELLI, Roberta;PEDRAZZONI, Mario;GIULIANI, Nicola;
1996-01-01

Abstract

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.
1996
Lack of increased serum interleukin 6 and soluble IL6 receptor concentrations in patients with thyroid diseases following recombinant human interferon a therapy / Minelli, Roberta; Girasole, G; Pedrazzoni, Mario; Giuliani, Nicola; Schianchi, C; Giuberti, T; Braverman, L. E.; Salvi, M; Roti, E.. - In: JOURNAL OF INVESTIGATIVE MEDICINE. - ISSN 1081-5589. - 44:(1996), pp. 370-374.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11381/1496397
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