title: Lack of increased serum interleukin-6 and soluble IL-6 receptor concentrations in patients with thyroid diseases following recombinant human interferon alpha therapy.
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.
authors.affiliation: Centro per lo Studio, Prevenzione, Diagnosi e Cura delle Tireopatie, Universitá degli Studi di Parma, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Minelli
authors.forename: G
authors.initials: G
authors.lastname: Girasole
authors.forename: M
authors.initials: M
authors.lastname: Pedrazzoni
authors.forename: N
authors.initials: N
authors.lastname: Giuliani
authors.forename: C
authors.initials: C
authors.lastname: Schianchi
authors.forename: T
authors.initials: T
authors.lastname: Giuberti
authors.forename: L E
authors.initials: LE
authors.lastname: Braverman
authors.forename: M
authors.initials: M
authors.lastname: Salvi
authors.forename: E
authors.initials: E
authors.lastname: Roti
mesh_terms: D015703:Antigens, CD / Q000032:analysis*; D005260:Female; D006521:Hepatitis, Chronic / Q000628:therapy; D006801:Humans; D006980:Hyperthyroidism / Q000097:blood / Q000209:etiology; D016898:Interferon-alpha / Q000009:adverse effects* / Q000627:therapeutic use; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D018123:Receptors, Interleukin / Q000032:analysis*; D019947:Receptors, Interleukin-6; D011994:Recombinant Proteins / Q000009:adverse effects / Q000627:therapeutic use; D013959:Thyroid Diseases / Q000097:blood / Q000209:etiology*; D013971:Thyrotoxicosis / Q000097:blood / Q000209:etiology
chemical_list: D015703:Antigens, CD; D016898:Interferon-alpha; D015850:Interleukin-6; D018123:Receptors, Interleukin; D019947:Receptors, Interleukin-6; D011994:Recombinant Proteins