title: [Increased serum soluble Fas ligand in hyperthyroid Graves' disease].
abstract: The interaction of Fas with its ligand (FasL) regulates a number of physiological and pathophysiological process of cell death or apoptosis. Recent studies suggest that Fas and Fas ligand (FasL) interactions among thyrocytes from patients with Hashimoto disease which is caused by thyroid autoimmunity may contribute to clinical hypothyroidism. The role of Fas-FasL interaction in the pathophysiology of Graves' disease has not well been determined. The serum levels of soluble Fas (sFas) and FasL (sFasL) were measured in 48 Japanese patients with Graves' disease (U; untreated hyperthyroidism, T; hyperthyroidism under treatment, E; euthyroidism under treatment and R; remission), destructive thyroiditis (D), subacute thyroiditis (S) and 40 normal controls using commercially available ELISA kits. The levels of sFas (mean +/- SD, ng/ml) were 0.93 +/- 0.30 in normal controls (n = 32), 2.41 +/- 1.28 in U (n = 19), 2.44 +/- 0.79 in T (n = 16), 2.37 +/- 0.55 in E (n = 12), and 2.30 +/- 0.11 in R (n = 6), 2.42 +/- 0.37 in D (n = 3) and 2.68 +/- 0.17 in S (n = 3). There were no significant differences of sFas levels among any groups. While, the mean levels of sFasL (ng/ml) of normal controls were 0.058 +/- 0.02 (n = 40), and those of patients with hyperthyroid Graves' disease (U; 0.34 +/- 0.09 and T; 0.26 +/- 0.05), were significantly higher than those in normal controls (p < 0.005) and with subacute thyroiditis (0.097 +/- 0.001, vs U; p < 0.01, vs T; p < 0.05) but not different from those in E, R and D (E; 0.34 +/- 0.09, R; 0.25 +/- 0.07 and D; 0.31 +/- 0.11, respectively). There was a significant correlation between serum thyrotropin receptor antibody (TRAb) and free thyroxine levels (p < 0.01) while there were no correlation between sFas and sFasL levels and TRAb or free thyroxine levels. The results indicate that the Fas-FasL system contributes to the pathophysiology of hyperthyroid Graves' disease although serum sFas and sFasL levels do not appear to be useful indicators in evaluating disease activity.
authors.affiliation: Clinical Laboratory Medicine, Kochi Medical School, Nankoku.
authors.forename: K
authors.initials: K
authors.lastname: Takeda
authors.forename: E
authors.initials: E
authors.lastname: Ohara
authors.forename: T
authors.initials: T
authors.lastname: Kaneda
authors.forename: K
authors.initials: K
authors.lastname: Hashimoto
authors.forename: M
authors.initials: M
authors.lastname: Sasaki
mesh_terms: D015551:Autoimmunity; D015415:Biomarkers / Q000097:blood; D053222:Fas Ligand Protein; D006111:Graves Disease / Q000276:immunology / Q000503:physiopathology*; D006801:Humans; D008562:Membrane Glycoproteins / Q000097:blood*; D012995:Solubility; D019014:fas Receptor / Q000097:blood*
chemical_list: D015415:Biomarkers; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019014:fas Receptor