Introduction-objective: Fas-mediated thyroid cell apoptosis is differentially regulated in autoimmune thyroid disease (AITD) being up-regulated in Hashimotos thyroiditis (HT) and down-regulated in Graves disease (GD). The soluble form of Fas (sFas), lacking the transmembrane domain due to alternative splicing may inhibit apoptosis by binding to Fas ligand. In this preliminary study we examined whether sFas is also differentially expressed in patients with AITD.
Materials and methods: We studied 32 newly diagnosed patients, 17 with HT in subclinical hypothyroidism (35.47±13.74 years), 6 with hypothyroid HT (35.67±14.88 years) and 9 with GD (32.5±10.67 years). We also examined 9 age-matched healthy controls (30.22±11.18 years). In all subjects we measured serum sFas by ELISA together with thyroid function indices and thyroid antibodies.
Results: There was a non significant decrease in sFas levels in patients with subclinical hypothyroidism (2.37±0.66 ng/ml) compared to controls (2.8±0.75 ng/ml) but not in patients with clinical hypothyroidism (3.25±1.15 ng/ml). However, in patients with GD, mean sFas levels (4.47±1.0 ng/ml) were significantly higher compared with controls (P=0.001) and patients with HT (P=0.005).
Conclusion: sFas is differentially regulated in patients with AITD. The elevated sFas in GD may reflect reduced full length membrane Fas and may have a role in the inhibition of Fas-mediated apoptosis of thyrocytes in this condition.
01 - 05 Apr 2006
European Society of Endocrinology