title: Soluble Fas is increased in hyperthyroidism independent of the underlying thyroid disease.
abstract: In Hashimoto's thyroiditis, Fas-induced apoptosis is one of the mechanisms leading to cell destruction, whereas thyroid tissue in Graves' disease is prevented from it. The soluble form of the Fas molecule produced by alternative splicing prevents from apoptosis. We measured soluble Fas in the sera of 112 patients with Graves' disease, 21 patients with toxic goiter, and 24 patients with subclinical hyperthyroidism due to suppressive therapy with levothyroxine after near-total resection of the thyroid gland for nodular goiter. Soluble Fas was increased in thyrotoxic patients, toxic goiter, and patients with subclinical hyperthyroidism. Decreased levels of soluble Fas were found in euthyroid patients with Graves' disease after surgery, whereas soluble Fas was normal in euthyroid patients with Graves' disease receiving antithyroid drug treatment and in patients in stable remission. There was a good correlation between soluble Fas with free T(3) (r = 0.6) and free T(4) (r = 0.5). Our results show that soluble Fas is increased in hyperthyroidism independent of the underlying thyroid disease.
authors.affiliation: Department of Endocrinology, Heinrich Heine University, D-40225 Dusseldorf, Germany. feldkamj@uni-duesseldorf.de
authors.forename: J
authors.initials: J
authors.lastname: Feldkamp
authors.forename: E
authors.initials: E
authors.lastname: Pascher
authors.forename: M
authors.initials: M
authors.lastname: Schott
authors.forename: P
authors.initials: P
authors.lastname: Goretzki
authors.forename: J
authors.initials: J
authors.lastname: Seissler
authors.forename: W A
authors.initials: WA
authors.lastname: Scherbaum
mesh_terms: D000328:Adult; D017209:Apoptosis / Q000187:drug effects; D018450:Disease Progression; D005260:Female; D006111:Graves Disease / Q000097:blood*; D006801:Humans; D006980:Hyperthyroidism / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011989:Receptors, Thyrotropin / Q000378:metabolism; D013971:Thyrotoxicosis / Q000378:metabolism; D014284:Triiodothyronine / Q000097:blood; D019014:fas Receptor / Q000378:metabolism*
chemical_list: D011989:Receptors, Thyrotropin; D019014:fas Receptor; D014284:Triiodothyronine