title: Soluble endothelium-associated adhesion molecules in patients with Graves' disease.
abstract: The targeting and recruitment of inflammatory cells to vascular endothelium in Graves' disease (GD) is mediated by intercellular adhesion molecule-1 (ICAM-1), endothelial leucocyte adhesion molecule-1 (ELAM-1), and vascular cell adhesion molecule-1 (VCAM-1). We have studied serum levels of soluble ICAM-1 (sICAM-1), soluble ELAM-1 (sELAM-1), and soluble VCAM-1 (sVCAM-1) in patients with GD (n = 21) and in patients with iodine-deficient goitre (IDG) (n = 23). The serum levels of sICAM-1 were markedly elevated in patients with GD before treatment with thiamazole (median 560 ng/ml versus 185 ng/ml in patients with IDG). In addition, elevated serum concentrations of sELAM-1 (median 85 ng/ml versus 33 ng/ml, respectively) and sVCAM-1 (median 42 ng/ml versus 15 ng/ml, respectively) were observed in patients with GD (P < 0.01 for all). The serum levels of sELAM-1 and sVCAM-1 dropped significantly after initiation of therapy and were within the normal range after 4, and 8 weeks of therapy, respectively. Serum levels of sICAM-1 were elevated even after 8 weeks of therapy. Serum levels of sVACM-1 and sICAM-1 correlated with the serum concentrations of anti-thyroid-stimulating hormone (TSH)-receptor antibodies (TSHR-R) (n = 21; r = 0.929 and r = 0.810, respectively) and anti-thyroid peroxidase antibodies (TPO-Ab) (n = 21; r = 0.673 and r = 0.750, respectively). However, no correlation between sELAM-1 and TPO-Ab, TSHR-R, and anti-thyroglobulin antibodies (Tg-Ab), respectively, could be found. In addition to thyroid hormones and autoantibodies, serum concentrations of sELAM-1 and sVCAM-1, but not sICAM-1, could be useful as clinical markers for disease activity.
authors.affiliation: Department of Infectious Diseases, Internal Medicine I, University of Vienna, Austria.
authors.forename: C
authors.initials: C
authors.lastname: Wenisch
authors.forename: D
authors.initials: D
authors.lastname: Myskiw
authors.forename: B
authors.initials: B
authors.lastname: Parschalk
authors.forename: T
authors.initials: T
authors.lastname: Hartmann
authors.forename: K
authors.initials: K
authors.lastname: Dam
authors.forename: W
authors.initials: W
authors.lastname: Graninger
mesh_terms: D001323:Autoantibodies / Q000097:blood*; D015815:Cell Adhesion Molecules / Q000097:blood*; D019040:E-Selectin; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D006042:Goiter / Q000378:metabolism; D006111:Graves Disease / Q000188:drug therapy / Q000378:metabolism*; D006801:Humans; D007124:Immunoenzyme Techniques; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007455:Iodine / Q000172:deficiency; D008297:Male; D008713:Methimazole / Q000627:therapeutic use; D013963:Thyroid Hormones / Q000097:blood; D013974:Thyroxine / Q000627:therapeutic use; D019010:Vascular Cell Adhesion Molecule-1
chemical_list: D001323:Autoantibodies; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D013963:Thyroid Hormones; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D008713:Methimazole; D007455:Iodine; D013974:Thyroxine