title: Soluble adhesion molecules and cytokines in patients with myasthenia gravis treated by plasma exchange.
abstract: Plasma exchange (PE) is an effective therapeutic method used in patients with myasthenia gravis (MG) refractory to common therapy and/or with life-threatening respiratory complications. Except for acetylcholine receptor antibodies (AChRAbs), some other inflammatory mediators possibly activated in MG may also be removed during PE. Serum levels of soluble adhesion molecules (sICAM-1 and sVCAM-1), IL-6 and soluble receptors for IL-2 (sIL-2R), IL-6 (sIL-6R) and TNF alpha (sTNF-R II) were measured in 20 MG patients assigned to treatment with PE. On the basis of the serum levels of AChRAb the patients were subdivided into 2 groups (8 patients with low AChRAb, 12 patients with high AChRAb). Soluble adhesion molecules and cytokines were measured before the first and last PE, at the end of the first PE and in the samples of plasma filtrate obtained during the first PE. Before the first PE patients with MG had higher serum levels of sICAM-1, sVCAM-1, sIL-2R and sTNF-R II than controls. Both after the first PE and during the course of PE, a substantial decrease in serum levels of AChRAb, sICAM-1 and sVCAM-1 was recorded. However, serum levels of sIL-2R and sTNF-R II were not significantly influenced by either a single treatment or during the course of PE. There were high levels of AChRAb, soluble adhesion molecules and soluble cytokine receptors in plasma filtrates too. Patients with high circulating AChRAb had higher serum levels of sICAM-1 and sVCAM-1 than patients with low AChRAb. Increased serum levels of soluble adhesion molecules and soluble cytokine receptors in patients with MG suggest some systemic activation of the immune response which is more pronounced in patients with high circulating AChRAb. PE led to the decrease in serum AChRAb and soluble adhesion molecules due to their effective filtration but, on the other hand, serum levels of soluble cytokine receptors were not influenced by PE, in spite of their effective filtration which is probably counteracted by their increased production, possibly stimulated by the contact of the blood with the synthetic membrane.
authors.affiliation: 1st Department of Medicine, 1st School of Medicine, Charles University, Prague, Czech Republic.
authors.forename: V
authors.initials: V
authors.lastname: Tesar
authors.forename: E
authors.initials: E
authors.lastname: Jelínková
authors.forename: M
authors.initials: M
authors.lastname: Jirsa
authors.forename: M
authors.initials: M
authors.lastname: Bakosová
authors.forename: P
authors.initials: P
authors.lastname: Pitha
authors.forename: V
authors.initials: V
authors.lastname: Chábová
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000097:blood; D015815:Cell Adhesion Molecules / Q000097:blood*; D016207:Cytokines / Q000097:blood*; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009157:Myasthenia Gravis / Q000097:blood* / Q000628:therapy*; D010951:Plasma Exchange; D011950:Receptors, Cholinergic / Q000276:immunology; D015375:Receptors, Interleukin-2 / Q000097:blood; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D012995:Solubility; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D001323:Autoantibodies; D015815:Cell Adhesion Molecules; D016207:Cytokines; D015850:Interleukin-6; D011950:Receptors, Cholinergic; D015375:Receptors, Interleukin-2; D018124:Receptors, Tumor Necrosis Factor; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1