Abstract

Rheumatic mitral stenosis (MS) is a late complication of acute rheumatic fever and it probably takes a minimum of 2 years after the onset of acute rheumatic fever for severe MS to develop.1 There is usually a long interval (10 to 20 years) between an episode of rheumatic carditis and the clinical presentation of symptomatic MS. Adhesion molecules are expressed on vascular endothelium and on immune and inflammatory cells. The fundamental role of cellular adhesion molecules in immunologic and inflammatory conditions has been elucidated in the last few years. They play a role in the migration of cells to sites of inflammation, transmigration of lymphocytes, and in immune effector functions. The molecules intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin are expressed on vascular endothelium and serve as ligands for counter receptors on circulating inflammatory cells.2 This study examined the serum levels of the adhesion molecules ICAM-1, VCAM-1, and E-selectin in patients with rheumatic MS and compared then with such levels in healthy control subjects.

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