A study on the role of vascular factors in pathogenesis of polymyositis / 中华神经科杂志

ABSTRACT

Objective To study the expression of intercellular adhesion molecule-1 (ICAM-1), interleukin-1? (IL-1?) and ultrastructure changes in capillaries and to explore whether capillaries may play a role in the pathogenesis of polymyositis (PM). Methods Ten cases of patients with PM were collected. Control group 1 consists of 6 patients with other myopathies,Control group 2 consists of 2 muscle specimens without clinical and histological evidence of a neuromuscular disorder. An immunohistochemical technique was applied to indentify the expression of ICAM-1 and IL-1? in capillaries in the PM group, Control group 1 and Control group 2. The first analysis was a qualitative assessment. For the second analysis, the number of positive mononuclear cells and capillaries of the whole tissue section from each patient and control was estimated for all the immunologic markers investigated. 10 PM patients were also examined by electron microscopy in order to observe capillary changes in muscles. Results We found that the capillaries in tissues from PM (median (64?20)/mm~2 of tissue, ranging 44—106/mm~2) were significantly less than those from controls (median (157?46)/mm~2 of tissue, ranging 93—213/mm~2) (t=-4.523, P=0.003). A significantly higher number of capillaries expressed IL-1? in the PM group than in the Control group 1(median 15/mm~2 of tissue (ranging 6—46/mm~2) vs 3/mm~2 of tissue (ranging 0—16/mm~2)) (t=3.721, P=0.003). There was no significant difference between PM group and Control group 1 in the number of capillaries expressing ICAM-1 (t=0.529,P=0.617). However, ICAM-1 expressions in endothelial cells of capillaries were stronger in PM patients as IL-1?. Electronic microscopy found capillary changes in 6 PM patients, showing as thickening and duplication of basement membrane, swelling of endothelial cells, stenosis or occlusion of vessels.Conclusion Our findings indicate that capillary changes might take a role in the pathogenesis of PM.