Morphologic change of the internal elastic lamina in Buerger's disease

Morphologic features and pathogenesis of arterial changes occurring in Buerger's disease (thromboangiitis obliterans) are still controversial. This study describes histopathologic features of medium sized arteries from patients with Buerger's disease, particularly of the internal elastic lamina in relation to the immunologic mechanism of the injury. Seventeen segments of occluded arteries (femoral or popliteal arteries) from 17 patients with Buerger's disease were analyzed by histopathological and immunohistochemical methods. The most characteristic features were total luminal obliteration, together with a varying degree of recanalization and deposition of hemosiderin pigments. Detailed analysis, however, showed marked undulation and multiplication of the internal elastic lamina (100%) associated with basophilic degeneration and delicate linear calcification (47%). Lymphocytic infiltration along the internal elastic lamina was seen in 71% and was associated with localized edema. Lymphocytes along the lamina were consistently positive for T cell marker. Mild to moderate fibrosis was present at the media in 24%. Adventitial changes included mild, nonspecific and irregular fibrosis seen in 53%. Immunologic injury to the internal elastic lamina associated with T-lymphocytic infiltration might be the initial morphogenetic mechanism of the thrombotic occlusion and organization of medium-sized arteries in Buerger's disease.

Alteraciones de la ultraestructura del músculo esquelético en la enfermedad de Buerger: reporte de un caso / Ultrastructure alterations of skeletal muscle in Buerger's disease

La tromboangeitis obliterante (TAO) o enfermedad de Buerger ha sido considerada una forma de vasculitis relacionada etiológicamente con el hábito tabáquico. De acuerdo a la revisión de la literatura, no existen estudios previos acerca del compromiso muscular en esta enfermedad, esto nos estimuló a reportar el caso de un paciente afectado de la mencionada patología y con signos clínicos evidentes de alteración muscular. Por ese motivo, se realizó biopsia muscular por punción percutánea, con aguja tipo Bergstrom, del músculo cuadriceps femoris. Se procesaron las muestras por métodos convencionales para microscopía electrónica de transmisión. De acuerdo a los resultados ultraestructurales, las alteraciones que se producen en los capilares intramusculares son de tipo isquémico. Igualmente, la presencia de atrofia nos señala un posible daño neural en esta enfermedad. Algunas de las alteraciones observadas en los capilares y en relación con el infiltrado presente podrían sugerir un componente autoinmune en la etiología de la enfermedad