ABSTRACT
Takayasu's arteritis (TA) is an acute inflammatory disease of unknown etiology, characterized by stenotic lesions in the aorta and its main branches that usually occurs in young women. However, it seems that older (middle-aged) cases of Takayasu's arteritis with chronic ongoing vasculitis are now being found more often, at least in Japan. Histopathological analysis in the acute phase of TA reveals extensive inflammation characterized by massive cell infiltration, destruction of the media, the adventitia around the vasa vasorum, and intimal hyperplasia, causing stenotic lesions. When destructive changes of the vessel wall predominate, it occasionally causes dilated lesions presenting as aneurysms (1). Vascular inflammation sometimes persists even after acute inflammation apparently subsides. Local vasculitis may latently occur without apparent inflammatory manifestations in the periphery, resulting in vascular damage that may evolve into lesions with pathological features resembling atherosclerotic aortic aneurysm. There is evidence of an association between Takayasu's arteritis and specific human leukocyte antigen (HLA) genes such as HLA-B52, -B39, and MICA (2-10). A recent report describes a close correlation between serum levels of inflammatory cytokines such as interleukin (IL)-6 and RANTES (regulated on activation, normal T cell expressed and secreted) with disease activity (11), suggesting a role of activated monocytes and T cells in the pathogenesis of TA. Some of the immunological mechanisms relevant in TA may also be involved in the formation of atherosclerotic aortic aneurysms (12-14). However, the precise mechanism of vessel injury as well as the primary cause that triggers the autoimmune process involved in both vascular diseases are still unknown and remain to be clarified.
