ABSTRACT
The schematic sequence of events in TAO pathogenesis can be described as follows: genetic disposition, smoking, triggering of the autoimmune reaction, vascular wall swelling and damage, and local thrombosis. The clear understanding of this pattern is essential for the development of a treatment strategy for TAO patients. Peripheral endothelium-dependent vasodilatation was shown to slow down in patients with TAO, while non-endothelial mechanisms of vasodilatation remain unchanged.13 The role of hyperhomocysteinemia in TAO pathogenesis is unclear.14 One cannot exclude the interaction between such thrombophilic states as antiphospholipid syndrome and TAO.15
