Akademik Veri Yönetim Sistemi
Clinical and Experimental Rheumatology, cilt.25, 2007 (SCI-Expanded, Scopus)
We propose that in BS the current evidence is in favour of the assertion that atherosclerosis is not increased to a considerable degree or to the degree seen in classic autoimmune diseases. Among the reasons to be considered are: a) the episodic nature of the inflammation, b) the general tendency for the disease activity to pass away with the passage of time and c) the more disease burden on the venous, rather than the arterial vessels in BS. One might also entertain the idea that the atherosclerosis is not part of BS because it is not a "true to form" autoimmune disease (63). A similar reasoning might also be made for the observations of not finding increased atherosclerosis in another chronic inflammatory condition, ankylosing spondylitis (64). On the other hand, the observed atherosclerosis both in Takayasu arteritis (9) and Wegener's granulomatosis (10) can be ascribed to the intense arterial inflammation in either of these conditions. Finally we believe the debate about the clinical importance of increased IMT and ECD as markers of the clinical atherosclerosis can be solved only by well-run, prospective studies. © Copyright Clinical and Experimental Rheumatology 2007.