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In addition to this attack, which might be caused by homocysteinylation of the vascular wall proteins by homocysteine and/or its oxidized products (homocysteic acid, homocysteine sulfinic acid, and homocysteine thiolactone), in vitro and in vivo work suggests that reduced homocysteine can inhibit endothelial cell turn-over (Wang et al, 1997) and promote smooth muscle cell proliferation (Lubec et al, 1996b

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Research highlights that overlapping clinical features with common anemia contribute significantly to delayed diagnosis and suboptimal early management [11][12]