Abdominal Aortic Aneurysm and its Correlation to Plasma Homocysteine, and Vitamins

Abstract

This study confirms significantly higher levels of plasma homocysteine in AAA patients but lower levels of B12. Use of supplemental vitamins that should lower plasma homocysteine may modify vascular disease progression. Clinical trials in this direction are warranted.

Plasma and aqueous humour levels of homocysteine in exfoliation syndrome

“…Schumacher and co-workers observed an association between aneurysms of the abdominal aorta and ocular exfoliation [36]. On the other hand, later, a high incidence of elevated Hcy levels was found in patients who suffered an abdominal aortic aneurysm [38,50].…”

Pathophysiology of Abdominal Aortic Aneurysm – Genetic Factors and Homocysteine Metabolism

“…An emerging pattern of atherosclerosis was detected in these patients and it was concluded that genetic defects in homocysteine metabolism and associated homocysteinuria was responsible for these vascular lesions (Guilliams, 2004). Endothelial vascular injury and atherosclerosis was subsequently demonstrated through intravenous infusion of Hcy in an animal model (Warsi et al, 2004). Several studies followed this, reporting the association between Hcy concentrations and vascular disease and more recent large scale meta-analyses have supported these findings (Castro et al, 2006).…”

“…Hcy can also be metabolised to cystathionine, an intermediate of the non-essential amino acid cysteine. Vitamin B6 is necessary for this transulphuration reaction to occur ( Figure 1) (Warsi et al, 2004;Guilliams, 2004;Moroz et al, 2007;Castro et al, 2006) Excess levels of Hcy are excreted to the plasma where the liver and kidney are the organs achieving catabolism and excretion of Hcy. Despite this, mild hyperHcy is present in 5-7% of the general population, due to either inherited or acquired dietary deficiencies of vitamin B6, B12 and folic acid.…”

“…The exact mechanism of MMPs interactions with other inflammatory cytokines, inflammatory cells, microbes and aortic wall tissue is unknown. MMPs can be activated by a range of stimuli including other MMPs, cytokines released by the inflammatory cells, elastin degradation products, microbes such as chlamydiae pneumoniae, reactive oxygen species, and mechanical alteration in the aortic wall stress (Warsi et al, 2004). Several genetic polymorphisms are associated with MMP and some have been linked with increased frequency in AAA (Thompson et al, 2008;Sandford et al, 2007).…”

“…High concentration of MMP-2 is found in small AAA suggesting its role in early AAA formation (Crowther et al, 2000). MMP-12 is highly expressed in tissue along the leading edge of AAA suggesting a role in AAA initiation (Warsi et al, 2004). MMP-1, MMP-3, MMP-8, MMP-13 are collagenases involved in degradation of extracellular matrix during aortic wall remodelling (Tromp et al, 2004;Pyo et al, 2000;Sinha et al, 2006;Petersen et al, 2000;Crowther et al, 2000;Abdul-Hussien et al, 2007).…”