Abstract
Experiments conducted in recent years on animals and research works worldwide show a linkage between calprotectin and occurrence and development of the abdominal aortic aneurysm (AAA). Additionally, a correlation between the level of the receptor for advanced glycation end products (RAGE) and the diameter of the abdominal aorta was found. The purpose of this study was to investigate whether calprotectin and the RAGE plasma level may be a biomarker of human AAA occurrence. We determined two groups of research participants: a group of 32 patients aged 53–88 undergoing primary endovascular aneurysm repair and a control group of 43 volunteers aged 59–82 without the AAA. All the patients from the study group had their blood samples drawn in order to determine the level of calprotectin and RAGE in plasma. The second follow-up examination was carried out after three months. The concentration of calprotectin and RAGE in plasma was determined with the use of the immunoenzymatic method (ELISA). The study showed that patients with the AAA had significantly higher mean calprotectin and RAGE plasma levels (p = 0.0001 and p = 0.0002, respectively) as compared to the control group. After the AAA repair operations, the level of concentration of the calprotectin decreased significantly (p = 0.0002). So far, no studies on the connection between the increase of the calprotectin and RAGE in the patient’s plasma with the AAA have been published. Calprotectin may be a promising biomarker related to the occurrence of AAA. Larger studies are needed to fully elucidate and confirm the role of calprotectin in the development and progression of the aneurysm.
Highlights
Dilation of the abdominal aorta above 50% of the diameter of a healthy aorta is considered an abdominal aortic aneurysm (AAA)
Numerous biological factors have been identified that contribute to AAA occurrence, e.g., serum elastin peptides (SEP), plasmin-antiplasmin (PAP) complexes, metalloproteinase-2 (MMP-2), metalloproteinase-9 (MMP-9), P-elastase, cystein C, tissue plasminogen activator, interferon-gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), interleukin-8 (Il-8), interleukin-6 (Il-6), macrophage migration inhibitory factor (MIF), osteopontin, osteoprogerin, fibrynogen, homocysteine, Staphylococcus sp., Chlamydophila pneumoniae, Treponema pallidum, and arachidonic acid [3]
Our findings suggest that calprotectin may be a promising biomarker for the occurrence of the AAA
Summary
Dilation of the abdominal aorta above 50% of the diameter of a healthy aorta is considered an abdominal aortic aneurysm (AAA). AAA is a complex, multifactorial disease with both genetic and environmental risk factors. The diameter of the AAA gradually increases and the larger ones are at higher risk of rupture. There are a lot of studied factors, which have impact on how fast the aneurysm grows, they comprise, amongst others: hypertension, smoking tobacco, hypercholesterolemia, genetic factors, chronic obstructive pulmonary disease, atherosclerosis as a general inflammatory process destructing aorta walls, and bacterial or viral infection [1,2]. Numerous biological factors have been identified that contribute to AAA occurrence, e.g., serum elastin peptides (SEP), plasmin-antiplasmin (PAP) complexes, metalloproteinase-2. In some cases, biomarkers such as arachidonic acid [4] and MMP-9 [5] have been evaluated as indicators of possible success of the AAA therapy
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