Background: Abdominal Aortic Aneurysm (AAA) remains a surgical challenge. There are many recognizable markers associated with the formation of AAA. Previous experiments carried out on animal models have shown a correlation between serum calprotectin and the occurrence of AAA. Objective: This study aimed to evaluate the level of calprotectin as a potential diagnostic biomarker in patients with diagnosed AAA. Methods: The study group consisted of 75 patients aged 35-75 years assigned to two groups: a control group (n=43) of healthy subjects without AAA and a study group (n=32) of patients with a diagnosed AAA. The first calprotectin test was performed upon patient admission to the hospital, and the second control test was performed after three months. The concentration of calprotectin in plasma was determined using the Immunoenzymatic Method (ELISA) with the commercially available Assaypro Kit (AssayMax™ Human Calprotectin ELISA Kit), as well as the sandwich method with polyclonal antibodies to human calprotectin and peroxidase enzyme. Results & Discussion: Serum calprotectin levels in AAA patients were three times higher than in healthy subjects (p<0.05). A statistically significant twofold decrease in calprotectin concentration was observed after AAA surgery compared to the control group (p<0.05). Conclusion: Calprotectin levels can be an important marker in the detection of AAA. In conclusion, AAA patients showed a threefold increase in serum calprotectin level and a twofold decrease in this marker after AAA surgery.

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.

An abdominal aortic aneurysm (AAA) is a dilatation of the abdominal aorta greater than 50% of the diameter of a healthy aorta. Previous experimental studies confirm the effect of calprotectin (CAL) on the onset of arterial pathology. It has been suggested that low levels of soluble receptors for advanced glycation end products (RAGEs) increase levels of cytokines that lead to the inhibition of matrix metalloproteinases (MMPs), affecting AAA formation. This study aimed to analyze the correlation of levels of RAGE and CAL with AAA diameter. A group of 32 patients aged 50–75 with diagnosed AAA was enrolled in the study. This group of patients was further divided into three subgroups based on AAA diameter: (1) 5.5 cm. Peripheral blood was drawn from all participants on admission to measure the serum CAL and RAGE levels. An enumeration survey was performed three months after AAA surgical treatment. CAL and RAGE plasma levels were measured with the enzyme-linked immunosorbent assay (ELISA). The median CAL levels were 2273.0 ng/mL before and 1217.0 ng/mL after treatment. There was a statistically significant decrease in CAL levels following the surgical treatment (p = 0.003). The correlation analysis between CAL levels and RAGE levels before and after surgical treatment showed no statistically significant correlations. In addition, there were no statistically significant correlations between CAL and RAGE levels with AAA size. In conclusion, CAL levels appear to be a significant marker in patients with AAA. There is an almost twofold decrease in CAL levels after AAA excision.

Abdominal aortic aneurysms (AAA) affect 2.4% of the population, with men being five times more likely to be affected than women. The development of AAA is linked to changes in the elastin and vascular wall collagen. The enzymes that damage the cell wall are called metalloproteinases. AAA forms as a result of damage to elastic fibres and the loss of the property of reversible deformation of the aortic wall. The degradation of elastin and other stem proteins in the aortic wall is caused by metalloproteinases and serine proteases, accompanied by cysteine proteases and asparagine proteases. Increased calprotectin levels are observed in AAA patients in comparison to patients with a healthy aorta. A significant role in the pathogenesis of AAA and its rupture is played by inflammatory response cells; proteases of the tissue plasma coagulation and fibrinolysis. Plasminogen activator and plasmin accelerate the degradation of the aortic wall. Microbial involvement of C. pneumoniae, Helicobacter pylori, CMV, and HIV is considered in this inflammatory reaction. The local activation of platelets and the plasma coagulation system leads to the formation of a mural thrombus filling the lumen of the aneurysm. The mural thrombus shows a high tissue factor (TF) activity. The formation of AAA is conditioned by a combination of multiple factors. The factors impacting the formation of AAA discovered so far include genetic factors, sex, age, lifestyle (abuse of alcohol, tobacco misuse, obesity, stress), health conditions (hypertension, high cholesterol level, atherosclerosis), and infectious factors: bacteria, viruses, and other microorganisms.

Calprotectin is a calcium-binding protein involved in inflammatory processes. In the context of abdominal aortic aneurysm (AAA), elevated levels of calprotectin may indicate immune system activation and chronic inflammation, which are among the mechanisms contributing to the development and progression of AAA. The receptor for advanced glycation end-products (RAGE) is a receptor that binds various ligands, including advanced glycation end-products formed during the glycation of proteins and lipids under oxidative stress conditions. Activation of RAGE is associated with inflammatory processes, oxidative stress, and tissue remodeling, which may contribute to the weakening of the aortic wall and aneurysm formation. The main objective of this study was to evaluate the effectiveness of both biomarkers in distinguishing patients with abdominal aortic aneurysm. A total of 27 patients with diagnosed AAA were included in the study. The control group consisted of 27 patients without AAA. Plasma levels of calprotectin and sRAGE were measured in both groups. Statistical analysis included the Shapiro–Wilk test, Mann–Whitney U test, and the Hosmer-Lemeshow (H-L) test. The likelihood of having AAA was found to be over one hundred times greater in individuals classified into the AAA group based on a decision tree model using calprotectin and sRAGE levels, compared to those classified into the no-AAA group. Calprotectin concentration was identified as a stronger predictor of AAA than sRAGE. The optimal cut-off value for plasma calprotectin was determined as ≥1136 ng/mL, yielding a sensitivity of 81.5% and a specificity of 100.0% for discriminating AAA patients from controls. It may be beneficial in future studies to explore non-invasive approaches, such as measuring calprotectin levels in stool and sRAGE in urine, as a potential screening method for AAA. Monitoring the concentrations of these biomarkers in bodily fluids, as a non-invasive method, could support screening efforts for AAA.