The Role of Serum Calprotectin as a New Marker in Abdominal Aortic Aneurysms – A Preliminary Report

Hauzer, Willy; Ferenc, Stanisław; Rosińczuk, Joanna; Gnus, Jan

doi:10.2174/1389201021666201117095215

Cited by 6 publications

(3 citation statements)

References 28 publications

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“…For example, Hauzer et al observed increased levels of calprotectin in patients with AAA compared to controls, and interestingly, these levels were reduced after surgery. 15 They also found differences in the levels of soluble receptor for advanced glycation end products (RAGE) between the two groups, 16 but were unable to establish a correlation between both markers (calprotectin or RAGE) and aortic diameter, probably due to limited sample size. 17 In contrast, our control group comprised healthy volunteers and carotid endarterectomy patients with severe atherosclerosis, who were analyzed separately to determine whether calprotectin would be able to differentiate AAA from other vascular diseases.…”

Section: Discussionmentioning

confidence: 99%

Calprotectin as a new inflammatory marker of abdominal aortic aneurysm: A pilot study

Plana,

Oto,

Herranz

et al. 2024

Vasc Med

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Introduction: Abdominal aortic aneurysm (AAA) is a relevant clinical problem due to the risk of rupture of progressively dilated infrarenal aorta. It is characterized by degradation of elastic fibers, extracellular matrix, and inflammation of the arterial wall. Though neutrophil infiltration is a known feature of AAA, markers of neutrophil activation are scarcely analyzed; hence, the main objective of this study. Methods: Plasma levels of main neutrophil activation markers were quantified in patients with AAA and a double control group (CTL) formed by healthy volunteers (HV) and patients with severe atherosclerosis submitted for carotid endarterectomy (CE). Calprotectin, a cytoplasmic neutrophil protein, was quantified, by Western blot, in arterial tissue samples from patients with AAA and organ donors. Colocalization of calprotectin and neutrophil elastase was assessed by immunofluorescence. Results: Plasma calprotectin and IL-6 were both elevated in patients with AAA compared with CTL ( p ⩽ 0.0001) and a strong correlation was found between both molecules ( p < 0.001). This difference was maintained when comparing with HV and CE for calprotectin but only with HV for IL-6. Calprotectin was also elevated in arterial tissue samples from patients with AAA compared with organ donors ( p < 0.0001), and colocalized with neutrophils in the arterial wall. Conclusions: Circulating calprotectin could be a specific AAA marker and a potential therapeutical target. Calprotectin is related to inflammation and neutrophil activation in arterial wall and independent of other atherosclerotic events.

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Section: Discussionmentioning

confidence: 99%

Calprotectin as a new inflammatory marker of abdominal aortic aneurysm: A pilot study

Plana,

Oto,

Herranz

et al. 2024

Vasc Med

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“…Patients with AAA also display an increased level of calprotectin in comparison to patients with a healthy aorta. That level decreases significantly after the removal of AAA [11,12].…”

Section: Pathogenesis Of Aaa Formationmentioning

confidence: 93%

Pathogenesis of abdominal aortic aneurysms from the vascular surgeon perspective – knowledge summary

HAUZER¹,

Gnus

HAUZER

et al. 2022

J Educ Health Sport

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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.

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“…Similarly, miRNA profiling produced under-expressed and overexpressed sequences suggesting the role in regulatory mechanisms [ 25 , 26 , 27 ]. Tissue factors related with inflammatory infiltrates and matrix degradation, such as pentraxin [ 28 ], galectin [ 29 ], calprotectin [ 30 , 31 ], kallikrein [ 32 ], and granzyme [ 33 ], correlate with the presence of AAA and might help in identifying patients at risk of AAA rupture ( Figure 2 ).…”

Section: Biomarkers and Compounds In Abdominal Aortic Aneurysms (Untreated Disease)mentioning

confidence: 99%

Biomarkers in EndoVascular Aneurysm Repair (EVAR) and Abdominal Aortic Aneurysm: Pathophysiology and Clinical Implications

et al. 2022

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Circulating biomarkers have been recently investigated among patients undergoing endovascular aortic aneurysm repair (EVAR) for abdominal aortic aneurysm (AAA). Considering the plethora of small descriptive studies reporting potential associations between biomarkers and clinical outcomes, this review aims to summarize the current literature considering both the treated disease (post EVAR) and the untreated disease (AAA before EVAR). All studies describing outcomes of tissue biomarkers in patients undergoing EVAR and in patients with AAA were included, and references were checked for additional sources. In the EVAR scenario, circulating interleukin-6 (IL-6) is a marker of inflammatory reaction which might predict postoperative morbidity; cystatin C is a promising early marker of post-procedural acute kidney injury; plasma matrix metalloproteinase-9 (MMP-9) concentration after 3 months from EVAR might help in detecting post-procedural endoleak. This review also summarizes the current gaps in knowledge and future direction of this field of research. Among markers used in patients with AAA, galectin and granzyme appear to be promising and should be carefully investigated even in the EVAR setting. Larger prospective trials are required to establish and evaluate prognostic models with highest values with these markers.

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The Role of Serum Calprotectin as a New Marker in Abdominal Aortic Aneurysms – A Preliminary Report

Cited by 6 publications

References 28 publications

Calprotectin as a new inflammatory marker of abdominal aortic aneurysm: A pilot study

Calprotectin as a new inflammatory marker of abdominal aortic aneurysm: A pilot study

Pathogenesis of abdominal aortic aneurysms from the vascular surgeon perspective – knowledge summary

Biomarkers in EndoVascular Aneurysm Repair (EVAR) and Abdominal Aortic Aneurysm: Pathophysiology and Clinical Implications

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