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Query: UMLS:C0162871 (
abdominal aortic aneurysm
)
8,664
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The aim of the study was to evaluate the ability of following biomarkers as diagnostic tools and risk predictors of
AAA
: C-reactive protein, interleukin-6,
pentraxin-3
, galectin-3, procollagen type III N-terminal peptide, C-terminal telopeptide of type I collagen, high-sensitive troponin I, and brain natriuretic peptide. Seventy-two patients with an
AAA
and 100 healthy individuals were enrolled into the study. We assessed individual biomarker performance and correlation between the
AAA
diameter and biomarker levels, and also, a multivariate logistic regression was used to design a possible predictive model of
AAA
growth and rupture risk. We identified following four parameters with the highest potential to find a useful place in
AAA
diagnostics: galectin-3,
pentraxin-3
, interleukin-6, and C-terminal telopeptide of type I. The best biomarkers in our evaluation (galectin-3 and
pentraxin-3
) were
AAA
diameter-independent. With the high AUC and
AAA
diameter correlation, the high-sensitive troponin I can be used as an independent prognostic biomarker of the upcoming heart complications in
AAA
patients. Authors recommend to add biomarkers as additional parameters to the current
AAA
patient management. Main addition value of biomarkers is in the assessment of the
AAA
with the smaller diameter. Elevated biomarkers can change the treatment decision, which would be done only based on
AAA
diameter size. The best way how to manage the
AAA
patients is to create a reliable predictive model of
AAA
growth and rupture risk. A created multiparameter model gives very promising results with the significantly higher efficiency compared with the use of the individual biomarkers.
...
PMID:Blood biomarker panel recommended for personalized prediction, prognosis, and prevention of complications associated with abdominal aortic aneurysm. 3125 18
Information about the tissue characteristics of abdominal aortic aneurysms (AAAs), some of which may be reflected in the serum, can help to elucidate
AAA
pathogenesis and identify new
AAA
biomarkers. This information would be beneficial not only for diagnostics and follow-up but also for potential therapeutic intervention. Therefore, the aim of our study was to compare the expression of structural proteins, immune factors (T and B lymphocytes, macrophages, neutrophils and
pentraxin 3
(
PTX3
)), osteoprotegerin (OPG), microvessels and hypoxic cells in
AAA
and nonaneurysmal aortic walls. We examined specimens collected during surgery for
AAA
repair (n = 39) and from the abdominal aortas of kidney donors without
AAA
(n = 8). Using histochemical and immunohistochemical methods, we quantified the areas positive for smooth muscle actin, desmin, elastin, collagen, OPG, CD3, CD20, MAC387, myeloperoxidase,
PTX3
, and hypoxia-inducible factor 1-alpha and the density of CD31-positive microvessels.
AAA
samples contained significantly less actin, desmin, elastin and OPG, more collagen, macrophages, neutrophils, T lymphocytes, B lymphocytes, hypoxic cells and
PTX3
, and a greater density of vasa vasorum (VV) than those in non-
AAA
samples. Hypoxia positively correlated with actin and negatively correlated with collagen. Microvascular density was related to inflammatory cell infiltrates, hypoxia,
PTX3
expression and
AAA
diameter. The lower OPG expression in AAAs supports the notion of its protective role in
AAA
remodeling.
AAA
contained altered amounts of structural proteins, implying reduced vascular elasticity.
PTX3
was upregulated in
AAA
and colocalized with inflammatory infiltrates. This evidence supports further evaluation of
PTX3
as a candidate marker of
AAA
. The presence of aortic hypoxia, despite hypervascularization, suggests that hypoxia-induced neoangiogenesis may play a role in
AAA
pathogenesis. VV angiogenesis of the
AAA
wall increases its vulnerability.
...
PMID:Inflammatory cell infiltrates, hypoxia, vascularization, pentraxin 3 and osteoprotegerin in abdominal aortic aneurysms - A quantitative histological study. 3170 88