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Patterns of markers of inflammation, coagulation and vasoconstriction during follow-up of abdominal aortic aneurysms

Flondell-Sité, Despina LU ; Lindblad, Bengt LU and Gottsäter, Anders LU (2012) In International Angiology 31(3). p.276-282
Abstract
AIM:

The etiology of abdominal aortic aneurysm (AAA) includes inflammation, coagulation, and endothelial dysfunction. We have prospectively evaluated relations between these mechanisms and AAA growth. Tumour necrosis factor (TNF)-α, interleukin (IL)-6, endothelin (ET)-1, CD40 ligand and the complex formed between activated protein C (APC) and protein C inhibitor (PCI) were measured annually and related to AAA growth during up to 5 years in 206 patients with conservatively followed AAA.



METHODS:

We evaluated 163 patients up to 1 year, 126 patients up to 2 years, 83 patients up to 3 years, 53 patients up to 4 years, and 33 patients up to 5 years. The total number of patient follow-up years was... (More)
AIM:

The etiology of abdominal aortic aneurysm (AAA) includes inflammation, coagulation, and endothelial dysfunction. We have prospectively evaluated relations between these mechanisms and AAA growth. Tumour necrosis factor (TNF)-α, interleukin (IL)-6, endothelin (ET)-1, CD40 ligand and the complex formed between activated protein C (APC) and protein C inhibitor (PCI) were measured annually and related to AAA growth during up to 5 years in 206 patients with conservatively followed AAA.



METHODS:

We evaluated 163 patients up to 1 year, 126 patients up to 2 years, 83 patients up to 3 years, 53 patients up to 4 years, and 33 patients up to 5 years. The total number of patient follow-up years was 458.



RESULTS:

ET-1 remained unchanged except for a tendency to increase in the third and fourth years of follow-up. TNF-α decreased significantly during the first year and thereafter increased back to baseline values. There were no changes in IL-6, CD40 ligand, and APC-PCI complex. When patients in the highest and lowest quartiles of AAA growth up to 5 years follow-up were compared, APC-PCI complex levels tended to be higher (P=0.06) in the highest quartile of growth at three years (0.45 µg/l [i.q.r. 0.40-0.77] versus 0.28 µg/L [i.q.r. 0.14-0.36]). Δ-values of ET-1 and TNF-α did not show any correlation to growth. The 14 AAA patients that ruptured during follow-up did not differ from patients with non-ruptured AAA regarding biomarkers.



CONCLUSION:

In conclusion, none of the investigated mediators could be used to predict growth or rupture, or help to prolong intervals between ultrasound examinations in follow-up of AAA patients. (Less)
Please use this url to cite or link to this publication:
author
; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Aortic aneurysm, abdominal, CD40 ligand, Endothelin-1, Growth, Interleukin-6, Tumour necrosis factor-alpha
in
International Angiology
volume
31
issue
3
pages
7 pages
publisher
Minerva Medica
external identifiers
  • wos:000306574600011
  • pmid:22634983
  • scopus:84864780409
  • pmid:22634983
ISSN
1827-1839
language
English
LU publication?
yes
id
e5a1bde2-b2b6-4634-984a-4670f8c0ec4d (old id 2608410)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/22634983?dopt=Abstract
date added to LUP
2016-04-01 10:16:53
date last changed
2025-10-14 10:57:59
@article{e5a1bde2-b2b6-4634-984a-4670f8c0ec4d,
  abstract     = {{AIM:<br/><br>
The etiology of abdominal aortic aneurysm (AAA) includes inflammation, coagulation, and endothelial dysfunction. We have prospectively evaluated relations between these mechanisms and AAA growth. Tumour necrosis factor (TNF)-α, interleukin (IL)-6, endothelin (ET)-1, CD40 ligand and the complex formed between activated protein C (APC) and protein C inhibitor (PCI) were measured annually and related to AAA growth during up to 5 years in 206 patients with conservatively followed AAA.<br/><br>
<br/><br>
METHODS:<br/><br>
We evaluated 163 patients up to 1 year, 126 patients up to 2 years, 83 patients up to 3 years, 53 patients up to 4 years, and 33 patients up to 5 years. The total number of patient follow-up years was 458.<br/><br>
<br/><br>
RESULTS:<br/><br>
ET-1 remained unchanged except for a tendency to increase in the third and fourth years of follow-up. TNF-α decreased significantly during the first year and thereafter increased back to baseline values. There were no changes in IL-6, CD40 ligand, and APC-PCI complex. When patients in the highest and lowest quartiles of AAA growth up to 5 years follow-up were compared, APC-PCI complex levels tended to be higher (P=0.06) in the highest quartile of growth at three years (0.45 µg/l [i.q.r. 0.40-0.77] versus 0.28 µg/L [i.q.r. 0.14-0.36]). Δ-values of ET-1 and TNF-α did not show any correlation to growth. The 14 AAA patients that ruptured during follow-up did not differ from patients with non-ruptured AAA regarding biomarkers.<br/><br>
<br/><br>
CONCLUSION:<br/><br>
In conclusion, none of the investigated mediators could be used to predict growth or rupture, or help to prolong intervals between ultrasound examinations in follow-up of AAA patients.}},
  author       = {{Flondell-Sité, Despina and Lindblad, Bengt and Gottsäter, Anders}},
  issn         = {{1827-1839}},
  keywords     = {{Aortic aneurysm, abdominal; CD40 ligand; Endothelin-1; Growth; Interleukin-6; Tumour necrosis factor-alpha}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{276--282}},
  publisher    = {{Minerva Medica}},
  series       = {{International Angiology}},
  title        = {{Patterns of markers of inflammation, coagulation and vasoconstriction during follow-up of abdominal aortic aneurysms}},
  url          = {{http://www.ncbi.nlm.nih.gov/pubmed/22634983?dopt=Abstract}},
  volume       = {{31}},
  year         = {{2012}},
}