Patterns of markers of inflammation, coagulation and vasoconstriction during follow-up of abdominal aortic aneurysms
(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:
https://lup.lub.lu.se/record/2608410
- author
- Flondell-Sité, Despina LU ; Lindblad, Bengt LU and Gottsäter, Anders LU
- organization
- publishing date
- 2012
- 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
- 2024-02-12 08:17:16
@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}}, }