uu.seUppsala University Publications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Expansion of small-diameter abdominal aortic aneurysms is not reflected by the release of inflammatory mediators IL-6, MMP-9 and CRP in plasma
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Vascular Surgery.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Vascular Surgery.
Uppsala University, Units outside the University.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Vascular Surgery.
2009 (English)In: European Journal of Vascular and Endovascular Surgery, ISSN 1078-5884, Vol. 37, no 4, 420-424 p.Article in journal (Refereed) Published
Abstract [en]

Abdominal aortic aneurysm (AAA) is a common disease that develops gradually over several years and is characterised by weakening and dilatation of the aortic wall. AAAs also demonstrates a marked inflammatory infiltrate throughout the aortic wall. Chlamydophila pneumoniae (C. pneumoniae), is a common bacterium. About 50% of the population has been infected in adolescence. Thirteen studies report the presence of either C. pneumoniae or its antigens in 35-100% of AAA specimens.

The overall aim of this thesis was to evaluate the possible role of C. pneumoniae in inflammatory response and expansion of AAA from a clinical point of view.

In paper I, viable C. pneumoniae was detected in a majority of 26 patients with AAA having open surgery. Patients operated for AAA had higher C. pneumoniae antibodies titers than controls. In paper II, 247 patients were randomised in a double-blind trial, to evaluate the effect of azithromycin on the expansion of small AAAs. No such effect was seen and there was no correlation between C. pneumoniae antibody titers and AAA expansion. In paper III, 42 patients with AAA were compared to 100 age- and sex matched controls with normal aortas. C. pneumoniae antibodies were analysed in plasma samples obtained at screening, and in samples from a study conducted 5-15 (mean 12) years previously on the same population. There was no significant difference between the groups. In paper IV, were 211 patients were analysed, we could not find an association between levels in plasma of three markers of inflammation (IL-6, MMP-9 and CRP) and AAA expansion. A significant reduction in AAA expansion rate was found in patients treated with a combination of ASA and statins.

In conclusion, viable C. pneumoniae is found at the scene of the crime, but we were unable to reverse or halt expansion of AAA with antibiotic treatment. C. pneumoniae antibody titers cannot be used, to detect small AAA, or to evaluate AAA expansion. From a clinical point of view, based on the methods and analyses used in this thesis, the role of C. pneumoniae in the inflammatory response and expansion of abdominal aortic aneurysms is limited.

Abstract [en]

OBJECTIVES: The aim of this study was to evaluate a possible correlation between plasma levels of interleukin-6 (IL-6), metalloproteinase-9 (MMP-9) and C-reactive protein (CRP) and the expansion of small abdominal aortic aneurysms (AAAs). DESIGN: Patients were selected from a prospective randomised clinical trial and categorised in two groups, in which one group received active treatment (azithromycin) and the other received placebo. No statistical difference in the expansion rate of AAAs between the groups was found and the two groups were considered as one cohort in the present study. MATERIAL AND METHODS: In this study, 213 patients with AAAs between 35 and 49 mm were followed-up with ultrasound examination every 6th month. Blood samples were taken on two occasions (6 months apart). IL-6 and MMP-9 were analysed on one occasion using Quantikine analysing kits (R&D Systems, Inc., USA). CRP was analysed using sensitive-CRP method. RESULTS: Levels of IL-6, MMP-9 and CRP did not correlate with AAA expansion. Neither was there any correlation between statin medication and changes in MMP-9 levels over the 6-month period. Patients on statins had a lower expansion rate than those not taking statins: 0.16 versus 0.25 cm per year. CONCLUSION: No correlation was found between levels of circulating IL-6, MMP-9, CRP and the expansion of small-diameter AAAs, indicating no clinical use of these markers in AAA surveillance.

Place, publisher, year, edition, pages
2009. Vol. 37, no 4, 420-424 p.
Keyword [en]
Abdominal aortic aneurysm, Chlamydophila pneumoniae, inflammation, statin, expansion, randomised clinical trial, MMP-9, IL-6, CRP, azithromycin.
National Category
Surgery
Research subject
Surgery
Identifiers
URN: urn:nbn:se:uu:diva-108599DOI: 10.1016/j.ejvs.2008.11.027ISI: 000265199400008PubMedID: 19119028OAI: oai:DiVA.org:uu-108599DiVA: diva2:236652
Available from: 2009-09-24 Created: 2009-09-24 Last updated: 2010-01-12Bibliographically approved
In thesis
1. The Role of Chlamydophila Pneumoniae in the Inflammatory Response and Expansion of Abdominal Aortic Aneurysms
Open this publication in new window or tab >>The Role of Chlamydophila Pneumoniae in the Inflammatory Response and Expansion of Abdominal Aortic Aneurysms
2009 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Abdominal aortic aneurysm (AAA) is a common disease that develops gradually over several years and is characterised by weakening and dilatation of the aortic wall. AAAs also demonstrates a marked inflammatory infiltrate throughout the aortic wall. Chlamydophila pneumoniae (C. pneumoniae), is a common bacterium. About 50% of the population has been infected in adolescence. Thirteen studies report the presence of either C. pneumoniae or its antigens in 35-100% of AAA specimens.

The overall aim of this thesis was to evaluate the possible role of C. pneumoniae in inflammatory response and expansion of AAA from a clinical point of view.

In paper I, viable C. pneumoniae was detected in a majority of 26 patients with AAA having open surgery. Patients operated for AAA had higher C. pneumoniae antibodies titers than controls. In paper II, 247 patients were randomised in a double-blind trial, to evaluate the effect of azithromycin on the expansion of small AAAs. No such effect was seen and there was no correlation between C. pneumoniae antibody titers and AAA expansion. In paper III, 42 patients with AAA were compared to 100 age- and sex matched controls with normal aortas. C. pneumoniae antibodies were analysed in plasma samples obtained at screening, and in samples from a study conducted 5-15 (mean 12) years previously on the same population. There was no significant difference between the groups. In paper IV, were 211 patients were analysed, we could not find an association between levels in plasma of three markers of inflammation (IL-6, MMP-9 and CRP) and AAA expansion. A significant reduction in AAA expansion rate was found in patients treated with a combination of ASA and statins.

In conclusion, viable C. pneumoniae is found at the scene of the crime, but we were unable to reverse or halt expansion of AAA with antibiotic treatment. C. pneumoniae antibody titers cannot be used, to detect small AAA, or to evaluate AAA expansion. From a clinical point of view, based on the methods and analyses used in this thesis, the role of C. pneumoniae in the inflammatory response and expansion of abdominal aortic aneurysms is limited.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2009. 85 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 485
Keyword
Abdominal aortic aneurysm, Chlamydophila pneumoniae, inflammation, aspirin, statin, expansion, randomised clinical trial
National Category
Surgery
Research subject
Surgery
Identifiers
urn:nbn:se:uu:diva-108867 (URN)978-91-554-7617-5 (ISBN)
Public defence
2009-11-06, Auditorium Minus, Museum Gustavianum, Akademigatan 3, Uppsala, 13:00 (English)
Opponent
Supervisors
Available from: 2009-10-16 Created: 2009-10-01 Last updated: 2009-10-16Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed

Authority records BETA

Karlsson, Lars

Search in DiVA

By author/editor
Karlsson, Lars
By organisation
Department of Surgical SciencesVascular SurgeryUnits outside the University
In the same journal
European Journal of Vascular and Endovascular Surgery
Surgery

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 423 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf