PMID- 22157685
OWN - NLM
STAT- MEDLINE
DCOM- 20120508
LR  - 20120319
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
VI  - 51
IP  - 4
DP  - 2012 Apr
TI  - Antibodies to common infectious agents in coronary artery disease patients with 
      and without rheumatic conditions.
PG  - 679-85
LID - 10.1093/rheumatology/ker251 [doi]
AB  - OBJECTIVES: The mechanism linking inflammation to atherosclerosis is unknown. We 
      have previously demonstrated a high occurrence of inflammation in the aortic 
      adventitia of patients with coronary artery disease (CAD), which was more 
      pronounced in patients with inflammatory rheumatic diseases (IRDs), and which 
      might be involved in the pathogenesis of cardiovascular disease. In theory, 
      infections might play a role in the pathogenesis of vascular inflammation or 
      atherosclerosis, or both. This study compared seropositivity and the burden of 
      several common infections in patients with CAD, both with and without IRD, and in 
      healthy controls (HCs). Moreover, we looked for relationships between the 
      examined antibodies and inflammatory infiltrates in the aortic adventitia. 
      METHODS: We examined sera for Chlamydophila pneumoniae, Mycoplasma pneumoniae, 
      Helicobacter pylori, CMV, Streptococcus pyogenes, parvovirus B19, HBV and HCV 
      with commercially available serological tests in 67 patients with IRD, 52 
      patients without IRD and 30 HCs. RESULTS: We observed neither any statistically 
      significant differences in the examined antibodies between the groups nor a 
      difference in the burden of infection. Except for a protective effect of 
      mycoplasma immunoglobulin A (IgA), we did not find any other associations between 
      the examined antibodies and the occurrence of aortic adventitial mononuclear cell 
      infiltrates. CONCLUSION: Our study does not support the notion that chronic 
      infections or infectious burden contribute to accelerated occurrence of CAD in 
      IRD. Mycoplasma IgA was related to a lower occurrence of aortic adventitial 
      inflammation.
FAU - Grub, Carola
AU  - Grub C
AD  - Department of Medical Microbiology, Hospital Innlandet Trust, Lillehammer NO 
      2609, Norway. carolagrub@hotmail.com
FAU - Brunborg, Cathrine
AU  - Brunborg C
FAU - Hasseltvedt, Viggo
AU  - Hasseltvedt V
FAU - Aukrust, Pal
AU  - Aukrust P
FAU - Forre, Oystein
AU  - Forre O
FAU - Almdahl, Sven Martin
AU  - Almdahl SM
FAU - Hollan, Ivana
AU  - Hollan I
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20111211
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
RN  - 0 (Antibodies, Bacterial)
RN  - 0 (Antibodies, Viral)
RN  - 0 (Immunoglobulin A)
SB  - IM
MH  - Aged
MH  - Antibodies, Bacterial/blood
MH  - Antibodies, Viral/blood
MH  - Aorta/pathology
MH  - Bacterial Infections/*complications/immunology
MH  - Case-Control Studies
MH  - Connective Tissue/pathology
MH  - Coronary Artery Disease/*microbiology/pathology
MH  - Female
MH  - Humans
MH  - Immunoglobulin A/blood
MH  - Male
MH  - Middle Aged
MH  - Pneumonia, Mycoplasma/immunology
MH  - Rheumatic Diseases/*complications
MH  - Virus Diseases/*complications/immunology
EDAT- 2011/12/14 06:00
MHDA- 2012/05/09 06:00
CRDT- 2011/12/14 06:00
PHST- 2011/12/14 06:00 [entrez]
PHST- 2011/12/14 06:00 [pubmed]
PHST- 2012/05/09 06:00 [medline]
AID - ker251 [pii]
AID - 10.1093/rheumatology/ker251 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2012 Apr;51(4):679-85. doi: 10.1093/rheumatology/ker251. 
      Epub 2011 Dec 11.