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Lack of association between vascular dementia and Chlamydia pneumoniae infection: a case-control study
Authors:Soo?Chan Carusone,Marek?Smieja,William?Molloy,Charlie?H?Goldsmith,Jim?Mahony,Max?Chernesky,Judy?Gnarpe,Tim?Standish,Stephanie?Smith,Mark?Loeb  author-information"  >  author-information__contact u-icon-before"  >  mailto:loebm@mcmaster.ca"   title="  loebm@mcmaster.ca"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author
Affiliation:(1) Department of Clinical Epidemiology and Biostatistics, McMaster University, 1200 Main St. W., L8N 3Z5 Hamilton, Canada;(2) Department of Pathology and Molecular Medicine, , 1200 Main St. W., L8N 3Z5 Hamilton, Canada;(3) Hamilton Regional Laboratory Medicine Program, , 50 Charlton Ave. E., L8N 4A6 Hamilton, Canada;(4) St. Peter's Centre for Studies in Aging, St. Peter's Hospital, 88 Maplewood Ave., L8M 1W9 Hamilton, Canada;(5) Department of Medicine, McMaster University, 1200 Main St. W., L8N 3Z5 Hamilton, Canada;(6) Department of Medical Microbiology and Immunology, University of Alberta, T6G 2H7 Edmonton, Canada
Abstract:

Background

Chronic inflammation appears to play a role in the pathogenesis of vascular dementia. Given the association between Chlamydia pneumoniae and stroke, the possibility exists that previous exposure to C. pneumoniae may play a role in vascular dementia. The objective of this study was to determine if there was an association between serological evidence of C. pneumoniae infection or inflammatory markers with vascular dementia.

Methods

28 case-patients with vascular dementia at a geriatric clinic and 24 caregiver-controls were tested for C. pneumoniae IgG and IgA antibodies. The association between vascular dementia and C. pneumoniae titres as well as inflammatory markers was estimated by using both conditional logistic regression and stratified logistic regression.

Results

When matched cases were compared to controls, there was no significant difference in elevated C. pneumoniae specific IgG antibodies (titre ≥ 1:32), odds ratio [OR] 1.3 (95% confidence intervals [CI] 0.3 to 6.0), p = 0.71, or in elevated C. pneumoniae specific IgA antibodies (titre ≥ 1:16), OR 2.0 (95%CI 0.5 to 8.0), p = 0.33 indicative of past or persistent C. pneumoniae infection. Similarly, no difference in high IgG or IgA antibody levels (IgG titre ≥ 1:512 or IgA titre ≥ 1:64) between the two groups, indicative of recent C. pneumoniae infection, was found, OR 0.4 (95%CI 0.1 to 2.1), p = 0.27. For C-reactive protein (CRP), the mean difference between 18 matched pairs (case – control) was – 3.33 mg/L. There was no significant difference between cases and controls when comparing log transformed values, OR 0.03 (95%CI 0.00 to 2.89), p = 0.13 or comparing CRP values above or below the median, OR 0.8 (95%CI 0.2 to 3.4), p = 0.71. For fibrinogen, the mean difference between pairs (case – control) was -0.07 g/L. There was no statistical difference between cases and controls when comparing log transformed values, OR 0.6 (95%CI 0.0 to 31.2), p = 0.79 or between fibrinogen values above and below the median, OR = 0.5 (95%CI 0.1 to 2.0), p = 0.50.

Conclusion

We found no evidence for a significant association between C. pneumoniae infection, inflammatory markers such as CRP and fibrinogen, and vascular dementia.
Keywords:
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