ArticleInflammation2002
No causal association between inflammation and Chlamydia pneumoniae in patients with chronic ischemic arterial disease.
Article in Inflammation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Chlamydia pneumoniae-Mediated Inflammation in Atherosclerosis: A Meta-Analysis.Mediators of inflammation · 2015Pooled it
- Atherosclerosis: process, indicators, risk factors and new hopes.International journal of preventive medicine · 2014Review
- Risk factors in coronary atherosclerosis athero-inflammation: the meeting point.Thrombosis journal · 2003Article
- Increased prevalence of Chlamydophila pneumoniae but not Epstein-Barr antibodies in essential hypertensives.Journal of human hypertension · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The C-reactive protein, Chlamydia-specific IgG antibody, and fibrinogen were assayed in the serum of 159 patients with arterial disease (the arterial group) and 203 patients with heart valve prostheses (the valvular group) and no demonstrable coronary disease. In the arterial group, the Chlamydia pneumoniae antibody was > or = 1:32 for 67.3% (107/159) of the patients, the C-reactive protein was elevated in 41.5% (66/159), and the fibrinogen was elevated in 27.7% (44/159). In the valvular group, the C. pneumoniae antibody was > or = 1:32 for 59.1% (120/203) of the patients; the C-reactive protein was elevated in 34.0% (69/203), and the fibrinogen was elevated in 17.2% (35/203). Of 107 patients in the arterial group with C. pneumoniae titers > or = 1:32, only 26 (24.3%) had elevated fibrinogen (426 +/- 29 mg/dL) and 44 (41.1%) had elevated C-reactive protein (1.06 +/- 0.52 mg/dL). Similarly, of the 120 patients in the valvular group with C. pneumoniae titers > or = 1:32, 17 (14.2%) had elevated fibrinogen (409 +/- 29 mg/dL) and 34 had elevated C-reactive protein (0.99 +/- 1.1 mg/dL). Correlated poorly was C. pneumoniae with C-reactive protein and fibrinogen levels. Only the fibrinogen level could be discriminated between the arterial and the valvular group. These results suggest that no causal association exists between inflammation and C. pneumoniae. A highly significant correlation between C-reactive protein and fibrinogen levels was found.
Indexed as
Identifiers
11936753What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.