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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Haematologica
2018 ; 103
(7
): 1245-1250
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C-reactive protein and risk of venous thromboembolism: results from a
population-based case-crossover study
#MMPMID29674505
Grimnes G
; Isaksen T
; Tichelaar YIGV
; Brox J
; Brękkan SK
; Hansen JB
Haematologica
2018[Jul]; 103
(7
): 1245-1250
PMID29674505
show ga
Long-term, low-grade inflammation does not seem to be a risk factor for venous
thromboembolism. The impact of acute inflammation, regardless of cause, on risk
of venous thromboembolism is scarcely studied. We aimed to investigate the impact
of acute inflammation, assessed by C-reactive protein, on short-term risk of
venous thromboembolism. We conducted a case-crossover study of patients with
venous thromboembolism (n=707) recruited from a general population. Information
on triggers and C-reactive protein levels were retrieved from hospital records
during the 90 days before the event (hazard period) and in four preceding 90-day
control periods. Conditional logistic regression was used to obtain ?
coefficients for change in natural log (ln) transformed C-reactive protein from
control to hazard periods and to determine corresponding odds ratios for venous
thromboembolism. Median C-reactive protein was 107 mg/L in the hazard period, and
ranged from 7 mg/L to 16 mg/L in the control periods. The level of C-reactive
protein was 58% (95% CI 39-77%) higher in the hazard period than in the control
periods. A one-unit increase in ln-C-reactive protein was associated with
increased risk of venous thromboembolism (OR 1.79, 95% CI 1.48-2.16). The risk
estimates were only slightly attenuated after adjustment for immobilization and
infection. In stratified analyses, ln-C-reactive protein was associated with
increased risk of venous thromboembolism in cases with (OR 1.55, 95% CI
1.01-2.38) and without infection (OR 1.77, 95% CI 1.22-2.57). In conclusion, we
found that acute inflammation, assessed by C-reactive protein, was a trigger for
venous thromboembolism.