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Timing of C‐reactive protein increment in acute traumatic stress: relevance for CRP determinations in acute cardiovascular events
Author(s) -
Segal Ortal,
Behrbalk Eyal,
Shapira Itzhak,
Otremsky Itzhak,
Berliner Shlomo,
Halpern Pinkhas,
Serov Jack,
Arbel Yaron
Publication year - 2008
Publication title -
stress and health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.009
H-Index - 61
eISSN - 1532-2998
pISSN - 1532-3005
DOI - 10.1002/smi.1181
Subject(s) - medicine , myocardial infarction , c reactive protein , white blood cell , acute stroke , biomarker , stroke (engine) , inflammation , cardiology , body mass index , gastroenterology , biochemistry , chemistry , tissue plasminogen activator , engineering , mechanical engineering
It is not clear whether acute stress of a few hours duration is capable of increasing the concentration of C‐reactive protein (CRP), a valuable biomarker in patients with acute myocardial infarction or stroke. Therefore, we measured the concentration of CRP in patients who presented with an acute fracture and in whom we can assume that the CRP concentrations prior to the event were within the normal limits. There were 20 patients with bone fractures and 20 gender‐ and body mass index (BMI)‐matched controls aged 52 ± 27 and 51 ± 21 years, respectively [mean ± standard deviation (SD)]. The patients were examined 3.2 ± 2.5 h (mean ± SD) after their actual trauma and presented with modestly elevated concentrations of CRP (2.7 ± 2.1 mg/L) as compared with the controls (2 ± 2.2 mg/L). At the same time, the expected increment in the white blood cell count was noted in the patients (12.4 ± 3 × 10 3 /mL) as opposed to the controls (7.1 ± 1.9, p < 0.001). We conclude that the expected increment in CRP within a few hours after the onset of acute traumatic stress is modest. The findings are relevant for stressful conditions of acute myocardial infarction and stroke that present within a few hours after the onset of pain and in which elevated CRP levels might represent the causative inflammation and are not necessarily a result of the acute stress/infarction per se. Copyright © 2008 John Wiley & Sons, Ltd.