F McKechnie1, S Lewis, G Mead. 1. Royal Infirmary of Edinburgh, Room S1642, Little France Crescent, Edinburgh EH164SA, UK. gillian.e.mead@ed.ac.uk
Abstract
BACKGROUND: The aetiology of fatigue after stroke is unknown. We explored the relationship between fatigue and C-reactive protein (CRP) as a marker of inflammation. METHODS: This cross-sectional study recruited inpatients with a stroke (onset within the previous three months) over a five-week period. Those with dysphasia or confusion severe enough to prevent informed consent and those with current infection were excluded. A semi-structured interview determined a) fulfillment of a case definition for fatigue and b) severity of fatigue (fatigue assessment scale, FAS). Venous blood was taken for CRP. A hospital anxiety and depression score (HADS) was used to screen for emotional distress. RESULTS: Of the 28 patients recruited (mean age 72.7 years, proportion men 47%), 15 (53%) fulfilled the case definition for fatigue. C-reactive protein data were logarithmically transformed for analysis. C-reactive protein levels did not differ significantly between those with and without fatigue, according to the case definition (=28, p=0.35). After exclusion of those with pre-stroke fatigue and those with high scores on the HADS (suggestive of emotional distress), the geometric mean CRP of the fatigued group was 16.04 mg/l (95% CI: 7.12-36.14) compared with 5.16 mg/l (95% CI: 2.7-9.85) in the non-fatigued group (n=21, p=0.025, unpaired t test), but the relationship between FAS and CRP was not statistically significant (r=0.37, p=0.098). CONCLUSION: This pilot study is the first to demonstrate an association between fatigue after stroke and higher CRP, after excluding patients with pre-stroke fatigue and those with probable mood disorders. If this finding is confirmed in a larger number of patients, it might provide a target for treating fatigue after stroke.
BACKGROUND: The aetiology of fatigue after stroke is unknown. We explored the relationship between fatigue and C-reactive protein (CRP) as a marker of inflammation. METHODS: This cross-sectional study recruited inpatients with a stroke (onset within the previous three months) over a five-week period. Those with dysphasia or confusion severe enough to prevent informed consent and those with current infection were excluded. A semi-structured interview determined a) fulfillment of a case definition for fatigue and b) severity of fatigue (fatigue assessment scale, FAS). Venous blood was taken for CRP. A hospital anxiety and depression score (HADS) was used to screen for emotional distress. RESULTS: Of the 28 patients recruited (mean age 72.7 years, proportion men 47%), 15 (53%) fulfilled the case definition for fatigue. C-reactive protein data were logarithmically transformed for analysis. C-reactive protein levels did not differ significantly between those with and without fatigue, according to the case definition (=28, p=0.35). After exclusion of those with pre-stroke fatigue and those with high scores on the HADS (suggestive of emotional distress), the geometric mean CRP of the fatigued group was 16.04 mg/l (95% CI: 7.12-36.14) compared with 5.16 mg/l (95% CI: 2.7-9.85) in the non-fatigued group (n=21, p=0.025, unpaired t test), but the relationship between FAS and CRP was not statistically significant (r=0.37, p=0.098). CONCLUSION: This pilot study is the first to demonstrate an association between fatigue after stroke and higher CRP, after excluding patients with pre-stroke fatigue and those with probable mood disorders. If this finding is confirmed in a larger number of patients, it might provide a target for treating fatigue after stroke.
Authors: N Jennifer Klinedinst; Rosemary Schuh; Steven J Kittner; William T Regenold; Glenn Kehs; Christine Hoch; Alisha Hackney; Gary Fiskum Journal: J Bioenerg Biomembr Date: 2019-01-07 Impact factor: 2.945
Authors: Kate Noonan; Sheila G Crewther; Leeanne M Carey; Michaela C Pascoe; Thomas Linden Journal: Clin Interv Aging Date: 2013-01-22 Impact factor: 4.458