http://onlinelibrary.wiley.com/doi/10.1111/ijs.12022/abstract;jsessionid=5BCB8F56E42B7F750C6E98F8AFEB6ABA.d03t03
Background
In
animal models, the spleen contracts after acute ischemic stroke,
followed by release of inflammatory cells leading to secondary brain
injury.
Aims
We aim to characterize splenic responses in patients with acute ischemic stroke.
Methods
In
this prospective observational study, we measured daily spleen sizes
with abdominal ultrasound in 30 patients with suspected acute ischemic
stroke. Splenic ultrasounds were also performed in 20 healthy
individuals.
Results
A
generalized estimating equation, longitudinal regression model for
adjusted spleen measurements showed the difference between baseline
spleen volume (within six-hours of stroke onset) and the volume at the
last measured time point (up to seven-days) to be statistically
significant (volume difference of 51·9 cm3, P =
0·04). Healthy controls had significantly smaller day-to-day variations;
the maximum observed difference in mean spleen volume between any two
time points was 9·5 cm3, with the average change over the period of observation being 1·24 cm3.
A statistically significant negative association was also observed
between the pattern of change of total white blood cell count and spleen
volume (P = 0·01). An analysis of individual cases
demonstrated possible associations between daily spleen volume changes
and clinical course.
Conclusions
We
hypothesize that the spleen may initially contract after ischemic
stroke followed by a re-expansion and that it contributes to ischemic
brain injury mediated via cellular components. Characterization of the
splenic response after stroke and its contribution to cerebral ischemic
injury has the potential to provide new opportunities for the
development of novel stroke therapies.
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