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Changes in spleen size in patients with acute ischemic stroke: a pilot observational study

Authors


  • The first two authors contributed equally to this work.
  • Conflict of interest: James C. Grotta is a consultant for Lundbeck. Sean Savitz is a Consultant for KM Pharmaceutical and received honoraria from Kyorin Pharmaceutical.
  • Funding: This work was made possible in part by funding from Bentsen Stroke Center and Howard Hughes Medical Institute.

Correspondence: Sean Savitz, Department of Neurology, University of Texas Medical School, 6431 Fannin, MSB 7.125, Houston, TX 77030, USA.

E-mail: sean.i.savitz@uth.tmc.edu

Abstract

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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