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 17 January 2018

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News

Inflamatory markers in cadaveric versus living-donor livers

Cold ischemia causes platelet deposition and neutrophil infiltration after reperfusion of cadaveric liver allografts, find doctors in the latest issue of Transplantation.

News image

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Prolonged cold storage of organs for transplantation may lead to inflammatory damage upon reperfusion.

In this study, doctors from England investigated whether organs from living donors experience less damage upon reperfusion than those retrieved from cadaver donors. The team obtained biopsies from 23 cadaveric and 10 living-related donor liver transplants, both before and 2 hours after reperfusion.

Cryosections were stained with antibodies against neutrophils, platelets, activated platelets, and endothelium.
Living-related donor liver allografts showed minimal changes postreperfusion.
Transplantation

The team found that the LRD liver allografts showed minimal changes postreperfusion.

However, in cadaver allografts, neutrophil infiltration was detected in 22%. Increased expression of von Willebrand factor (vWF), CD41, and P-selectin occurred in 48%, 30%, and 13% of allografts, respectively.

In cadaver allografts with deposition of activated platelets expressing either P-selectin or vWF, the cold ischemia time was significantly longer (885 versus 608 minutes, 776.8 versus 559 minutes, respectively).

Increases in neutrophils and platelets after reperfusion were not significantly associated with clinical events posttransplant.

However, in cadaver transplants that experienced early acute rejection, the mean cold ischemia time was significantly longer than in allografts with no rejection (732 versus 480 minutes).

Dr Wayel Jassem's team concluded, "This study demonstrates that in the clinical situation, cold ischemia causes platelet deposition and neutrophil infiltration after reperfusion of cadaveric liver allografts".

"These early inflammatory events may contribute to make the graft more susceptible to acute rejection".

Transplant 2003; 76(11): 1599-1603
18 December 2003

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