Transfusion-transmissible infections and transfusion-related immunomodulation AbstractThe risk of acquiring a transfusion-transmitted infection has declined in recent years. However, after human immunodeficiency virus and hepatitis B and C virus transmission were successfully reduced, new pathogens are threatening the safety of the blood supply, especially in the face of rising numbers of immunocompromised transfusion recipients. Despite new standards in the manufacture and storage of blood products, bacterial contamination still remains a considerable cause of transfusion-related morbidity and mortality. Better allograft survival in kidney transplant patients and higher cancer recurrence rate in surgical oncology patients after allogeneic blood transfusions highlighted a previously underestimated side-effect: transfusion-related immunomodulation (TRIM). The precise pathomechanism still remains uncertain; however, its mostly deleterious effects--such as a higher incidence of postoperative or nosocomial infections--is increasingly accepted. Although transfusion-related immunomodulation is thought to be mediated mainly by donor white blood cells, the benefit of leukoreduction on overall mortality and on infectious complications is highly debatable. Transfusion-transmissible infections and Transfusion-related immunomodulation Transfusion-transmissible infections and Transfusion-related immunomodulation AbstractThe risk of acquiring a transfusion-transmitted infection has declined in recent years.
Background Transfusing blood products may induce inflammatory reactions within the vascular compartment potentially leading to a systemic inflammatory response. Experiments were designed to assess the inflammatory potential of different blood products in an endothelial cell-based in vitro model and to compare baseline levels of potentially activating substances in transfusion products. Methods The inflammatory response from pre-activated (endotoxin-stimulated) and non-activated endothelial cells as well as neutrophil endothelial transmigration in response to packed red blood cells (PRBC), platelet concentrates (PC) and fresh frozen plasma (FFP) was determined. Baseline inflammatory mediator and lipid concentrations in blood products were evaluated. Results Following incubation with all blood products, an increased inflammatory mediator release from endothelial cells was observed. Platelet concentrates, and to a lesser extent also FFP, caused the most pronounced response, which was accentuated in already pre-stimulated endothelial cells. Inflammatory response of endothelial cells as well as blood product-induced migration of neutrophils through the endothelium was in good agreement with the lipid content of the according blood product. Conclusion Within the group of different blood transfusion products both PC and FFP have a high inflammatory potential with regard to activation of endothelial cells. Inflammation upon blood product exposure is strongly accentuated when endothelial cells are pre-injured. High lipid contents in the respective blood products goes along with an accentuated inflammatory reaction from endothelial cells.
Background Liver hypertrophy induced by partial portal vein occlusion (PVL) is accelerated by adding simultaneous parenchymal transection ("ALPPS procedure"). This preclinical experimental study in pigs tests the hypothesis that simultaneous ligation of portal and hepatic veins of the liver also accelerates regeneration by abrogation of porto-portal collaterals without need for operative transection. Methods A pig model of portal vein occlusion was compared with the novel model of simultaneous portal and hepatic vein occlusion, where major hepatic veins draining the portal vein-deprived lobe were identified with intraoperative ultrasonography and ligated using pledgeted transparenchymal sutures. Kinetic growth was compared, and the portal vein system was then studied after 7 days using epoxy casts of the portal circulation. Portal vein flow and portal pressure were measured, and Ki-67 staining was used to evaluate the proliferative response. Results Pigs were randomly assigned to portal vein occlusion (n = 8) or simultaneous portal and hepatic vein occlusion (n = 6). Simultaneous portal and hepatic vein occlusion was well tolerated and led to mild cytolysis, with no necrosis in the outflow vein-deprived liver sectors. The portal vein-supplied sector increased by 90 ± 22% (mean ± standard deviation) after simultaneous portal and hepatic vein occlusion compared with 29 ± 18% after PVL (P < .001). Collaterals to the deportalized liver developed after 7 days in both procedures but were markedly reduced in simultaneous portal and hepatic vein occlusion. Ki-67 staining at 7 days was comparable. Conclusion This study in pigs found that simultaneous portal and hepatic vein occlusion led to rapid hypertrophy without necrosis of the deportalized liver. The findings suggest that the use of simultaneous portal and hepatic vein occlusion accelerates liver hypertrophy for extended liver resections and should be evaluated further. Introduction Portal vein occlusion by ligation (PVL) or embolization is a wellestablished method to improve the safety of extended liver resections by inducing liver hypertrophy before resection.1, 2, 3 The novel procedure associating liver partition and portal vein ligation (ALPPS) indicated that kinetic growth of the future liver remnant can be increased by adding a parenchymal transection between the portal vein-supplied and portal vein-deprived part of the liver.4 A recent pig study from our laboratory suggested that the parenchymal transection in ALPPS leads to an abrogation of extensive porto-portal neocollaterals between the portal vein-supplied and the portal vein-deprived side of the liver.5 Porto-portal collaterals are common in PVL and also occur in portal vein embolization; these collaterals are known to blunt hypertrophy, and their complete abrogation may well be the cause for the astounding effectiveness of parenchymal transection in ALPPS. Based on the concept that abrogation of collaterals is a key requirement for rapid hypertrophy, we postulated that simultaneous occlusion of hepatic ...
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