What'S New in SHOCK, June 2017?

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Every month, SHOCK greets its readers with a treasure trove of publications that includes review articles and clinical and basic science studies covering the areas of shock, trauma, sepsis, inflammation, ischemia and reperfusion, and related conditions. The 2017 June issue of SHOCK is no exception. The articles published in this edition demonstrate that, with high-quality investigation, many questions can be answered, and many new others are revealed. For the benefit of the reader, each publication in this June edition of SHOCK is briefly summarized below.
Endothelial cell activation contributes to sepsis-related organ failure by increasing vascular permeability, the production of inflammatory mediators, and leukocyte migration to the sites of inflammation. Sphingosine-1-phosphate (S1P) is an endothelial-regulating lipid. Recently, circulating levels of S1P were found to be decreased in patients with sepsis. In the first review article of this issue of SHOCK, Winkler et al. (1) summarize S1P's effects on the endothelial function, discuss S1P's potential use as a biomarker, and consider therapeutic strategies targeting S1P and its receptors to treat inflammation and sepsis. The authors review preclinical studies showing how circulating S1P activates S1PR1, S1PR2, or S1PR3 receptors, ultimately leading to lower surface expression of adhesion molecules, increased endothelial cell barrier function, and decreased production of pro-inflammatory cytokines. They also discuss the existing clinical studies showing decreased levels of S1P in patients with infection, highlighting the finding that S1P levels and the SOFA score were equally potent to diagnose septic shock. Finally, the authors review existing S1P-targetting agents.
Host defense peptides, or antimicrobial peptides, are innate immunity effector molecules released in response to infection. Ho et al. (2) conducted a systematic review and located 87 unique studies of host defense peptides in sepsis. The best-characterized peptides were cathelicidin, defensin, and hepcidin, which regulate the immune response, pyroptosis, and coagulation. Cathelicidin and defensin were mostly reported in adult sepsis, while hepcidin in neonatal sepsis. Many studies used the endotoxemia model, limiting the interpretation of their relevance for infection. Additionally, most studies employed a cross-sectional design. The authors concluded that innate defense peptides have been insufficiently evaluated as sepsis diagnostic or prognostic biomarkers, and propose that future studies employ a longitudinal design and consider a panel of multiple peptides.
Hemothorax is a potential source of blood for autotransfusion. However, hemothorax blood appears to have hypercoagulable properties that may aggravate acute traumatic coagulopathy. To better understand the coagulation-changing effects of plasma and cellular microparticles from hemothorax blood, Mitchell et al. (3) studied samples from 17 adult trauma patients. Hemothorax plasma and microparticles were found to induce hypercoagulability by reducing clotting and clotting formation times, and increasing the α angle. Hemothorax plasma inhibited platelet aggregation and contained high levels of fibrin degradation products and tissue factor. Hemothorax plasma also had high counts of microparticles, which were enriched in pro-thrombotic factors such as phosphatidylserine and tissue factor. Hemothorax plasma also had a significant loss of high molecular weight von Willebrand factor multimers. The authors concluded that hemothorax plasma hypercoagulability is likely due to microparticles expressing high levels of tissue factor and phosphatidylserine. On the other hand, the same microparticles in hemothorax plasma caused platelet dysfunction, which may be made more severe by depletion of high molecular weight von Willebrand factor multimers. In summary, these observations suggest that autologous transfusion of hemothorax blood may indeed aggravate acute traumatic coagulopathy.
MicroRNAs (miRNAs) regulate the expression of genes involved in normal lung physiology and inflammatory diseases of the lung, but they have not been studied in patients with acute respiratory distress syndrome (ARDS). To determine how miRNAs change during ARDS, Narute et al.
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