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What's New In Shock, May 2011?

The May 2011 issue of Shock once again provides an excellent selection of clinical and laboratory investigations plus two timely review articles. The first review addresses the important clinical issue of genetic factors that predispose to complications in trauma patients. Hildebrand et al. (1) provide a comprehensive review of articles that study single-nucleotide polymorphisms of genes critical for the immune and inflammatory responses following trauma. This review will serve as a valuable resource for those seeking to use genomic information to tailor treatment in this very heterogeneous group of patients. The second review addresses a practical laboratory issue of measurement of infarct size in studies of myocardial ischemia. A common difficulty in interpreting the literature is trying to compare results from fundamentally different experimental models. Mersmann et al. (2) provide a concise but comprehensive and systematic review of cardiac ischemia/ reperfusion models in mice. This very pragmatic survey should be a required citation for all future studies on cardiac ischemia/ reperfusion in a murine model. As outlined by Hildebrand et al. (1), the response to trauma and sepsis is very heterogeneous such that rational therapy requires accurate staging of patient status. A potentially valuable approach for such staging is the development of biomarkers. The May issue offers four clinical studies, all focused on staging and biomarkers in sepsis. Oxygen delivery to tissues is an important parameter to monitor, but invasive approaches increase the risk of morbidities. Mesquida et al. (3) evaluated whether StO2 could serve as an acceptable surrogate for measurements made using a pulmonary artery catheter (PAC). They compared measurements using near-infrared spectroscopy of StO2 with DO2 measured via a PAC in 15 patients in early septic shock. Although a StO2 less than 75% was significantly associated with severe decrease in DO2, moderate but potentially clinically relevant decreases in DO2 were not accurately predicted by StO2, indicating that this method does not have sufficient sensitivity to replace PAC measurements. The next three articles examined potentially novel biomarkers. Schulte et al. (4) evaluated peroxiredoxin levels as a marker for oxidative stress in septic patients. They studied preserved serum samples from 79 medical intensive care unit patients by comparing the secreted form of peroxiredoxin (Prx4) with other biomarkers, physiologic status (Acute Physiology And Chronic Health Evaluation), and organ failure (Sequential Organ Failure Assessment) scores as well as outcome. Prx4 levels in serum correlated significantly with a variety of biomarkers of inflammation as well as with Acute Physiology And Chronic Health Evaluation and Sequential Organ Failure Assessment scores. Interestingly, it also distinguished between septic and nonseptic inflammation. These results suggest that Prx4 may be a valuable biomarker in septic patients and indicate that further prospective studies are needed. It is well known that circulating cytokine profiles reflect inflammatory status. Krzystek-Korpacka et al. (5) investigated the cytokine midkine, which is normally expressed in gestation and restricted to just a few organs in adults. They measured midkine levels in serum of 38 septic and 82 inflammatory bowel disease patients as well as 87 control subjects. Elevated midkine levels were much more common in septic than in inflammatory bowel disease patients. It also remained elevated in shock but gradually decreased with severe sepsis and was highest in patients with Gram-positive infections. These results suggest that midkine may be useful in assessing status of septic patients, but further studies would be needed to evaluate its sensitivity. The final clinical study examined serum heat shock protein 70 (HSP70) levels as a marker for oxidant status and outcome in sepsis. Gelain et al. (6) studied HSP70 serum levels in 15 patients (8 with severe sepsis and 7 with septic shock) and 24 control subjects. Overall, HSP70 levels were elevated n septic patients, but this was restricted to those who also had elevated markers for oxidative stress (e.g., thiobarbituric acid reactive substances [TBARS]), whereas patients without evidence of oxidative stress had normal HSP70. Patients with increased HSP70 also had increased mortality, indicating the importance of oxidative stress in outcome in sepsis. The article by Kobba et al. (7) provides an interesting perspective on the HSP70 story. They studied the heat shock paradox (heat shock then inflammation leads to protection; inflammation then heat shock increases injury) in cardiac myocytes and the potential role of heat shock factor (HSF) in mediating this paradox. Using TNF-! followed by heat shock in rat cardiac myocytes, they found that this specifically increased HSP60 expression but not HSP32 (heme oxygenase). Inhibition of HSF-1 action prevented HSP induction as well as increased apoptosis, indicating that the heat shock paradox is likely mediated by HSF-1Y dependent induction of HSP60. The remaining laboratory investigations in this month’s issue address potential novel therapeutic approaches to shock and sepsis. Two of these focus on liver injury. McNeal et al. (8) studied the role of receptor interacting protein 1 (RIP-1) hepatocyte death in sepsis. Adapter protein RIP-1 is thought to contribute to activation of necrosis in hepatocytes in response to TNF-!, so they tested whether inhibiting it either by siRNA or pharmacologic methods would improve survival and decrease liver injury in sepsis. Contrary to expectations, inhibition of RIP-1 actually increased mortality causing the