Critical care : the official journal of the Critical Care Forum
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Editorial Comment
Should heparin-binding protein levels be routinely monitored in patients with severe sepsis and septic shock?
Heparin-binding protein (HBP), also known as azurocidin, has multiple functions in the inflammatory process, especially during severe infections. Beside its antimicrobial properties, HBP may induce vascular leakage leading to extravascular efflux, which is an important pathophysiologic event in the development of septic shock. Not surprisingly, high HBP plasma levels are found in severe sepsis patients and in septic shock patients as well as in serious infections associated with endothelial damage. ⋯ Moreover, 50% of nonseptic patients developed infection while hospitalized in the ICU, and to classify them as truly nonseptic patients is problematic. Second, there is a lack of a routine diagnostic method for HBP analysis. Nevertheless, if the results of the present study are validated in large clinical trials in different ICU populations and cost-effectiveness data become available, the serial HBP measurements will have a promising future.
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Sepsis is one of the leading causes of mortality in non-cardiac intensive care units, and the need for markers of progression and severity are high. Also, treatment of sepsis is highly debated and potential new targets of treatment are of great interest. In the previous issue of Critical Care Kumaraswamy and colleagues have investigated whether plasma apolipoprotein M (apoM) is affected during different grades of sepsis, septic shock and systemic inflammatory response syndrome. ⋯ This identifies apoM as a potential new biomarker in sepsis. It also underscores the possibility that altered high-density lipoprotein in sepsis patients can affect the course of disease. Thus, since apoM is the carrier of Sphingosine-1-P (S1P), a molecule with great influence on vascular barrier function, the study presented raises the interest and relevance for further studies of apoM and S1P in relation to sepsis and inflammation.
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Editorial Comment
Sepsis in transit: from clinical to molecular classification.
In the previous issue of Critical Care, Maslove and colleagues studied circulating neutrophil transcriptional expression to discover and validate a molecular subclassification of adult patients with sepsis. The authors divided patients into small derivation (n = 55) and validation (n = 71) cohorts. Their complex methodology included partitioning around medoid and hierarchical clustering methods to define two transcriptionally distinct subtypes of sepsis. ⋯ Interestingly, most patient characteristics did not differ between groups, except for an increase in the proportion of severe sepsis in molecular subtype 1. Possible confounders of this study were the small sample size, population stratification, and lack of information regarding drug interventions, all of which support the need for more studies with larger cohorts that include transcriptional profiles. This thought-provoking hypothesis-generating study could lead to a new neutrophil expression-based molecular classification of adult sepsis.
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Editorial Comment
Contrast-induced nephropathy: attributable incidence and potential harm.
Contrast-induced nephropathy is a common form of hospital-acquired acute kidney injury. Incidence is low in patients with normal renal function but increases in high-risk patients. Patients with contrast-induced nephropathy have higher in-hospital complication rates and mortality. ⋯ In the previous issue of Critical Care, Cely and colleagues showed an unexpectedly low incidence of contrast-induced nephropathy in critically ill patients receiving radiographic contrast material for computerized tomography. We should note that it is difficult to establish the true frequency and impact of the contrast nephrotoxicity because of many other causes for acute kidney injury in this population. Moreover, the impact on long-term kidney function and the possible effect of this insult on the recovery of renal function when associated with other causes of acute kidney injury are unknown.
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Hydroxyethylstarch (HES) 200/0.5 is associated with renal failure. Several studies have suggested that renal function is affected but the subsequent arguments leave the clinician in no man's land. A recent study in Critical Care by Simon and colleagues using a two hit animal model of shock demonstrates that the use of a higher molecular weight starch, HES 200/0.5, is associated with impaired renal function when compared with ringers acetate, gelatin or a lower molecular weight starch, HES 130/0.42. ⋯ Added to the previous evidence, the renal effects of HES200/0.5 are probably real. Many clinicians have already moved to the lower molecular weight starches on the basis of doubt rather than certainty, but this study tips the balance. The cause remains elusive and the lack of a mechanism should be seen as a problem.