Abstract
The present report highlights the most important papers appearing in Critical Care and other major journals about severe sepsis, the systemic inflammatory response and multiorgan dysfunction over the past year. A number of these clinical and laboratory studies will have a considerable impact on the sepsis research agenda for years to come. The steroid controversy, the debate over tight glycemic control, the colloid versus crystalloid issue, the value of selective decontamination of the digestive tract, the enlarging role of biomarkers, the value of genomics and rapid diagnostic techniques have all been prominently featured in recent publications. Basic research into novel predictive assays, genetic polymorphisms, and new molecular methods to risk-stratify and to determine treatment options for sepsis have occupied much of the Critical Care publications relating to sepsis pathophysiology in 2008. We will attempt to briefly summarize what we consider to be the most significant contributions to the sepsis literature over the last year, and their likely ramifications in the future, for critical care clinicians, clinical investigators and basic researchers alike.
Highlights
2008 was a significant year in Critical Care, with a number of landmark papers being published in sepsis research in this journal and in other publications
The results of this study were in keeping with those published by Hagiwara and colleagues, where danaparoid improved survival in an endotoxin-induced lung injury model and was associated with decreased production of high mobility group box 1 (HMGB-1) and proinflammatory cytokines [42]
Carriers of the polymorphism had an increased frequency of early death from infection along with higher Simplified Acute Physiology Score II compared with wild-type genotypes. This 982C>T variant was accompanied by significantly lower HMGB-1 blood levels (P
Summary
2008 was a significant year in Critical Care, with a number of landmark papers being published in sepsis research in this journal and in other publications. The results of this study were in keeping with those published by Hagiwara and colleagues, where danaparoid improved survival in an endotoxin-induced lung injury model and was associated with decreased production of high mobility group box 1 (HMGB-1) and proinflammatory cytokines [42] It remains to be seen whether danaparoid will be taken forward in clinical trials of sepsis given the recent negative results of heparin in a severe sepsis trial [43]. In an important study on the outcome effects of polymorphisms of the HMGB-1 gene locus on human chromosome 13, Kornblit and colleagues reported the first evidence of the HMGB-1 genotype’s impact on the risk of systemic inflammatory response and sepsis [47] These investigators performed a long-term, 4-year study comparing HMGB-1 sequencing data in 239 ICU patients with HMGB-1 blood levels and clinical outcomes. Gene association reports in the ICU literature are improving with respect to statistical methods and analytic detail but have further room for improvement [48]
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