Recent advances in sepsis research: novel biomarkers and therapeutic targets.

Sepsis remains a common cause of death in the intensive care units worldwide. However, in the last decade a significant development could be noticed in sepsis research regarding diagnostic markers that can help the physicians to recognize the disease in the early phase, which is the clue of the successful treatment of sepsis. This development provided the identification of new molecules and structures (i.e. cytokines, cell surface markers, receptors) that are potential biomarkers of sepsis in the clinical settings. Besides, the advance in the understanding of the pathophysiologic, immunologic and biochemical pathway of sepsis has made the way for assignment of new drug targets in the therapy of sepsis. This review aims to provide a summary about these novelties regarding our knowledge about sepsis published in the medical literature recently. We will describe the presumed pathophysiological role and diagnostic value of sepsis markers that are used even more widely in the clinical practice (i.e. procalcitonin, IL-6), summarize the data regarding the sepsis marker candidates that are investigated in some initial study (i.e. matrix metalloproteinases, microRNA fingerprints), and we will discuss substances that may be specific markers for certain organ failures related to sepsis (i.e. neutrophil gelatinase-derived lipocalin in acute renal failure). Furthermore, we will review the mediators of the immuno-inflammatory cascade in sepsis concerning their potential applicability as therapeutic targets in the treatment of this often lethal disease. In addition, we present some insights into the identification of genetic markers of sepsis.

Circulating endothelial cell count, plasma vWF and soluble ICAM-1 levels following primary or elective percutaneous coronary intervention.

BACKGROUND: Percutaneous coronary intervention (PCI) is an important therapeutic strategy in patients with ischaemic heart disease. Our aim was to clarify the extent of endothelial injury induced by PCI in stable angina (SA) or in acute ST-elevation myocardial infarction (STEMI). METHODS: Circulating endothelial cell (CEC) count, von Willebrand factor (vWF) and soluble intercellular adhesion molecule-1 (sICAM-1) levels were determined pre-, post-, 24 and 96h after PCI in patients with SA (n=23) and with STEMI (n=28). To provide control data regarding the effect of angiography itself stable angina patients with coronarography only (n=23) were enrolled. RESULTS: PCI and coronarography in stable angina patients caused measurable, but only non-significant elevation of CEC count and plasma vWF (p=NS). In STEMI, significantly higher baseline CEC count (p=0.019) and vWF plasma levels (p=0.046) were found compared to SA with PCI/or coronarography. After PCI, explicit increase in CEC count was observed (significant peak at 24h) (p=0.036). Positive correlation was found between baseline CKMB and CEC count at 24h (r=0.51, p<0.05). CONCLUSION: Both coronary angiography and elective PCI cause only mild endothelial injury. However, in patients with STEMI, not only the procedure itself but myocardial ischemia and the ongoing atherothrombotic process might be responsible for the prolonged and more pronounced endothelial damage.