2,833 publications from this institution
AZD9773 rapidly and efficiently decreased plasma tumor necrosis factor-α concentration in patients with severe sepsis/septic shock, but this effect did not translate into clinical benefit.
Severe sepsis, defined as sepsis associated with acute organ dysfunction, results from a generalized inflammatory and procoagulant host response to infection. Coagulopathy in severe sepsis is commonly associated with multiple organ dysfunction, and often results in death. The molecule that is central to these effects is thrombin, although it may also have anticoagulant and antithrombotic effects through the activation of Protein C and induction of prostacyclin. In recent years, it has been recognized that chemicals produced by endothelial cells play a key role in the pathogenesis of sepsis. Thrombomodulin on endothelial cells coverts Protein C to Activated Protein C, which has important antithrombotic, profibrinolytic and anti-inflammatory properties. A number of studies have shown that Protein C levels are reduced in patients with severe infection, or even in inflammatory states without infection. Because coagulopathy is associated with high mortality rates, and animal studies have indicated that therapeutic intervention may result in improved outcomes, it was rational to initiate clinical studies.
This multicenter observational study reveals the common occurrence of anemia and the large use of blood transfusion in critically ill patients. Additionally, this epidemiologic study provides evidence of an association between transfusions and diminished organ function as well as between transfusions and mortality.
Acute kidney injury (AKI) is a serious and as yet incompletely understood disorder in which sudden impairment of kidney function occurs secondary to one or more of a variety of underlying conditions. This disorder is very common in (elderly) ICU patients and is associated with very high mortality. Many of those who survive suffer from permanent kidney failure and other long-term morbidities, which may include cardiovascular disease and immune dysfunction. Epidemiologic evidence suggests that AKI is not a single disease, but a syndrome comprised of multiple, often coexisting, etiologies. Being usually part of multiorgan failure syndrome, it calls for multiple organ support therapy. The publication at hand contains sections on prerenal azotemia syndromes, dying 'of' or 'with' AKI, pathophysiology of sepsis-induced acute kidney injury, developments in prevention/treatment/rehabilitation, and renal support. Reporting the latest recommendations from experts, it provides valuable information for those that are interested in understanding the disorder and its treatment options.
Magnesium (Mg) is an essential ion for life and is involved in many important biological processes. Mg deficiency may have serious consequences and has been implicated in many diseases. Assessment of Mg status is difficult because Mg is essentially intracellular and there is no simple, rapid and accurate laboratory test to determine total body Mg. New, non-invasive techniques are being developed that could be used in the near future. Mg therapy is clearly indicated in "torsade de pointes" and preeclampsia. Mg therapy is not recommended in the treatment of acute myocardial infarction, stroke or non-severe acute asthma. Nevertheless, Mg administration may be useful to reduce cerebral ischemic events after aneurysmal subarachnoid hemorrhage or in the treatment of severe acute asthma, specifically in children. Finally, the potential post-operative analgesic effect of Mg is still debated and results from new, larger clinical trials may help clarify this issue. This article reviews physiological functions and pharmacology of Mg status as well as the causes, clinical manifestations, and treatment of Mg deficiency. The possible analgesic effects of Mg in the postoperative period are also reviewed.
SCOPUS: ar.j
Hyperlactataemia, a marker of poor prognosis in intensive care patients, is most frequently found in cases of acute circulatory failure ; however, it may be due to factors other than cellular hypoxia. The level of blood lactate is determined by the balance between its production and its elimination, which can be influenced by various factors. For example, the influence of medication on blood lactate levels should not be underestimated, whether in anaesthesiology, with the use of propofol, or with certain anti-retrovirals in HIV seropositive patients. And in oncology, blood lactate can derive from anaerobic metabolism, characteristic of tumour cells. The differential diagnosis of hyperlactataemia can, therefore, sometimes be more complex than initially thought.
