BMJ  2007;335:1219-1220 (15 December), doi:10.1136/bmj.39399.552245.80 (published 23 November 2007)

Editorials

Antithrombin III in critically ill patients

Evidence shows that it does not improve outcomes and increases the risk of bleeding

The first 150 words of the full text of this article appear below.

Antithrombin III, first described in 1939 as a cofactor of heparin, is one of the most important physiological inhibitors of coagulation.¹ Absence of this cofactor is regarded as incompatible with life, and acquired deficiency—for example, in sepsis—is associated with a high risk of venous thrombosis. In the 1960s researchers found a link between coagulation abnormalities and infection,² and the anti-inflammatory characteristics of antithrombin III were reported more recently.³ These discoveries have helped us understand how sepsis develops. In the past 15 years, several clinical trials have investigated whether giving antithrombin III to patients who are deficient in this factor—such as those with sepsis, pre-eclampsia, and traumatic brain injury—improves outcomes. Overall, it had no effect on mortality, although it did improve secondary end points in some trials.

In their systematic review in this week’s BMJ, Afshari and colleagues assess the effects of giving antithrombin III to critically ill . . . [Full text of this article]

¹ Clinic of Anaesthesia and Intensive Care Medicine, University Hospital Marburg, 35033 Marburg, Germany, ² Institute of Theoretical Surgery, Philipps-University Marburg, 35033 Marburg, Germany

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Antithrombin III in critically ill patients

Arash Afshari, et al.
bmj.com, 19 Dec 2007 [Full text]