Editorials

Antithrombin III in critically ill patients

BMJ 2007; 335 doi: https://doi.org/10.1136/bmj.39399.552245.80 (Published 13 December 2007) Cite this as: BMJ 2007;335:1219
  1. A Torossian, associate professor of anaesthesia and intensive care medicine1,
  2. J Graf, associate professor of cardiology and intensive care medicine1,
  3. A Bauhofer, associate professor of theoretical surgery2
  1. 1Clinic of Anaesthesia and Intensive Care Medicine, University Hospital Marburg, 35033 Marburg, Germany
  2. 2Institute of Theoretical Surgery, Philipps-University Marburg, 35033 Marburg, Germany
  1. alexander-torossian{at}t-online.de

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

    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 injuryimproves 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 …

    View Full Text

    Sign in

    Log in through your institution

    Free trial

    Register for a free trial to thebmj.com to receive unlimited access to all content on thebmj.com for 14 days.
    Sign up for a free trial

    Subscribe