%0 Journal Article %T Targeted treatment of acute respiratory distress syndrome with statins¡ªa commentary on two phenotype stratified re-analysis of randomized controlled trials %A Dennis C. J. J. Bergmans %A Lieuwe D. J. Bos %A Nanon F. L. Heijnen %A Ronny M. Schnabel %A on behalf of the DARTS consortium %J SCIE-indexed Journal %D 2019 %R 10.21037/jtd.2019.01.23 %X No immunomodulatory pharmacological interventions have been found effective for the acute respiratory distress syndrome (ARDS) despite identification of potentially effective drugs in preclinical studies (1,2). A frequently mentioned reason is the clinical and biological heterogeneity of ARDS (2). In attempts to quantify this heterogeneity, etiological, physiological-, and biological phenotypes have been explored (2-4). A classification based on a physiological phenotype by PaO2/FiO2 ratio, is included in the Berlin definition as ¡®oxygenation criterion¡¯ and discriminates between mild, moderate and severe ARDS (2). Recently, two biological phenotypes have been identified: ¡®hyper-inflammatory¡¯ and ¡®hypo-inflammatory¡¯, depending on levels of; pro-inflammatory markers, coagulopathy, severe shock, and metabolic derangement (4). These two biological phenotypes, also called ¡°subphenotypes¡±, have different outcomes with a high mortality in the ¡®hyper-inflammatory¡¯ phenotype and a low mortality in the ¡®hypo-inflammatory¡¯ phenotype. Furthermore, the biological phenotypes show a differential treatment responses to PEEP-strategies and fluid management (4,5). There is no data on a differential response to immunomodulatory treatments %U http://jtd.amegroups.com/article/view/26633/html