Literature DB >> 11772319

Clinical developments for treating ARDS.

Stephanie Eaton1, Greg Martin.   

Abstract

Acute respiratory distress syndrome (ARDS), is characterised by capillary permeability and pulmonary oedema formation and may complicate a variety of medical and surgical illnesses. As a self-perpetuating state of inflammatory derangement, acute lung injury (ALI)/ARDS is manifest clinically as rapid development of radiographic infiltrates, severe hypoxaemia and reduced lung compliance. Over the years, researchers have made significant progress in elucidating the pathophysiology of this complex syndrome. Therapies targeting specific pathophysiologic steps in the development or persistence of this syndrome are in various stages of laboratory and clinical testing. Results to date have shown nitric oxide (NO) to improve oxygenation in the majority of patients but fail to improve mortality. Surfactant replacement has had limited success in adults, but new formulations and delivery methods may prove beneficial. Several inflammatory mediator-targeted therapies have progressed successfully through early clinical evaluation. Among these, neutrophil elastase inhibitors have shown the most promise and are currently undergoing Phase III trials. Other mediator-targeted therapies, such as prostaglandin E1, IL-10 and platelet activating factor antagonists, have not been found efficacious in large clinical trials of ARDS. However, these therapies, along with coagulation modulators, may have a favourable impact on ARDS by improving outcomes in sepsis, the greatest risk factor for developing this condition. In the interim, supportive care through improvements in mechanical ventilation are beneficial, while specific fluid balance and nutrition strategies may prove advantageous.

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Year:  2002        PMID: 11772319     DOI: 10.1517/13543784.11.1.37

Source DB:  PubMed          Journal:  Expert Opin Investig Drugs        ISSN: 1354-3784            Impact factor:   6.206


  5 in total

1.  Effects of urinary trypsin inhibitor on lipopolysaccharide-induced acute lung injury in rabbits.

Authors:  Hong-Beom Bae; Cheol-Won Jeong; Mei Li; Hyung-Seok Kim; Sang-Hyun Kwak
Journal:  Inflammation       Date:  2012-02       Impact factor: 4.092

2.  Staphylococcus aureus induces microglial inflammation via a glycogen synthase kinase 3beta-regulated pathway.

Authors:  Yi-Lin Cheng; Chi-Yun Wang; Wei-Ching Huang; Cheng-Chieh Tsai; Chia-Ling Chen; Ching-Fen Shen; Chia-Yu Chi; Chiou-Feng Lin
Journal:  Infect Immun       Date:  2009-07-13       Impact factor: 3.441

3.  Glycogen synthase kinase-3 negatively regulates anti-inflammatory interleukin-10 for lipopolysaccharide-induced iNOS/NO biosynthesis and RANTES production in microglial cells.

Authors:  Wei-Ching Huang; Yee-Shin Lin; Chi-Yun Wang; Cheng-Chieh Tsai; Hsiang-Chi Tseng; Chia-Ling Chen; Pei-Jung Lu; Po-See Chen; Li Qian; Jau-Shyong Hong; Chiou-Feng Lin
Journal:  Immunology       Date:  2008-10-29       Impact factor: 7.397

4.  The use of neutrophil elastase inhibitor in the treatment of acute lung injury after pneumonectomy.

Authors:  Sang Kwon Lee; Bong Soo Son; Jung Joo Hwang; Kil Dong Kim; Do Hyung Kim
Journal:  J Cardiothorac Surg       Date:  2013-04-08       Impact factor: 1.637

5.  Candidate genes and pathogenesis investigation for sepsis-related acute respiratory distress syndrome based on gene expression profile.

Authors:  Min Wang; Jingjun Yan; Xingxing He; Qiang Zhong; Chengye Zhan; Shusheng Li
Journal:  Biol Res       Date:  2016-04-18       Impact factor: 5.612

  5 in total

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