1. Motamedi SM, Posadas-Calleja

J, Straus S, Bates DW et al. The efficacy of computer-enabled discharge interventions: a systematic review. BMJ Qual Saf 2011; 20: 403–415. 2. Callen J, McIntosh J, Li J. Accuracy of medication documentation in hospital discharge summaries: A retrospective analysis of medication transcription errors in manual and electronic discharge summaries. International Journal of Medical Informatics 2010; 79: 58–64. “
“K. Sonnexa,b, H. Alleemuddera, Sunitinib L-C. Chena aUniversity of Nottingham, Nottingham, UK, bNottingham University Hospitals, Nottingham, UK ICS have been shown to reduce the decline in lung function in COPD. However, it is thought that smoking causes resistance to the effects of ICS. Never-smokers, ex-smokers and light smokers had a better improvement in lung function1 after six months ICS use than current and heavy smokers. ‘Steroid resistance’ due to smoking may cause lower efficacy selleck products of ICS in this patient group but further work is required. It has been shown that smoking accelerates the loss in lung function (as measured by forced

expiratory volume in 1 second; FEV1) and increases mortality in Chronic Obstructive Pulmonary Disease (COPD) patients.1 Later stages of COPD may require regular treatment with inhaled corticosteroids (ICS) in addition to bronchodilators. One of the mechanisms by which ICS exerts its effect is by acting on enzyme histone deacetylase 2 (HDAC2) to suppress the release of inflammatory mediators.2 ICS have been shown

to reduce exacerbation rates and possibly reduce the decline in FEV1 in comparison to placebo.1 However, there is some evidence that smoking inactivates HDAC2, resulting in smokers being resistant to the effects of ICS.2 The aim of this research was to conduct a systematic review of the evidence that smoking affects efficacy of ICS in COPD. An electronic database search of PubMed, Ovid Medline, Ovid Embase and Cochrane Library (2000–2014) was performed using appropriate free text and MeSH terms. The reference lists of the retrieved papers were searched for retrieving further relevant studies. Fully published RCTs evaluating the use of ICS Vasopressin Receptor in COPD adults and stratifying the participants by smoking status were included. Review articles, abstracts, papers which are not fully published or published in languages other than English were not included. Retrieved trials that include COPD patients with asthma, lung cancer and pneumonia were excluded. Ethics approval was not required. A total of 44 studies were identified, 40 were excluded because participants were not stratified according to smoking status or the population did not meet the inclusion criteria. Of the remaining four trials, one was not randomised and was thus excluded. COPD severity varied across the studies ranging from mild to very severe. Two types of ICS were studied as monotherapy or in combination with salbutamol or salmeterol: fluticasone and budesonide.