Objective: Controversy remains as to whether low-dose corticosteroids can reduce the mortality and morbidity of acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS) without increasing the risk of adverse reactions. We aimed to evaluate all studies investigating prolonged corticosteroids in low-to-moderate dose in ALI or ARDS.
Data Sources: MEDLINE, EMBASE, Current Content, and Cochrane Central Register of Controlled Trials, and bibliographies of retrieved articles.
Study Selection: Randomized controlled trials (RCTs) and observational studies reported in any language that used 0.5-2.5 mg.kg.d of methylprednisolone or equivalent to treat ALI/ARDS.
Data Extraction: Data were extracted independently by two reviewers and included study design, patient characteristics, interventions, and mortality and morbidity outcomes.
Data Synthesis: Both cohort studies (five studies, n = 307) and RCTs (four trials, n = 341) showed a similar trend toward mortality reduction (RCTs relative risk 0.51, 95% CI 0.24-1.09; p = 0.08; cohort studies relative risk 0.66, 95% CI 0.43-1.02; p = 0.06). The overall relative risk was 0.62 (95% CI 0.43-0.91; p = 0.01). There was also improvement in length of ventilation-free days, length of intensive care unit stay, Multiple Organ Dysfunction Syndrome Score, Lung Injury Scores, and improvement in Pao2/Fio2. There was no increase in infection, neuromyopathy, or any major complications. There was significant heterogeneity in the pooled studies. Subgroup and meta-regression analyses showed that heterogeneity had minimal effect on treatment efficacy; however, these findings were limited by the small number of studies used in the analyses.
Conclusion: The use of low-dose corticosteroids was associated with improved mortality and morbidity outcomes without increased adverse reactions. The consistency of results in both study designs and all outcomes suggests that they are an effective treatment for ALI or ARDS. The mortality benefits in early ARDS should be confirmed by an adequately powered randomized trial.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1097/CCM.0b013e31819fb507 | DOI Listing |
Am J Respir Cell Mol Biol
January 2025
Lady Davis Institute for Medical Research, Montreal, Quebec, Canada;
Iron regulatory protein 2 (IRP2), a post-transcriptional regulator of cellular iron metabolism has been associated with susceptibility to chronic obstructive pulmonary disease (COPD). Resistive breathing (RB) is the hallmark of the pathophysiology of obstructive airway diseases, especially during exacerbations, where increased mechanical stress is imposed on the lung. We have previously shown that RB, through tracheal banding, mimicking severe airway obstruction, induces pulmonary inflammation and injury in previously healthy mice.
View Article and Find Full Text PDFAm J Respir Cell Mol Biol
January 2025
Duke Medicine, Medicine, Durham, North Carolina, United States.
Becoming more frequent due to climate change, ozone (O) exposures can cause lung injury. Alveolar type 2 (AT2) cells and hyaluronan (HA), a matrix component, are critical to repairing lung injury and restoring homeostasis. Here, we define the impact of HA on AT2 cells following acute O exposure.
View Article and Find Full Text PDFAm J Respir Cell Mol Biol
January 2025
Second Military Medical University First Hospital, Department of Respiratory and Critical Care Medicine, Shanghai, China;
Identifying inflammation-induced leukocyte subsets and their derived circulating factors has been instrumental in understanding the progession of ALI/ARDS. Nevertheless, how primary inflammation-induced non-leukocyte populations in distal organs contribute to ALI/ARDS remains poorly defined. Here, we report one population of erythroblast-like cells (Ter-cells) deriving from megakaryocyte- erythroid progenitor cells with a unique Ter-119+CD45-CD71+ phenotype in ALI/ARDS.
View Article and Find Full Text PDFHepatol Commun
November 2024
Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Background: Liver fibrosis is caused by chronic toxic or cholestatic liver injury. Fibrosis results from the recruitment of myeloid cells into the injured liver, the release of inflammatory and fibrogenic cytokines, and the activation of myofibroblasts, which secrete extracellular matrix, mostly collagen type I. Hepatic myofibroblasts originate from liver-resident mesenchymal cells, including HSCs and bone marrow-derived CD45+ collagen type I+ expressing fibrocytes.
View Article and Find Full Text PDFCell Mol Life Sci
January 2025
School of Basic Medical Sciences, Xinxiang Medical University, #601 Jinsui Road, Xinxiang, 453003, Henan, China.
Herpes simplex virus type I (HSV-1) infection is associated with lung injury; however, no specific treatment is currently available. In this study, we found a significant negative correlation between FcRn levels and the severity of HSV-1-induced lung injury. HSV-1 infection increases the methylation of the FcRn promoter, which suppresses FcRn expression by upregulating DNMT3b expression.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!