1,721,010 research outputs found
Comment on: Endobronchial biopsy in the final diagnosis of chronic obstructive pulmonary disease and asthma: a clinicopathological study
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The importance of gastroenterological comorbidities in chronic obstructive disease and their manifestations
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The end-expiratory occlusion test for detecting preload responsiveness: a systematic review and meta-analysis
No full textBackground: We performed a systematic review and meta-analysis of studies assessing the end-expiratory occlusion test (EEXPO test)-induced changes in cardiac output (CO) measured by any haemodynamic monitoring device, as indicators of preload responsiveness. Methods: MEDLINE, EMBASE and Cochrane Database were screened for original articles. Bivariate random-effects meta-analysis determined the Area under the Summary Receiver Operating Characteristic (AUSROC) curve of EEXPO test-induced changes in CO to detect preload responsiveness, as well as pooled sensitivity and specificity and the best diagnostic threshold. Results: Thirteen studies (530 patients) were included. Nine studies were performed in the intensive care unit and four in the operating room. The pooled sensitivity and the pooled specificity for the EEXPO test-induced changes in CO were 0.85 [0.77–0.91] and 0.88 [0.83–0.91], respectively. The AUSROC curve was 0.91 [0.86–0.94] with the best threshold of CO increase at 5.1 ± 0.2%. The accuracy of the test was not different when changes in CO were monitored through pulse contour analysis compared to other methods (AUSROC: 0.93 [0.91–0.95] vs. 0.87 [0.82–0.96], respectively, p = 0.62). Also, it was not different in studies in which the tidal volume was ≤ 7 mL/kg compared to the remaining ones (AUSROC: 0.96 [0.92–0.97] vs. 0.89 [0.82–0.95] respectively, p = 0.44). Subgroup analyses identified one possible source of heterogeneity. Conclusions: EEXPO test-induced changes in CO reliably detect preload responsiveness. The diagnostic performance is not influenced by the method used to track the EEXPO test-induced changes in CO. Trial registration The study protocol was prospectively registered on PROSPERO: CRD42019138265
Idiopathic Pulmonary Fibrosis and Post-COVID-19 Lung Fibrosis: Links and Risks
Full text link: Idiopathic pulmonary fibrosis (IPF) is considered the paradigmatic example of chronic progressive fibrosing disease; IPF does not result from a primary immunopathogenic mechanism, but immune cells play a complex role in orchestrating the fibrosing response. These cells are activated by pathogen-associated or danger-associated molecular patterns generating pro-fibrotic pathways or downregulating anti-fibrotic agents. Post-COVID pulmonary fibrosis (PCPF) is an emerging clinical entity, following SARS-CoV-2 infection; it shares many clinical, pathological, and immune features with IPF. Similarities between IPF and PCPF can be found in intra- and extracellular physiopathological pro-fibrotic processes, genetic signatures, as well as in the response to antifibrotic treatments. Moreover, SARS-CoV-2 infection can be a cause of acute exacerbation of IPF (AE-IPF), which can negatively impact on IPF patients' prognosis. In this narrative review, we explore the pathophysiological aspects of IPF, with particular attention given to the intracellular signaling involved in the generation of fibrosis in IPF and during the SARS-CoV-2 infection, and the similarities between IPF and PCPF. Finally, we focus on COVID-19 and IPF in clinical practice
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