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Background/aims Although an increasing volume of research is emerging, rehabilitative treatment of patients with COVID-19 still continues to be a matter of great importance that must be explored further. The purpose of the present study was to describe the effects of inpatient rehabilitation in acute patients treated in a sub-intensive hospital setting during the COVID-19 pandemic. Methods A retrospective analysis was conducted based on the prospectively collected data of 192 patients with COVID-19 undergoing a physiotherapeutic regimen during their hospitalisation. Patients were admitted because of COVID-19-related pneumonia from the periods of 25 March-12 June 2020 and 2 November 2020-9 June 2021. This study investigated dyspnoea intensity using the modified Borg scale, motor function through the 1-minute sit-to-stand test, and daily walked distance. In a subset of 57 patients, handgrip strength and respiratory muscle function was also evaluated. Measurements were taken at baseline and discharge. Results Patients were classified according to the severity of their ratio of arterial oxygen partial pressure to fractional inspired oxygen (mean 225 ± 82 mmHg). At discharge to home or to another hospital facility, patients performed a mean of 12 repetitions (1-minute sit-to-stand test); dyspnoea intensity was 1.4 (modified Borg scale), and they were able to walk a mean distance of 266.7 metres. The mean handgrip strength of the dominant hand was 29.3 kg, the maximal inspiratory pressure was 43.5 cmH2O, and the maximal expiratory pressure was 59.1 cmH2O. Overall, significant differences before and after treatment were detected for all clinical variables. Dyspnoea improved by 0.7 points; walked distance by 200 metres; the number of repetitions at the 1-minute sit-to-stand test by 5.6; the handgrip strength by 1.2 kg (right hand) and 1.7 kg (left hand); maximal inspiratory pressure by 7.7 cmH2O; and maximal expiratory pressure by 9.5 cmH2O. Conclusions Patients obtained significant improvements in functional capacity, dyspnoea perception, handgrip strength and respiratory muscle function. In addition, the treatment was feasible and well tolerated by patients, and no adverse related events were observed in a sub-intensive care setting. [ABSTRACT FROM AUTHOR]

Background: For the first time we tested an association between the human multidrug resistance gene 1 (MDR1) polymorphisms (SNPs) and idiopathic pulmonary fibrosis (IPF). Several MDR1 polymorphisms are associated with pathologies in which they modify the drug susceptibility and pharmacokinetics. Materials and Methods: We genotyped three MDR1 polymorphisms of 48 IPF patients and 100 control subjects with Italian origins. Results: No evidence of association was detected. Conclusion: There are 50 known MDR1 SNPs, and their role is explored in terms of the effectiveness of drug therapy. We consider our small-scale preliminary study as a starting point for further research. [ABSTRACT FROM AUTHOR]

Purpose: Saber-sheath trachea is a specific radiographic parameter for chronic obstructive pulmonary disease (COPD), which consists of marked coronal narrowing associated with sagittal widening (tracheal index <2/3-0.67). The aim of this study was to investigate the correlation between saber-sheath trachea and clinical-radiological findings in a group of patients with COPD of varying severity. Materials and methods: We evaluated the chest radiographs of 71 patients with COPD distributed as follows: GOLD class I, 8/71 (11.3 %); class II, 34/71 (47.9 %); class III, 16/71(22.5 %); class IV, 13/71 (18.3 %). In 52/71 (73.2 %) patients we also evaluated chest computed tomography (CT) scans. We analyzed the prevalence of saber-sheath trachea and its correlation with the Tiffenau index, GOLD stage and radiological signs of COPD. Moreover, we evaluated the sensitivity, specificity and accuracy of chest radiography as compared to CT taken as the gold standard, and the correlation between the radiographic and CT tracheal index. Results: Saber-sheath trachea was found in 18/71 (25.4 %) patients, with a greater prevalence in patients with lower Tiffenau Index ( p = 0.02), GOLD stages III-IV and visual severity score 3 (severe) on chest CT. Saber-sheath trachea was not found to be related to other radiological signs of COPD. The sensitivity, specificity and accuracy values of radiography were 72.2, 97.0 and 88.5 %, with perfect concordance between the radiographic and CT tracheal index ( p < 0.00001). Conclusion: Saber-sheath trachea is linked to the functional severity of airway obstruction, but not to other radiological signs of COPD. Thus, evaluation of the trachea at chest radiography is strongly recommended. [ABSTRACT FROM AUTHOR]

Objectives. To investigate the effect of the cause of acute respiratory failure and the role of comorbidities both acute and chronic on the outcome of COPD patients admitted to Respiratory Intensive Care Unit (RICU) with acute respiratory failure and treated with NIV. Design. Observational prospective study. Patients and Methods. 176 COPD patients consecutively admitted to our RICU over a period of 3 years and treated with NIV were evaluated. In all patients demographic, clinical, and functional parameters were recorded including the cause of acute respiratory failure, SAPS II score, Charlson comorbidity index, and further comorbidities not listed in the Charlson index. NIV success was defined as clinical improvement leading to discharge to regular ward, while exitus or need for endotracheal intubation was considered failure. Results. NIV outcome was successful in 134 patients while 42 underwent failure. Univariate analysis showed significantly higher SAP II score, Charlson index, prevalence of pneumonia, and lower serum albumin level in the failure group. Multivariate analysis confirmed a significant predictive value for pneumonia and albumin. Conclusions. The most important determinants of NIV outcome in COPD patients are the presence of pneumonia and the level of serum albumin as an indicator of the patient nutritional status. [ABSTRACT FROM AUTHOR]

In idiopathic pulmonary fibrosis (IPF) patients the presence of missense polymorphisms (SNP) in members of the epidermal growth factor receptor (EGFR) family or their genetic association could influence the binding affinity of natural ligands, modifying the expression and the behavior of the correlated genes. EGFR family members are particularly involved in the epithelial injury and fibrotic process in IPF. Genetic variations in HER family of receptors may alter the possible therapeutic efficacy of EGFR inhibitors. This study aimed to analyze the relationships between IPF and specific EGF receptor family functional polymorphisms. We tested the presence of common EGFR, HER2 and HER3 non-synonymous SNPs in the peripheral blood of 20 Italian IPF patients and their association with the disease. Our data indicated that the HER2 variant allele frequency was significantly lower in patients than in controls, with an odds ratio of 0.31 (95% CI 0.080, 0.98). Our finding suggests that HER2 variant could be a protective factor against IPF onset. [ABSTRACT FROM AUTHOR]

Background: Although increased nitric oxide (NO) production in asthma is mediated largely by upregulation of the inducible form of nitric oxide synthase (iNOS, or NOS 2), some studies have suggested an important role for the usually constitutive neural NOS isoform (nNOS, or NOS 1). Aim: To investigate how NOS 1 may influence allergic inflammation, we used NOS 1 knockout mice and their wild-type (WT) controls. Methods: Mice were sensitized and challenged with ovalbumin (OVA) using a protocol known to upregulate NOS 2 in the airways. Results: In addition to expected increases in NOS 2 activity, OVA challenge led to increases in calcium-dependent NOS activity, which was accounted for by increased expression of NOS 1 at both mRNA (n = 5, p < 0.001) and protein levels (n = 5, p < 0.01). In NOS-1-deficient mice, OVA challenge induced less eosinophilia (n = 7, p < 0.05) and much less NO production (n = 10, p < 0.01) than in WT controls, reflecting not only the expected absence of NOS 1, but also lack of upregulation of NOS 2. This interaction appeared to be stimulus specific as NOS-1-deficient mice did upregulate NOS 2 following exposure to lipopolysaccharide (n = 5, p < 0.001). Conclusions: These findings underscore the importance of NOS 1 in allergic airway inflammation and suggest a mechanism by which NOS 1 may influence overall NO production in the airways. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]