Effect of pulmonary rehabilitation programme including either O2 inhalation or noninvasive ventilation in patients with chronic obstructive pulmonary disease.

Background: Pulmonary rehabilitation (PR) is crucial in managing chronic obstructive pulmonary disease (COPD) and enhancing functional capacity and health status. Oxygen therapy and noninvasive ventilation (NIV) may be needed to be incorporated into rehabilitation to augment the effectiveness of physical training. Objectives: To compare and assess the impact of the PR programme alone and with augmentation with O2 or NIV on COPD patients. Methods: Seventy-five COPD patients were equally divided into three groups: group 1 patients performed 8 week-PR programme only. Group 2 performed the PR programme while receiving O2. Group 3 completed the PR programme plus NIV. Modified Borg scale, VO2 max, modified Medical Research Council Dyspnea Scale, 6-minute walk test, COPD assessment test score, spirometric measures and arterial blood gases were assessed before and after the programme. Results: The outcome measurements showed meaningful improvement compared with the baseline in the three studied groups. However, VO2 max in group 3 showed higher significant improvement than both groups 1 and 2. Regarding 6-minute walk test, groups 2 and 3 had a higher significant improvement than group 1. COPD assessment test score in group 3 showed higher significant improvement than groups 1 and 2. Arterial blood gases in groups 2 and 3 showed significant increase in partial pressure of arterial oxygen and arterial oxygen saturation, but group 3 only had a significant decrease in PaCO2. Conclusion: O2 supplementation and NIV help severe to very severe COPD patients to perform higher exercise intensity, so they augment the benefits of PR.

Prognostic role of annexin A2 and cancer-associated fibroblasts in advanced non-small cell lung cancer: Implication in epithelial-mesenchymal transition and gefitinib resistance.

BACKGROUND: Despite advances in treatment of non-small cell lung cancer (NSCLC), its prognosis remains dismal. Development of drug resistance is a major obstacle against success of targeted epidermal growth factor receptor (EGFR) -tyrosine kinase inhibitors (TKI) therapy. This study aimed to assess the prognostic role of annexin A2 (ANXA2) expression, within both tumor cells and stroma, as well as cancer associated fibroblasts (CAFs) in NSCLC and to investigate their potential role in induction of epithelial mesenchymal transition (EMT) and resistance to gefitinib. METHOD: Immunohistochemistry was performed to evaluate tumoral and stromal ANXA2 expression and α-SMA-stained CAFs in 110 advanced NSCLC patients. Furthermore, STAT3 and E-cadherin mRNA expression was studied by quantitative reverse transcription PCR (qRT-PCR). RESULTS: Both tumoral and stromal ANXA2 as well as CAFs were significantly related to clinical stage IV and malignant pleural effusion, while tumoral ANXA2 was significantly related to poor tumor differentiation. EGFR mutation and high tumoral ANXA2 were independent factors for poor overall survival, whereas high stromal and tumoral ANXA2 and high CAFs were independent predictors for poor progression-free survival. Moreover, high ANXA2 and CAFs were significantly associated with high STAT3 and low E-cadherin mRNA expression. Focusing on EGFR mutated cases, gefitinib resistance was significantly associated with high tumoral and stromal ANXA2, high CAFs, high STAT3 and low E-cadherin. CONCLUSION: CAFs and ANXA2 could be considered as poor prognostic parameters in advanced NSCLC and are potential factors for gefitinib therapy resistance through EMT induction.

Acidic mammalian chitinase tuning after enteric helminths eradication in inflammatory respiratory disease patients.

AIM: This study aimed at investigating the presence of intestinal parasitic infections in inflammatory respiratory diseases patients during the disease attack, and measuring the acidic mammalian chitinase (AMCase) gene expression in blood before and after infection eradication. METHODOLOGY: This case-control study included 123 inflammatory respiratory diseases patients and 120 apparently healthy individuals. Repeated stool examination was done, while total and specific IgE were measured. AMCase gene expression was analysed by real time-polymerase chain reaction (RT-PCR). RESULTS: Infection was detected in 32.5% of the diseased and 23.25% of the healthy individuals. Higher rate of the helminthic infection was detected (23.57) in comparison to the protozoal (12.19%) in the patients. A significantly higher rate of infection with the chitin-rich helminths "Enterobius vermicularis & Hymenolepis nana" and level of anti-Dermatophagoide-IgE were reported in the patients (14.63%, 6.5% and 23.57%, respectively). AMCase expression was significantly higher in helminths-infected patients than the noninfected, or protozoa infected. After infection eradication, AMCase expression significantly declined in the previously helminth-infected patients (mean ± SD = 13.9 ± 3.918 before and 4.515 ± 1.93 after), but insignificantly affected in the protozoa infected (mean ± SD = 2.095 ± .285 before and 2.675 ± 1.181 after). CONCLUSION: Chitin-rich intestinal helminths are suspected to precipitate Th2-immune response in remote tissues by enhancing systemic AMCase expression through intestinal mucosa and macrophages irritation.

Pulmonary Function Tests Abnormalities in Children With Inflammatory Bowel Disease: Is It Common?

OBJECTIVE: The aim of the study was to evaluate the frequency and type of pulmonary dysfunction in newly diagnosed children with inflammatory bowel disease (IBD) and the correlation between pulmonary function tests (PFTs) and IBD activity. METHODS: It is an observational case-control study. One hundred newly diagnosed children with IBD were enrolled as the patient group, which was further subdivided into 52 with Crohn disease (CD) and 48 with ulcerative colitis (UC). Fifty healthy children matched for age, sex, height, and body mass index (BMI) served as the control group. PFTs in the form of forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), FEV1/FVC, residual volume (RV), total lung capacity (TLC), mid-forced expiratory flow of 25% to 75% (FEF 25%-75%) and diffusing capacity of the lung for carbon monoxide (DLCO) were evaluated in all studied children. PFTs were measured at diagnosis, every 6 months for a period of 3 years, during remission and at least once during activity in patient group. RESULTS: There was significant progressive deterioration in all PFTs in IBD patients compared with their PFTs at the start of the study (P < 0.05) except for FEV1/FVC, RV, and TLC (P > 0.05). There was significant deterioration during disease activity compared with remission state as regards FEV1, FVC, FEF 25% to 75%, and DLCO (P < 0.05). Significant negative correlation was found between disease activity in both UC and CD groups and FEV1, FVC, FEF 25% to 75%, and DLCO. CONCLUSIONS: Subclinical PFTs abnormalities are common in pediatric IBD even during remission period. So, periodic PFTs evaluation should be considered in the routine follow-up of IBD children.

NOD2 expression, DNA damage and oxido-inflammatory status in atopic bronchial asthma: Exploring their nexus to disease severity.

BACKGROUND: Allergic asthma is a chronically relapsing inflammatory airway disease with a complex pathophysiology. AIM: This study was undertaken to investigate the potential contribution of NOD2 signaling, proinflammatory cytokines, chitotriosidase (CHIT1) activity, oxidative stress and DNA damage to atopic asthma pathogenesis, as well as to explore their possible role as surrogate noninvasive biomarkers for monitoring asthma severity. METHODS: Sixty patients with atopic bronchial asthma who were divided according to asthma severity into 40 mild-moderate, 20 severe atopic asthmatics, in addition to thirty age-matched healthy controls were enrolled in this study. NOD2 expression in PBMCs was assessed by quantitative real-time RT-PCR. DNA damage indices were assessed by alkaline comet assay. Serum IgE, IL-17, IL-8 and 3-Nitrotyrosine levels were estimated by ELISA. Serum CHIT1and GST activities, as well as MDA levels, were measured. RESULTS: NOD2 mRNA relative expression levels were significantly decreased in atopic asthmatic cases relative to controls with lower values among severe atopic asthmatics. On the other hand, IL-17 and IL-8 serum levels, CHIT1 activity, DNA damage indices and oxidative stress markers were significantly increased in atopic asthmatic cases relative to controls with higher values among severe atopic asthmatics. The change in these parameters correlated significantly with the degree of decline in lung function. CONCLUSION: The interplay between NOD2 signaling, proinflammatory cytokines, CHIT1 activity, heightened oxidative stress and DNA damage orchestrates allergic airway inflammation and thus contributing to the pathogenesis of atopic asthma. These parameters qualified for measurement as part of new noninvasive biomarker panels for monitoring asthma severity.