Effect of Azithromycin on Lung Function and Pulmonary Exacerbations in Children with Post-infectious Bronchiolitis Obliterans. A Double-blind, Placebo-controlled Trial
Published on: 28th February, 2024
Introduction: Acute lower respiratory infection (ALRI) of viral etiology is a frequent consultation in pediatrics. Post-infectious bronchiolitis obliterans (PIBO) is a rare and potentially severe disorder following ALRI, characterized by partial or complete obstruction of the small airways by inflammatory tissue. There is evidence that macrolides reduce morbidity and mortality in diffuse panbronchiolitis, which may have similar inflammatory and obstructive components.We hypothesized that the effect of azithromycin (AZ) may improve lung function and reduce pulmonary exacerbations in PIBO.MethodsStudy design: A double-blind, randomized, placebo-controlled trial.Patients: We enrolled patients with PIBO followed-up at the Pulmonology department between 5 years to 18 years.Treatment regimen: The patients were randomized to receive active drug or placebo three times a week. Clinical evaluation: Clinical evaluation, pulse oximetry, lung function, and 6-min walk test were performed before and after study initiation and at 1, 3, and 6 months.CT scan and a quality of life questionnaire were performed at the beginning and the end of the Study.Results: 29 patients, 15 in G1 (10 males) and 14 in G2 (7 males) were included.There were no significant differences in FVC, FEV1, TLC, RV, or sGaw between the treatment group and controls. In addition, no significant differences were observed in exacerbations, quality of life questionnaire, or HRCT scan scores.Conclusion: No differences were observed between the groups. Further studies are necessary to allow us to find a better treatment, as azithromycin does not seem to be efficacious.
Why is Pain not Characteristic of Inflammation of the Lung Tissue?
Published on: 7th March, 2024
The article presents materials that make it possible to understand the reason for the absence of one of the classic signs of inflammatory processes in patients with acute pneumonia. The peculiarities of the functional significance of the lungs for the body are the reason that in the case of inflammation in the tissues of the organ, nature has provided for the presence of a more important adaptive mechanism instead of pain as a signal sign. Understanding the causes of the absence of pain in pneumonia in the initial period, which is most responsible for timely and effective care for these patients, allows us to look at the pathogenesis of the disease from a new point of view, which is of fundamental importance for the correction and selection of pathogenetic means of care.
Effect of TAK242 on MCP-1 and TGF-β in COPD Rats
Published on: 13th March, 2024
Objective: To investigate the mechanism of MCP-1 and TGF-β regulation by TAK242 in COPD rats. Methods: Thirty-six SD rats were randomly divided into normal, COPD control, and TAK242 groups. The normal group was freely fed, and the other groups used the method of fumigation plus lipopolysaccharide tracheal drip to establish an experimental animal model of COPD. After successful modeling, each experimental group received 0.9% NaCl solution and corresponding drugs by intraperitoneal injection for 7 d. After drug administration, lung function was examined; pathological changes in lung tissue were observed by light microscopy with hematoxylin-eosin staining; mRNA expression of MCP-1 and TGF-β was detected by q-PCR; and protein expression of MCP-1 and TGF-β in lung tissue was detected by Western blot and IHC, TGF-β protein expression in rat lung tissue. Results: Compared with the normal group, rats in the COPD control group showed signs and symptoms of COPD, decreased lung function, and increased expression of MCP-1 and TGF-β. The TAK242 group showed decreased expression of MCP-1 and TGF-β compared to the COPD control group. Conclusion: MCP-1, and TGF-β played a crucial role in the early stage of COPD fibrosis. TAK242 could ameliorate airway inflammation and inhibit the progression of COPD lung fibrosis in pre-existing rats in COPD model rats.
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