Exacerbations of Chronic Obstructive Pulmonary Disease (COPD) have a substantial effect on overall disease management, health system costs, and patient outcomes. However, exacerbations are often underdiagnosed or recognized with great delay due to several factors such as patients’ inability to differentiate between acute episodes and symptom fluctuations, delays in seeking medical assistance, and disparities in dyspnea perception. Self-management intervention plans, telehealth and smartphone-based programs provide educational material, counseling, virtual hospitals and telerehabilitation, and help COPD patients to identify exacerbations early. Moreover, biomarkers such as blood eosinophil count, fibrinogen, CRP, Serum amyloid A(SAA),together with imaging parameters such as the pulmonary artery-to-aorta diameter ratio, have emerged as potential predictors of exacerbations, yet their clinical utility is limited by variability and lack of specificity. In this review, we provide information regarding the importance of the early identification of exacerbation events in COPD patients and the available methods which can be used for this purpose.

We report a case of endogenous lipoid pneumonia secondary to long-term use of amiodarone (> 30 years) for atrial fibrillation in a 76-year-old Caucasian woman, presenting with cough and dyspnea. Endogenous Lipoid pneumonia is a rare underdiagnosed condition more prevalent in adults. It is usually asymptomatic and a diagnosis is generally made in patients who have become clinically unstable or when an abnormal lung shadow is found on a chest X-ray. In the case here described it was diagnosed by fiberoptic bronchoscopy with bronchoalveolar lavage (BALF) where fat-laden macrophages (oil red O stain) were identified. Since a history of use of oil-based products had been ruled out, amiodarone was deemed to be the most likely cause of lipoid pneumonia. The patient was managed with the replacement of amiodarone with digoxin and treated with oral prednisolone. The patient has remained clinically stable with radiological improvement during a follow-up of two years.

Current variations in asthma prevalence and clinical characteristics suggest that lifestyle choices including dietary habits, may affect the pathogenesis and/or clinical expression of the disease. The purpose of this study is to evaluate the association between adherence to Mediterranean diet (MD) and asthma control, considering disease severity. Adherence to MD was assessed through a questionnaire, the MD Adherence Screener (MEDAS), previously validated in Mediterranean populations. Each participant received a score ranging from 0 to 14. A score higher than 10 indicates high MD adherence. The level of asthma control was assessed by the Asthma Control Test and two groups were formed (controlled vs. partly controlled/uncontrolled). The study sample included 105 participants (34% males). About 45% of participants were severe asthmatics. Adherence to MD was associated with 14% higher, though not statistically significant, probability of controlled asthma in the overall study sample (OR = 1.14; 95% CI = 0.46-2.81) and 60% higher probability of controlled asthma among severe asthmatics (OR = 1.60, 95% CI = 0.46-5.59). These results indicate a possible association between adherence to MD and asthma control, but findings are restricted by the study's small sample size which does not allow asserting the inference.

Background: Chronic obstructive pulmonary disease (COPD) is a common disease characterized by progressive airflow obstruction, influenced by genetic and environmental factors. Eosinophils have been implicated in COPD pathogenesis, prompting the categorization into eosinophilic and non-eosinophilic endotypes. This study explores the association between eosinophilic inflammation and mRNA expression of ELAVL1, ZfP36, and HNRNPD genes, which encode HuR, TTP and AUF-1 proteins, respectively. Additionally, it investigates the expression of IL-9 and IL-33 in COPD patients with distinct eosinophilic profiles. Understanding these molecular associations could offer insights into COPD heterogeneity and provide potential therapeutic targets. Methods: We investigated 50 COPD patients, of whom 21 had eosinophilic inflammation and 29 had non-eosinophilic inflammation. Epidemiological data, comorbidities, and pulmonary function tests were recorded. Peripheral blood mononuclear cells were isolated for mRNA analysis of ELAVL1, ZfP36, and HNRNPD genes and serum cytokines (IL-9, IL-33) were measured using ELISA kits. Results: The study comprised 50 participants, with 66% being male and a mean age of 68 years (SD: 8.9 years). Analysis of ELAVL1 gene expression revealed a 0.45-fold increase in non-eosinophilic and a 3.93-fold increase in eosinophilic inflammation (p = 0.11). For the ZfP36 gene, expression was 6.19-fold higher in non-eosinophilic and 119.4-fold higher in eosinophilic groups (p = 0.07). Similarly, HNRNPD gene expression was 0.23-fold higher in non-eosinophilic and 0.72-fold higher in eosinophilic inflammation (p = 0.06). Furthermore, serum levels of IL-9 showed no statistically significant difference between the eosinophilic and non-eosinophilic group (58.03 pg/mL vs. 52.55 pg/mL, p = 0.98). Additionally, there was no significant difference in IL-33 serum levels between COPD patients with eosinophilic inflammation and those with non-eosinophilic inflammation (39.61 pg/mL vs. 37.94 pg/mL, p = 0.72). Conclusions: The data suggest a notable trend, lacking statistical significance, towards higher mRNA expression for the ZfP36 and HNRNPD genes for COPD patients with eosinophilic inflammation compared to those with non-eosinophilic inflammation.

Introduction: Flexible bronchoscopy and its new methods have revolutionized the era of the diagnosis, staging, and restaging of lung cancer. A rare late complication is post-bronchoscopy respiratory infection, but it is critical due to treatment delays, treatment cancellation, and death. The aim of this study is to identify risk factors for respiratory tract infection after bronchoscopy in patients with lung cancer. Methods: A retrospective single-center observational study of 182 hospitalized patients was conducted at U.G.H. “ATTIKON” who underwent bronchoscopy for diagnosis/staging/restaging of lung cancer from January 2022 to April 2023. Patients were divided into two groups based on whether or not they developed post-bronchoscopy respiratory infection. Results: Analyzing the data between the groups, several potential risk factors for infection were identified, including recent hospitalization for COVID-19 within the last month (OR: 6.16; p = 0.01), history of COPD (OR: 8; p = 0.03), presence of emphysema on CT scan (OR: 8; p = 0.03), endobronchial lesions causing ≥ 50% bronchial obstruction with inability to advance the bronchoscope (OR: 9.6; p < 0.01), increased white blood cell count (≥8.5 K/μL) before bronchoscopy (OR: 8; p = 0.03), and advanced stage IV non-small-cell lung cancer (OR: 9.67; p = 0.02). Conclusions: Comparing our results with previous studies on risk factors for respiratory infections after bronchoscopy, we found that recent hospitalization for SARS-CoV-2 infection was a unique finding in our study. With the increasing incidence of lung cancer worldwide and the critical role of bronchoscopy in diagnosis/staging/restaging, large multicenter studies are needed to identify these risk factors and develop strategies for early detection, treatment, and prevention.

Introduction: The coronavirus disease (COVID-19) is an infectious disease, caused by the SARS-CoV-2 virus, which causes severe respiratory disease. Critical ill patients often experience a condition known as Low T3 Syndrome (LT3S). Previous studies showed an association between low FT3 levels...