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.

Background: Coronavirus disease 2019 (COVID-19) has been a pandemic since 2020, and depending on the SARS-CoV-2 mutation, different pandemic waves have been observed. The aim of this study was to compare the baseline characteristics of patients in two phases of the pandemic and evaluate possible predictors of mortality. Methods: This is a retrospective multicenter observational study that included patients with COVID-19 in 4 different centers in Greece. Patients were divided into two groups depending on the period during which they were infected during the Delta and Omicron variant predominance. Results: A total of 979 patients (433 Delta, 546 Omicron) were included in the study (median age 67 years (54, 81); 452 [46.2%] female). Compared to the Omicron period, the patients during the Delta period were younger (median age [IQR] 65 [51, 77] vs. 70 [55, 83] years, p < 0.001) and required a longer duration of hospitalization (8 [6, 13] vs. 7 [5, 12] days, p = 0.001), had higher procalcitonin levels (ng/mL): 0.08 [0.05, 0.17] vs. 0.06 [0.02, 0.16], p = 0.005, ferritin levels (ng/mL): 301 [159, 644] vs. 239 [128, 473], p = 0.002, C- reactive protein levels (mg/L): 40.4 [16.7, 98.5] vs. 31.8 [11.9, 81.7], p = 0.003, and lactate dehydrogenase levels (U/L): 277 [221, 375] vs. 255 [205, 329], p < 0.001. The Charlson Comorbidity Index was lower (3 [0, 5] vs. 4 [1, 6], p < 0.001), and the extent of disease on computed tomography (CT) was greater during the Delta wave (p < 0.001). No evidence of a difference in risk of death or admission to the intensive care unit was found between the two groups. Age, cardiovascular events, acute kidney injury during hospitalization, extent of disease on chest CT, D-dimer, and neutrophil/lymphocyte ratio values were identified as independent predictors of mortality for patients in the Delta period. Cardiovascular events and acute liver injury during hospitalization and the PaO₂/FiO₂ ratio on admission were identified as independent predictors of mortality for patients in the Omicron period. Conclusions: In the Omicron wave, patients were older with a higher number of comorbidities, but patients with the Delta variant had more severe disease and a longer duration of hospitalization.

Background: Stewart’s approach is known to have better diagnostic accuracy for the identification of metabolic acid–base disturbances compared to traditional methods based either on plasma bicarbonate concentration ([HCO₃⁻]) and anion gap (AG) or on base excess/deficit (BE). This study aimed to identify metabolic acid–base disorders using either Stewart’s or traditional approaches in critically ill COVID-19 patients admitted to the ICU, to recognize potential hidden acid–base metabolic abnormalities and to assess the prognostic value of these abnormalities for patient outcome. Methods: This was a single-center retrospective study, in which we collected data from patients with severe COVID-19 admitted to the ICU. Electronical files were used to retrieve data for arterial blood gases, serum electrolytes, and proteins and to derive [HCO₃⁻], BE, anion gap (AG), AG adjusted for albumin (AG_adj), strong ion difference, strong ion gap (SIG), and SIG corrected for water excess/deficit (SIG_corr). The acid–base status was evaluated in each patient using the BE, [HCO₃⁻], and physicochemical approaches. Results: We included 185 patients. The physicochemical approach detected more individuals with metabolic acid–base abnormalities than the BE and [HCO₃⁻] approaches (p < 0.001), and at least one acid–base disorder was recognized in most patients. According to the physicochemical method, 170/185 patients (91.4%) had at least one disorder, as opposed to the number of patients identified using the BE 90/186 (48%) and HCO₃ 62/186 (33%) methods. Regarding the derived acid–base status variables, non-survivors had greater AG_adj, (p = 0.013) and SIG_corr (p = 0.035) compared to survivors. Conclusions: The identification of hidden acid–base disturbances may provide a detailed understanding of the underlying conditions in patients and of the possible pathophysiological mechanisms implicated. The association of these acid–base abnormalities with mortality provides the opportunity to recognize patients at increased risk of death and support them accordingly.

Invasive Aspergillus tracheobronchitis is a relatively rare form of invasive pulmonary aspergillosis characterized by invasion of the tracheobronchial tree by Aspergillus spp. Invasive pulmonary aspergillosis is predominantly detected in severely immunocompromised patients. Notably however, pulmonary and tracheobronchial cases of invasive aspergillosis have also been reported, particularly in the context of severe malaria caused by Plasmodium falciparum. Herein, we present a case of invasive Aspergillus tracheobronchitis in a patient with hairy cell leukemia and previous Plasmodium falciparum infection.

Previous studies have reported very different rates of human rhinovirus (HRV) and respiratory syncytial virus (RSV) genome detection in nasal and sputum samples, but not in bronchoalveolar lavage (BAL) and bronchial biopsy samples. Our study aimed to investigate the presence of HRV and RSV in the lungs of 31 consecutive patients with stable COPD (11 GOLD stage I, 11 II, and 9 III) and 22 control subjects (12 current or past smokers, and 10 non-smokers), who underwent diagnostic (e.g., lung cancer) and/or therapeutic (e.g., hemoptysis) fibreoptic bronchoscopy in a university hospital in Athens, Greece. Viral RNA of HRV and RSV were not detected in any of the samples of COPD patients or control subjects after being processed with real-time PCR.