Background: Since the confirmation of the first patient infected with SARS-CoV-2 in Spain in January 2020, the epidemic has grown rapidly, with the greatest impact on the region of Madrid. This article describes the first 2226 adult patients with COVID-19, consecutively admitted to La Paz University Hospital in Madrid. Methods: Our cohort included all patients consecutively hospitalized who had a final outcome (death or discharge) in a 1286-bed hospital of Madrid (Spain) from 25 February (first case admitted) to 19 April 2020. The data were manually entered into an electronic case report form, which was monitored prior to the analysis. Results: We consecutively included 2226 adult patients admitted to the hospital who either died (460) or were discharged (1766). The patients’ median age was 61 years, and 51.8% were women. The most common comorbidity was arterial hypertension (41.3%), and the most common symptom on admission was fever (71.2%). The median time from disease onset to hospital admission was 6 days. The overall mortality was 20.7% and was higher in men (26.6% vs. 15.1%). Seventy-five patients with a final outcome were transferred to the intensive care unit (ICU) (3.4%). Most patients admitted to the ICU were men, and the median age was 64 years. Baseline laboratory values on admission were consistent with an impaired immune-inflammatory profile. Conclusions: We provide a description of the first large cohort of hospitalized patients with COVID-19 in Europe. Advanced age, male sex, the presence of comorbidities and abnormal laboratory values were more common among the patients with fatal outcomes.

Uncontrolled, severe asthma remains a significant clinical challenge, affecting a small proportion of asthma patients worldwide. Despite advancements in treatment options, a subset of patients continues to experience frequent exacerbations, uncontrolled symptoms, and impaired quality of life. The advent of biological therapies has revolutionized the management of severe asthma, offering targeted treatments that address specific inflammatory pathways. This review provides a comprehensive overview of the efficacy and response criteria of biological treatments in severe asthma, focusing on clinical, functional, and inflammatory markers used to help in the evaluation of the biologic treatment. Key response criteria include symptom control, reduction in exacerbations, improvement in lung function, and a reduction in or the discontinuation of oral corticosteroids. Biomarkers such as blood eosinophils and exhaled nitric oxide (FeNO) are essential tools in guiding treatment adjustments. Real-world studies underscore the importance of personalized treatment strategies, as variability in response to biological therapies can be significant. The emergence of tools such as the FEOS score and EXACTO questionnaire offer quantitative measures for assessing biological response and guiding clinical decisions. Additionally, predictive factors for better or poorer responses, such as pre-treatment lung function and comorbidities, like obesity and rhinosinusitis, are critical in patient selection. This review highlights the need for ongoing reassessments and potential modifications of therapy in cases of suboptimal response. Practical considerations for switching biological therapies are discussed, emphasizing the importance of tailoring treatments to individual patient profiles and disease phenotypes. With the continued development of personalized medicine, the outlook for patients with severe asthma is improving, selecting specific biomarkers to improve the selection of the biologic treatment.

Advances in knowledge about clinical features, physiology, and underlying immunology are leading to targeted therapies and a new era of therapies. Biological treatments for severe asthma have changed the way this disease is managed, especially in patients who do not respond adequately to conventional treatments with corticosteroids and bronchodilators. These treatments block the action of different molecules involved in the immune response and in the inflammation of the airways, bronchoconstriction, bronchial hyperresponsiveness, and excessive mucus production. Currently, there are sufficient real-life data to corroborate the good results obtained in clinical trials by these type of drugs for severe asthma patients. Observational studies reveal their efficacy and safety, reducing exacerbations, leading to fewer emergency room visits and hospitalizations, and improving quality of life with better asthma control and better functional status.

Background: Lung cancer is the leading cause of death from cancer. Tobacco is related to the development of this type of tumor due to genetic alterations and to the secretion of certain biological markers. Bronchogenic carcinomas secrete a series of biological substances known as tumor markers. Some of these markers, such as carcinoembryonic antigen, neuron-specific enolase, tissue polypeptide antigen (TPA), tissue polypeptide-specific antigen (TPS) and CYFRA 21.1, possess clear clinical value when analyzed in bronchoalveolar lavage (BAL) of patients with lung malignancies, particularly when they are analyzed in the two BAL fractions, bronchial (BF) and alveolar (AF), being more increased in the BF. For this reason, we intend to demonstrate that smokers with cancer secrete more biological substances in the BF and that the concentrations of these markers are higher in the BAL of smokers than in that of non-smokers. Methods: The five aforementioned tumor markers were studied in the two BAL fractions of 52 lung cancer patients (46 smokers and 6 non-smokers). We performed BAL using 150 ml of 0.9% saline solution divided in three aliquots of 50 ml. The fluid obtained from the first 50 ml was the BF. The liquid from the other two aliquots was the AF. The five tumor marker concentrations were calculated in accord with the indications of the laboratory. Results: The TPA and TPS levels in the BAL of lung cancer patients were more increased in the BF than in the AF, even when the patients were divided into smokers and non-smokers. When we compared smokers with non-smokers, the smokers had higher levels of TPS in the BF and of TPA in the AF. Conclusions: Thus, we believe that the cellular alterations produced by tobacco are responsible for the secretion of these tumor markers.

This issue of Sleep and Breathing presents a section on sleep in COPD, a widespread disease consuming many health resources which is often diagnosed so late that little chance of reversibility remains. The early detection of the warning clinical signs can include sleep studies, mainly in the presence of arterial carbon dioxide levels higher than expected from pulmonary function tests. Two of the articles deal with hypercapnia and nocturnal hypoventilation in COPD; the third underlines the impact of tobacco smoking on snoring and on oxygen availability to tissues, showing a poor reliability of pulse oximetry in subjects with heavy smoking habits.

To evaluate KL-6 levels in medium-term post-COVID and to compare them in three groups categorised by the severity of COVID-19, we conducted a real-world, retrospective, cohort study. Data from the COVID-19 episode and follow-up during the post-COVID phase were extracted from the COVID@HULP and POSTCOVID@HULP databases, respectively. For the post-COVID period we included demographics, medical history, symptoms, quality of life, physical activity, anxiety and depression status and laboratory results. Patients were categorised into three groups based on the severity of COVID-19: Group 1 (inpatient critical), Group 2 (inpatient non-critical) and Group 3 (hospitalised at home). KL-6 was measured during the follow-up of the three groups. In all, 802 patients were included (Group 1 = 59; Group 2 = 296; Group 3 = 447 patients). The median age was 59 years (48–70), and 362 (45.2%) were males. At admission, fibrinogen and ferritin levels were lower in Group 3 than in the other groups (p < 0.001). Follow-up data were obtained 124 days (97–149) after the diagnosis of COVID-19. The median levels of fibrinogen, ferritin and KL-6 at follow-up were 336 mg/dL (276–413), 80.5 ng/mL (36–174.3) and 326 U/mL (240.3–440.3), respectively. KL-6 levels were lower in Group 3 than in the other groups (298 U/mL (231.5–398) vs. 381.5 U/mL (304–511.8) (Group 1) and 372 U/mL (249–483) (Group 2) (p < 0.001)). KL-6 was associated with ferritin (p < 0.001), fibrinogen (p < 0.001), D-dimer (p < 0.001) and gamma-glutamyl transferase (p < 0.001). KL-6 levels are less elevated at medium-term post-COVID follow-up in patients with mild COVID-19 than in those with moderate or severe disease. KL-6 is associated with systemic inflammatory, hepatic enzyme and thrombosis biomarkers.