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.
Anticoagulants are widely used in patients with pulmonary arterial hypertension (PAH) to prolong survival. However, there is a lack of robust evidence demonstrating the benefits of anticoagulants in PAH patients and very little is known about the complications of their use in this population. The objective of this study is to compare the safety of routine administration of oral anticoagulants between PAH patients who were and were not treated with oral anticoagulants. This observational, retrospective cohort study included consecutive patients with confirmed PAH from two centers: Brigham and Women’s Hospital in Boston and Hospital Universitario La Paz in Madrid from January 2009 to August 2015. The study group comprised patients who received therapeutic anticoagulation; patients who had never received anticoagulants were placed in the control group. Of the 201 included patients, 60.2% were treated with oral anticoagulants and 39.8% were not treated. The hazard ratio for major bleeding was 2.7 (95% confidence interval [CI] = 1.1–6.8; P = 0.036). The incidence rate for the anticoagulation group was 4.7 per 100 patient‐years (95% CI = 2.5–8.0). The most frequent major hemorrhage was gastrointestinal bleeding with 24 cases (72.7%). Prior bleeding, poor anticoagulation, HAS‐BLED score ≥3, diabetes, and number of medications were factors that increased the risk of major bleeding in patients using anticoagulants. The harmful effects of anticoagulants could outweigh the benefits in PAH patients. Therefore, anticoagulants should be prescribed on a case‐by‐case basis and should not be systematically recommended.