Allergic Bronchopulmonary Aspergillosis (ABPA) is an immune-mediated airway disease caused by hypersensitivity to Aspergillus fumigatus in genetically and immunologically susceptible people, most often those with asthma or Cystic Fibrosis (CF). Persistent luminal fungus, impaired mucociliary clearance, and exaggerated type 2 immunity interact to produce mucus plugging, eosinophilic inflammation, bronchiectasis, and, in advanced disease, respiratory failure. The 2024 International Society for Human and Animal Mycology (ISHAM) criteria require A. fumigatus sensitization and total immunoglobulin E (IgE) ≥500 IU/mL, together with supportive immunologic or imaging evidence. Sensitization without active ABPA is a related but distinct state and is not routinely treated. This narrative review integrates evidence on epidemiology, immunopathogenesis, diagnosis, clinical classification, radiology, differential diagnosis, complications, and treatment. Prednisolone or itraconazole monotherapy is appropriate for most acute disease; combined therapy is generally reserved for recurrent exacerbations. Therapeutic Drug Monitoring (TDM) is important during azole treatment. Biologics directed against IgE, interleukin (IL)-5/IL-5 receptor α, or IL-4 receptor α are increasingly used for treatment-dependent disease, but the evidence is mainly observational. Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) modulators may reduce airway fungal burden but create clinically important cytochrome P450 3A4 (CYP3A4) interactions with azoles. Response and relapse should be judged against a patient-specific stable IgE baseline together with symptoms and imaging.
Introduction/Objective Right heart strain (RHS) is a commonly occurring and significant complication of acute pulmonary embolism (PE). CTPA images often suggest pulmonary hypertension; however, diagnostic echocardiography is not always immediately available to confirm this. In this study, we assessed how accurately Computed Tomography Pulmonary Angiography (CTPA), troponin, and NT-proBNP predict evidence of RHS in patients with acute PE, compared with transthoracic echocardiography (TTE). Methods A total of 656 patients had CTPAs performed over 6 months at a tertiary university hospital. Studies positive for PE were then separated into those with and without reported CTPA evidence of RHS. Patients’ TTE, troponin-T, NT-proBNP, and D-dimer results were assessed, and potential relationships were explored. Results About 128 (19.5%) studies were positive for acute PE, and 25 patients with RHS on CTPA had TTEs, with 16 showing evidence of RHS. A total of 39 patients with PEs and no CTPA-reported RHS had TTEs, with 7 suggesting RHS. CTPAs showed a 69.6% sensitivity and 78.0% specificity in predicting RHS. NT-pro-BNP (cut-off 300pg/ml) and troponin-T (cut-off 34ng/L) showed higher sensitivity, 92.9% and 75%, respectively, and lower specificity, 33.3% and 58%, respectively, than CTPA. 329/656 (50%) had an alternative explanation for symptoms on CTPA, meaning only 30.5% of patients had no explanation for symptoms. Discussion While an accessible and useful test, CTPA is not as reliable in predicting RHS in patients with acute PE as TTE. Conclusion Patients diagnosed with a clinically significant PE should be considered for TTE regardless of whether or not RHS is evident on CTPA.
Introduction/Objective Current American Thoracic Society/European Respiratory Society (ATS/ERS) guidelines recommend Global Lung Initiative (GLI) reference equations for spirometry, lung volumes, and Diffusing Capacity of the Lungs for Carbon Monoxide (DLCO). The impact of adopting these reference equations remains unclear and may differ by race. Methods We conducted a cross-sectional study of Pulmonary Function Tests (PFT) performed at Grady Memorial Hospital in Atlanta, GA, from 2017 to 2024. PFT components and interpretive patterns were analyzed using current Grady reference equations, then compared with GLI, including race-neutral spirometry, and stratified by race. Results There were 7877 eligible patients; 7034 (89%) were Black, 529 (7%) were White, and 314 (4%) were Hispanic. Black patients had increased frequency of abnormal FEV1 (37.4% to 52.1%, p < 0.001), FVC (32.4% to 48.4%, p < 0.001), Total Lung Capacity (TLC) (6.7% to 40.8%, p < 0.001), and DLCO (30.3% to 45.3%, p < 0.001). White and Hispanic patients had decreases in abnormal FEV1 (48.0% to 38.0%, p < 0.001, and 29.0% to 20.7%, p < 0.001, respectively), decreases in abnormal FVC (38.0% to 26.1%, p < 0.001, and 26.1% to 18.2%, p < 0.001), increases in abnormal TLC (12.7% to 17.8%, p < 0.001, and 12.4% to 16.8%, p < 0.001) and no change in DLCO. 44.3% of Black, 16.8% of White, and 14.5% of Hispanic patients had a new interpretive pattern. Discussion In this health system with a predominantly Black patient population, transitioning our PFT reference equations to GLI increased detection of abnormalities and changed interpretive patterns, with greater effects in Black patients. Conclusion The health-system impact of implementing GLI reference equations is highly context-dependent, influenced by demographics and prior reference equations.
Introduction:Pulmonary hypertension (PH) is a frequent and serious complication of advanced chronic obstructive pulmonary disease (COPD) and is associated with a poor prognosis and limited treatment options. Current management focuses on optimizing COPD care, while the role of pulmonary vasodilators remains controversial. Ensifentrine, a dual phosphodiesterase (PDE) 3/4 inhibitor with bronchodilatory and anti-inflammatory properties, may offer a therapeutic benefit in COPD-associated PH. This study aims to retrospectively evaluate the effects of six months of nebulized ensifentrine on pulmonary hemodynamics and functional outcomes in patients with severe COPD and associated pre-capillary PH. Methods:We conducted a single-center, retrospective chart review of patients with GOLD stage III and IV COPD and confirmed pre-capillary PH (mean pulmonary artery pressure [mPAP] ≥20 mmHg, pulmonary vascular resistance [PVR] >2 Wood units, pulmonary capillary wedge pressure ≤15 mmHg). Five patients treated with nebulized ensifentrine (3 mg twice daily) between September 2024 and May 2025 were included. Hemodynamics via right heart catheterization (RHC) and 6-minute walk distance (6MWD) were measured at baseline and at 6 months. Results:The cohort (mean age 76 years, 60% male, mean FEV1 33.4% predicted) demonstrated severe emphysema and PH (baseline mPAP 53.2 mmHg, PVR 9.5 WU, cardiac index 2.5 L/min/m2). After 6 months, mean changes were as follows: • mPAP: decreased by 1.6 mmHg • Cardiac index: increased by 0.1 L/min/m2 • PVR: decreased by 1.0 WU • 6MWD: improved by 31 m • mMRC dyspnea score improved from 3.6 to 3.2 • CAT score from 23 to 21.6 • DLCO increased modestly (29%→31.2% predicted). • No adverse events, exacerbations, or hospitalizations were observed during this period. • The combination of ensifentrine with roflumilast was well tolerated. Discussion:Pulmonary hypertension in COPD is associated with worse outcomes, yet treatment options remain limited and uncertain. In this small retrospective case series of five patients with very severe COPD and confirmed pre-capillary PH, the addition of ensifentrine to optimized therapy was associated with modest but potentially meaningful improvements in symptoms, exercise capacity (6MWD), and select hemodynamic parameters, without worsening oxygenation. Its dual PDE3/PDE4 inhibition and inhaled delivery provide a plausible mechanism for bronchodilation, anti-inflammatory effects, and selective pulmonary vasodilation while minimizing ventilation-perfusion mismatch. However, the findings are highly preliminary given the very small sample size, lack of a control group, retrospective design, and significant selection bias, limiting generalizability and causal inference. Overall, the results are hypothesis-generating and suggest that ensifentrine may have therapeutic potential in COPD-associated PH, but larger, prospective, randomized trials are needed to confirm efficacy, safety, and its role in treatment algorithms. Conclusion:In this retrospective study, ensifentrine was safe and was associated with modest improvements in pulmonary hemodynamics and functional status in patients with severe COPD with pre-capillary PH. These preliminary findings warrant confirmation in larger, prospective, controlled trials.
Introduction Patients with Inflammatory Bowel Disease (IBD) may experience a range of extraintestinal pulmonary manifestations. Anti-TNFα therapy has emerged as a crucial treatment option for IBD patients. Despite the pro-inflammatory role of TNFα in pulmonary diseases, anti-TNFα therapy has no major value in their treatment. Therefore, this study aimed to investigate the prevalence of pulmonary manifestations and the impact of anti-TNFα therapy on lung function parameters in IBD patients. Methods Thirty two patients with IBD were recruited. These patients received pulmonary function tests prior to and at least 6 weeks after initiating anti-TNFα therapy. Pulmonary function was evaluated by standardized body plethysmography, including the measurement of lung diffusion capacity (DLCO SB). Results FEV1 and vital capacity (VC) were within normal range before and during anti-TNFα therapy. Mean residual volume (RV) was moderately increased before initiation of anti-TNFα therapy. RV decreased during the course of therapy, from 2.7 L (interquartile range (IQR) 2.04 - 3.06) or 159% (IQR 129.25 - 184.75) prior to anti-TNFα therapy to 2.5 L (IQR 2.14 - 3.00) or 138% (IQR 127.00 - 165.25) during anti-TNFα therapy ( p =0.031 for absolute values and p =0.014 for relative values. DLCO SB was slightly reduced before anti-TNFα therapy and decreased even further during anti-TNFα therapy, from 76.1% to 72%. Discussion Lung function tests in our IBD cohort were almost normal. FEV1 and VC were within normal range. RV was moderately increased, and DLCO SB was slightly decreased. These might indicate an extraintestinal involvement of IBD. During anti-TNFα therapy, RV slightly improved, whereas DLCO SB decreased even further, albeit only slightly. In our IBD cohort, anti-TNFα therapy did not significantly influence lung function parameters. Conclusion Our study shows that anti-TNFα therapy in Inflammatory Bowel Disease (IBD) only slightly changes lung function parameters, including diffusion capacity, at least in patients with mild IBD.
