Trigeminal neuralgia (TN) is a debilitating condition characterized by sudden, severe facial pain. IV medications for acute TN exacerbations have not been investigated in randomized controlled trials (RCTs). Oral medications are often insufficient for acute attacks, and surgery is not immediately available. We conducted an RCT to evaluate IV fosphenytoin therapy (IFT) as a rapid-acting rescue treatment for acute TN exacerbations. We hypothesized that, compared with placebo, IFT would reduce acute TN pain. This multicenter, double-blind, placebo-controlled phase 3 trial was conducted at 6 institutions (April 2023-April 2024). Patients with classical or idiopathic TN who were experiencing TN exacerbation (numerical rating scale [NRS] score ≥5) were recruited from emergency and outpatient settings, and all study drugs were administered during hospital admission. Participants were randomized 1:1 to IFT (initial dose: 18 mg/kg, maintenance: 7.5 mg/kg for 4 days) or placebo. The primary end point was the change in NRS pain scores from baseline to 120 minutes after the initial dose. Secondary end points included attack frequency, the proportion achieving ≥50% NRS score improvement, and adverse events. Data were collected by blinded personnel and analyzed using repeated-measures mixed-effects models. Of 31 participants screened, 22 were randomized; 1 placebo-assigned participant did not meet the NRS ≥5 criterion and was excluded, leaving 21 for analysis (IFT: 11; placebo: 10). Participants had a mean age of 65.2 years (range 42-83; 8 men, 13 women). Compared with placebo, IFT significantly reduced pain (NRS change: -6.1 vs -2.4; between-group difference -3.8; 95% CI -6.4 to -1.1; p = 0.008), decreased attack frequency within 24 hours (2.5 ± 5.3 vs 16.1 ± 19.6, difference -13.6; 95% CI -26.4 to -0.7), and increased the proportion achieving ≥50% NRS improvement (90.9% vs 40.0%, difference 50.9%; 95% CI 5.6%-81.6%). Adverse events (somnolence, hypotension, and nausea) were mild and transient. IFT provided rapid and well-tolerated pain relief in acute TN exacerbations. Although findings are preliminary because of the small sample size, IFT may be a viable short-term treatment option, meriting further investigation. Japan Registry of Clinical Trials, jRCT2011220043. Registered March 3, 2023. First enrollment April 25, 2023. jrct.mhlw.go.jp/en-latest-detail/jRCT2011220043. This study provides Class I evidence that in patients with acute TN exacerbations, IV fosphenytoin is superior to placebo in reducing pain intensity at 120 minutes.

Adjunctive pimavanserin in schizophrenia: A systematic review and meta-analysis with a focus on negative-symptom programmes.

Innate immunity and biomarkers of multiple sclerosis relapse versus remission.

A properly functioning cardiopulmonary system is essential for sustaining life, but can be compromised by acute exacerbations of cardiopulmonary conditions or progressive declines caused by degenerative diseases. Continuous cardiopulmonary monitoring has been proposed to improve the treatment of such impairments by enhancing triage in acute settings and facilitating the early detection and ongoing management of progressive disorders. In spite of this, suitable monitoring technologies are scarce. Existing systems often provide only coarse indicators of cardiopulmonary status or are too obtrusive for continuous use. We present reSPIRE, a chest-worn sensing system that acquires (S)eismocardiography, (P)hotoplethysmography, (I)mpedance pneumography and cardiography, surface (R)espiratory mechanomyography and electromyography, and (E)lectrocardiography signals. We validated the system on healthy participants (n=18) with controlled breathing maneuvers, incremental inspiratory and expiratory loading, and stationary cycling. Strong correlations were observed between wearable-derived indices of respiratory muscle force and inspiratory mouth pressure (Spearman: ρ=0.87, repeated measures: rrm=0.76). Significant phase-specific differences (p<0.001) in respiratory mechanomyography and electromyography band-powers were detected across both inspiratory and expiratory loading, leveraging respiratory phase context from the impedance pneuomgraphy signal. Tidal volume was accurately estimated from impedance pneumography, coefficient of determination (R2)=0.91, during sequences of spontaneous breathing and breathing while modulating rate and depth. Lastly, continuous tracking of hemodynamic (heart rate, pre-ejection period, impedance cardiography amplitude) and ventilatory changes was demonstrated throughout periods of cycling and recovery. These results demonstrate that the reSPIRE system's multimodal fusion enables precise monitoring of cardiopulmonary markers, advancing wearable-based monitoring and supporting its use in research of cardiopulmonary health.

The role of statins in reduction of acute exacerbations in chronic obstructive pulmonary disease (COPD) remains unclear. This systematic review and meta-analysis aimed to determine the preventive effect of statins on exacerbations in COPD patients. A systematic search was conducted in PubMed, Embase, Cochrane Library, and clinicaltrials.gov, without language restrictions. Randomized controlled trials (RCTs) on treatment of COPD with statins, compared with placebo, were reviewed. Estimated effects of included studies were pooled as risk ratios (RRs) and weighted mean differences (WMDs), with 95% confidence intervals (CIs). The certainty of evidence was assessed using the GRADE (Grading of Recommendations, Assessment, Development, and Evaluations) framework. Three RCTs (enrolling 1190 patients) met the inclusion criteria. Compared with placebo, the exacerbation related hospitalization rate (RR 0.87, 95% CI 0.77 to 0.97; GRADE = low) and severe exacerbation rate (RR 0.88, 95% CI 0.78 to 0.99; low) were significantly lower in statins groups. There was no statistically significant difference in moderate exacerbation rate (RR 0.71, 95% CI 0.48 to 1.04; very low), annualized exacerbation rate (WMD -0.21 per person-year, 95% CI -0.61 to 0.20; very low), and annualized moderate-to-severe exacerbation rate (WMD -0.21 per person-year, 95% CI -0.57 to 0.15; very low) between the two groups. In the absence of single-inhaler triple therapy (SITT), statins were associated with a reduction in severe exacerbations and hospitalization rates of COPD. Given the limitations of the evidence we found, further large-scale, high-quality studies are needed to clarify the impact of statins on prognosis and the beneficiary population. PROSPERO CRD42025644971.

The neutrophil-to-lymphocyte ratio (NLR) is a marker of systemic inflammation, with prognostic value in interstitial lung disease (ILD). However, the association between baseline NLR and the therapeutic efficacy of nintedanib remains unclear. This study investigates the relationship between baseline NLR values and clinical outcomes in patients with idiopathic pulmonary fibrosis (IPF) and progressive fibrosing-ILD (non-IPF ILD) receiving nintedanib therapy. This retrospective multicenter study included 406 patients-169 with IPF and 237 with non-IPF ILD-who initiated nintedanib treatment between 2019 and 2023 across 15 institutions in Japan. Patients were stratified into low- and high-NLR groups using a cutoff of 2.86. Comparative analysis assessed survival time, forced vital capacity (FVC) changes, and acute exacerbations. The high-NLR group demonstrated shorter median survival time in the overall study population (1,171 vs. 1,386days; p =0.025). In subgroup analyses, higher NLRs were associated with shorter survival time in patients with IPF (778 vs. 1,447days; p =0.006), but not in the non-IPF ILD group. While nintedanib mitigated FVC decline in most subgroups, this effect was attenuated in patients with IPF and high-NLR, with no statistically significant benefit (-8.63% vs. -6.71%). In multivariable analysis, NLR was not found to be an independent predictor of the annual relative FVC decline in any group. The incidence of acute exacerbations did not differ significantly between groups. While baseline NLR did not independently predict the annual relative FVC decline, it was identified as a significant independent predictor of survival time in patients with ILD, particularly those with IPF, following the initiation of nintedanib.

The recommendation regarding systemic corticosteroids in ventilated patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is unknown since most studies have excluded ventilated patients. Our study aims to investigate whether systemic steroids benefit the subgroup of AECOPD who require ventilation. We systematically searched PubMed, Cochrane, and Embase databases for randomized trials or observational studies comparing systemic steroids to placebo or no systemic steroids, up to April 2025. Outcomes of interest were intensive care unit (ICU) mortality, length of ICU stay, duration of ventilation, non-invasive ventilation (NIV) failure rate, hyperglycemia episodes, and ventilator-associated pneumonia (VAP). Six studies including 1596 ventilated AECOPD patients (including subgroups from larger ICU populations), were included in the systematic review. Of these 1424 contributed to the quantitative synthesis of at least one outcome. We performed sensitivity analysis for study type and mode of ventilation. ICU mortality was not significantly decreased in the systemic steroid group compared to placebo or no systemic steroids (Odds ratio (OR) = 1.09; 95% CI 0.62-1.91; p = 0.78; I²=0.0%). There was no statistically significant difference between the groups for duration of ventilation (Mean difference (MD) = -2.24; 95% CI -5.13 to 0.66; p = 0.13; I²=78.7%). In the subgroup of randomized controlled trials (RCTs), systemic steroids were associated with a shorter duration of ventilation (MD = -1.12 days; 95% CI -2.23 to 0.00; p = 0.049; I² = 59.9%). There was no difference between groups for length of ICU stay (MD = -1.60; 95% CI -3.32 to 0.12; p = 0.068; I²=68.5%). There was no statistically significant difference between groups for NIV failure (Odds ratio (OR) = 1.17; 95% CI 0.83-1.67; p = 0.37; I²=58.1%). Hyperglycemia episodes were significantly higher in the steroid group (OR = 2.38; 95% CI 1.56 to 3.62; p < 0.001; I²=0.0%). There was no significant difference in rates of VAP (OR = 1.19; 95% CI 0.80-1.77; p = 0.38; I²=0.0%). This meta-analysis suggests that critically ill AECOPD patients on ventilation may not derive a significant benefit from systemic steroids. CRD420251034592.

Unstable Exacerbating COPD: Unaddressed Modifiable Risk Factors or Unstable Despite Optimised Care.

Two phase 3, randomized trials of inhaled treprostinil for idiopathic pulmonary fibrosis (IPF) were conducted on the basis of preclinical and clinical evidence of an antifibrotic mechanism. TETON-2 was completed first, and results were published; the results of TETON-1 and of both trials combined are reported here. In the double-blind TETON-1 trial, we randomly assigned patients with IPF to receive inhaled treprostinil or placebo (12 breaths four times daily). The primary end point was the change in forced vital capacity (FVC) at week 52. Secondary end points, which were analyzed in a prespecified order to control for multiplicity, were clinical worsening (the first occurrence of death from any cause, hospitalization for a respiratory cause, or a relative decline of ≥10% in the percentage of predicted FVC) and acute exacerbation of IPF (each assessed in a time-to-event analysis), survival, change in percentage of predicted FVC, quality of life, and change in diffusion capacity of the lungs for carbon monoxide at week 52. A total of 598 patients underwent randomization and received at least one dose of treprostinil (299 patients) or placebo (299 patients). Of these, 434 completed the assessments through week 52 (218 in the treprostinil group and 216 in the placebo group). The mean age of the patients was 73.0 years, 77.3% were men, and 77.6% were receiving background antifibrotic therapy; the percentage of predicted FVC at baseline was 74.6%. The median change in FVC at week 52 was -43.3 ml (95% confidence interval [CI], -92.1 to -9.1) with treprostinil and -196.2 ml (95% CI, -227.1 to -155.6) with placebo (difference, 130.1 ml; 95% CI, 82.2 to 178.1; P<0.001). Clinical worsening occurred in 95 patients (31.8%) with treprostinil and in 133 patients (44.5%) with placebo (hazard ratio, 0.67; 95% CI, 0.52 to 0.88; P = 0.003). No significant difference was observed in the time to an IPF exacerbation, and no further inferences regarding secondary end points were made. The most frequent adverse event was cough (reported in 54.8% of the patients in the treprostinil group and 33.1% patients in the placebo group). Discontinuation of treprostinil or placebo occurred in 40.5% and 32.8% of the patients, respectively, with adverse event being the primary reason (20.7% and 14.7%). Efficacy and safety outcomes were similar in analyses of the combined trial data. In patients with IPF, treatment with inhaled treprostinil led to a smaller decline in FVC and fewer clinical-worsening events than placebo over the course of 52 weeks. (Funded by United Therapeutics; TETON-1 ClinicalTrials.gov number, NCT04708782.).

Studies report a high 28-day all-cause mortality rate in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). The specific prognostic value of lymphocyte subsets for critically ill patients remains unclear. We aimed to evaluate the association between lymphocyte subsets and 28-day all-cause mortality in patients with AECOPD admitted to the intensive care unit (ICU). We conducted a retrospective cohort study on patients with severe AECOPD admitted to our hospital from January 2022 to December 2025. Comparisons were made between the survivors and non-survivors. We used restricted cubic splines, and Receiver Operating Characteristic (ROC) curves to describe the association between lymphocyte-related indicators and 28-day all-cause mortality. To prevent overfitting and robustly identify independent risk factors, Boruta feature selection and LASSO regression were sequentially utilized, followed by multivariable logistic regression to construct a prognostic model. The study enrolled 382 patients. During the 28-day follow-up, 115 (30.1%) patients died, and 267 (69.9%) survived. Among all examined immune cells, the CD3 + CD4+ T lymphocyte count demonstrated the strongest predictive performance. CD3 + CD4+ T lymphocytes exhibited the best predictive performance with a cutoff value of 157.61/µL. A prognostic model incorporating CD3 + CD4+ T lymphocytes and other key clinical features showed excellent discriminative ability with an area under the curve (AUC) of 0.860. A marked decline in CD3 + CD4+ T lymphocytes (< 157.61/µL) is a significant and readily accessible independent risk factor for 28-day all-cause mortality in patients with AECOPD admitted to the ICU. A nomogram based on the multivariable logistic regression model provides a practical tool for early risk stratification and targeted immune monitoring in critical care settings.

A 58-year-old man underwent left lower lobectomy for lung cancer. During the postoperative follow-up, upper-lung field pulmonary fibrosis (upper-PF) radiologically consistent with pleuroparenchymal fibroelastosis, gradually emerged in the left upper lobe. Seventeen years after surgery, the patient presented with acute dyspnea. Chest computed tomography demonstrated bilateral ground-glass opacities, predominantly in the contralateral non-fibrotic lung. After excluding other potential causes of acute respiratory failure, an acute exacerbation of unilateral upper-PF was diagnosed and successfully treated with anti-inflammatory therapy. Chest physicians should recognize that an acute exacerbation can develop even in patients with unilateral upper-PF, although it might be extremely rare.

Patients with interstitial lung disease (ILD) often experience postoperative acute exacerbation (AE). There is a lack of consensus regarding the risk factors for postoperative AE. This study aimed to identify factors associated with postoperative AE in patients with ILD. Of 84,833 patients who underwent surgery under general anesthesia, we included 198 ILD patients. The patients were retrospectively divided into AE and non-AE groups. Exclusion criteria were those who were continuously on a ventilator preoperatively or postoperatively, and those with obvious infection. We investigated risk factors, adjusting for sex and pulmonary surgery. AE occurred within 30 days after surgery in 11 patients (5.6%) and six of these patients (55%) died. Preoperative C-reactive protein (CRP) levels were significantly higher in the AE group than in the non-AE group (OR, 1.06; 95% confidence interval [CI], 1.00-1.13; p = 0.048). Chest high-resolution computed tomography (CT) evaluation was performed according to the updated 2022 idiopathic pulmonary fibrosis guidelines. CT revealed that patients in the CT-defined usual interstitial pneumonia (UIP) group, comprising UIP and probable UIP patterns, were significantly more likely to experience AE than those in the non-CT-UIP group, which included indeterminate UIP and alternative diagnosis patterns (OR, 4.00; 95% CI, 1.19-15.04; p = 0.025). In patients with ILD, the risk of postoperative AE across all surgeries, including non-pulmonary surgery, was associated with high preoperative CRP levels and the CT-UIP pattern.

Microscopic polyangiitis (MPA) is a type of systemic inflammatory small vessel vasculitis that is frequently accompanied by interstitial lung disease (ILD). Acute exacerbations (AE) of ILD are fatal complications in patients with MPA and can be triggered by various factors, including infections. We report a case of AE of MPA-ILD following severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) infection. An 81-year-old male with MPA during remission maintenance therapy was hospitalized for Coronavirus disease 2019 (COVID-19) pneumonia. Treatment for SARS-CoV-2 infection improved his respiratory symptoms and radiological findings, but his respiratory condition suddenly deteriorated with a high fever on hospital day 52. Chest HRCT showed diffuse bilateral ground glass opacity, and we diagnosed AE of MPA-ILD. He was refractory to steroid pulse therapy and died on the second day after the onset of AE. Pathologic autopsy revealed hyaline membrane formation over the entire bilateral lobes, consistent with the exudative phase of the diffuse alveolar damage (DAD) pattern. Our case suggests that persistent immune activation during the post-acute phase of SARS-CoV-2 infection may contribute to delayed AE of MPA-ILD with a DAD pattern through macrophage-driven lung injury, given that ILD exacerbation occurred approximately two months after the onset of COVID-19 pneumonia.

Potassium-competitive acid blockers (P-CABs) are newer gastric acid suppressants used to treat gastroesophageal reflux disease (GERD), but evidence regarding their respiratory safety compared with proton pump inhibitors (PPIs) in patients with chronic obstructive pulmonary disease (COPD) remains limited. We conducted a target trial emulation study using the Korean National Health Insurance database. Patients aged ≥40 years with COPD who initiated P-CAB or PPI for GERD between 2019 and 2022 were included. Follow-up continued from treatment initiation until the earliest occurrence of the outcome, treatment discontinuation, switching to another drug class, death, or the end of the study period. The outcome was the occurrence of pneumonia or moderate-to-severe COPD exacerbations. Propensity score matching (1:3) was applied, and hazard ratios (HRs) with 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. Among the 560,987 eligible patients, 4671 P-CAB users and 14,013 PPI users were included after matching. P-CAB was not significantly associated with the risk of respiratory events compared with PPI, but a trend toward lower risks for pneumonia (aHR, 0.76; 95% CI, 0.54-1.07) and severe exacerbations (aHR, 0.60; 95% CI, 0.32-1.14) was observed. In patients with a Charlson Comorbidity Index ≤1, the risk of severe exacerbations was significantly lower (aHR, 0.31; 95% CI, 0.11-0.88). P-CABs showed lower risks of pneumonia and severe exacerbations compared with PPIs, although the differences were not statistically significant. Further long-term studies across diverse patient subgroups are warranted.

Progressive pulmonary fibrosis (PPF) is a clinical phenotype observed across various interstitial lung diseases (ILDs) other than idiopathic pulmonary fibrosis, characterized by worsening fibrosis on high-resolution computed tomography (HRCT), progressive decline in lung function, and deteriorating respiratory symptoms. Despite shared pathophysiological mechanisms, the rate of disease progression and clinical outcomes vary substantially according to each subtype of PPF. Key predictors of poor prognosis include advanced age, male sex, rapid lung function decline, hypoxemia, pulmonary hypertension, and radiologic features such as a usual interstitial pneumonia pattern and traction bronchiectasis. Genetic factors, particularly telomere shortening and mutations in telomere-related genes, have emerged as important determinants of prognosis and therapeutic response. Acute exacerbation of PPF is associated with poor short-term prognosis representing a major cause of morbidity and mortality in PPF. The introduction of antifibrotic therapies has significantly altered the management of PPF by slowing lung function decline. However, their impact on long-term survival remains under investigation.

PurposeChronic obstructive pulmonary disease (COPD) exacerbations significantly accelerate disease progression and increase mortality and healthcare utilization. While triple therapy (inhaled corticosteroids/long-acting β2-agonist/long-acting muscarinic antagonist [ICS/LABA/LAMA]) is commonly prescribed to manage COPD, its long-term real-world effectiveness following hospitalization for acute exacerbation of COPD remains unclear.Patients and MethodsThis retrospective cohort study included 500 patients hospitalized for severe COPD exacerbations at a tertiary hospital (2015–2023). Patients were classified as receiving triple therapy (ICS/LABA/LAMA) during or within 7 days after the index hospitalization or not. Primary outcomes were COPD-related readmission and all-cause mortality within three years; secondary analyses were stratified by prior exacerbation frequency, baseline FEV1 % predicted, and eosinophil count. Adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox models, with Kaplan–Meier methods for survival.ResultsAmong the study population, 329 patients (65.8%) received triple therapy. Overall, no significant differences were observed in three-year COPD-related readmission rates (adjusted hazard ratio [aHR]: 0.95, 95% confidence interval [CI]: 0.66–1.35) or all-cause mortality (aHR: 0.88, 95% CI: 0.57–1.36) between the groups. However, stratified analyses demonstrated significant benefits of triple therapy in patients with ≥2 exacerbations within one year prior to the index hospitalization (aHR for readmission: 0.14; aHR for mortality: 0.24) and showed numerically lower risks among those with baseline FEV1 ≥50% predicted (aHR for readmission: 0.57; aHR for mortality: 0.43).ConclusionTriple therapy was not associated with improved outcomes in the overall cohort but may be associated with better outcomes in selected high-risk subgroups. These findings should be interpreted with caution given the observational design and potential residual confounding. Further studies are warranted to confirm these findings and refine patient selection for triple therapy.

Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) frequently coexists with type 2 diabetes mellitus (T2DM) and is associated with substantial short-term mortality. However, patients with AECOPD and metabolic comorbidity represent a clinically heterogeneous subgroup, and admission-based tools with independent validation for early in-hospital mortality risk stratification in this population remain limited. In this multicenter retrospective cohort study, hospitalized patients with AECOPD and concomitant T2DM were consecutively enrolled and divided into a training cohort and an institutionally independent validation cohort from a separate hospital within the same city. Candidate predictors routinely available at admission were evaluated using multivariable logistic regression to develop a parsimonious prediction model for in-hospital mortality. Model performance was assessed in terms of discrimination, calibration, and clinical utility, and compared with established bedside scores, including the quick Sequential Organ Failure Assessment (qSOFA) and BAP-65. Elevated arterial carbon dioxide tension (PaCO₂), procalcitonin (PCT), and D-dimer measured early after admission were independently associated with in-hospital mortality. A simplified model incorporating these three variables demonstrated stable discrimination in both the training and validation cohorts, with an area under the receiver operating characteristic curve of approximately 0.79, and showed good calibration. Decision curve analysis indicated higher or non-inferior net clinical benefit across clinically relevant threshold probabilities compared with qSOFA and BAP-65. In hospitalized patients with AECOPD and T2DM, PaCO₂, PCT, and D-dimer were independently associated with in-hospital mortality. An admission-based model integrating these markers showed promising performance in multicenter data with independent hospital-based validation within the same city. Further validation in geographically distinct populations is needed before broader generalizability can be assumed.

Impact of E-Prescribing Protocols on Antimicrobial Prescribing for Common Infections in Greece: An Interrupted Time Series Analysis.

BackgroundAcute exacerbations of chronic obstructive pulmonary disease (AECOPD) drive disease progression and mortality. This study aims to investigate whether nutritional risk and sarcopenia independently predict (AECOPD) in patients with stable COPD.MethodsIn this single-center retrospective cohort study, 264 hospitalized patients with stable COPD were followed for 12 months. Nutritional risk was assessed using the Nutritional Risk Screening 2002. Sarcopenia was defined according to the Asian Working Group for Sarcopenia 2019 criteria. Appendicular skeletal muscle index (ASMI), handgrip strength, gait speed, and five-repetition sit-to-stand (5STS) time were measured. Independent predictors of AECOPD were identified using multivariable logistic regression. Discrimination was evaluated using the area under the receiver operating characteristic curve (AUC).ResultsDuring follow-up, 102 patients (38.6%) developed AECOPD. Patients with AECOPD exhibited higher rates of sarcopenia (64.71% vs. 32.72%, P < 0.001) and nutritional risk (64.71% vs. 39.51%, P < 0.001), alongside lower ASMI, reduced handgrip strength, slower gait speed, and prolonged 5STS time (all P < 0.01). After adjustment for age, sex, smoking history, forced expiratory volume in 1 second (FEV1)% predicted, and prior AECOPD, and comorbidity burden, both sarcopenia (OR 6.265, 95% CI 3.008–13.049) and nutritional risk (OR 3.016, 95% CI 1.571–5.793) remained independent predictors. ASMI demonstrated a protective association (OR 0.266, 95% CI 0.177–0.399), while TNF-α was positively associated with AECOPD risk (OR 1.175, 95% CI 1.044–1.322). The ASMI-based model achieved the highest discrimination (AUC 0.893).ConclusionSarcopenia and nutritional risk independently increase AECOPD risk in stable COPD. Incorporating muscle mass parameters into risk stratification may improve predictive accuracy.

Objective: To explore the clinical characteristics of bronchiectasis patients with different levels of peripheral blood eosinophils. Methods: This study was a retrospective study. A total of 162 stable non-cystic fibrosis bronchiectasis patients were enrolled from Capital Medical University, Beijing Tongren Hospital from June 2022 to May 2025. Among them, there were 79 males and 83 females, aging 20-85 (60.27±15.83) years. Blood eosinophil(EOS) count (cells/μl, 100 cells/μl=0.1×109/L) was used as the cut-off value to classify patients into high BEC (blood eosinophil count) group, (Blood EOS≥300 cells/μl), medium BEC group (100 cells/μl≤Blood EOS<300 cells/μl) and low BEC group (blood EOS<100 cells/μl). The differences in general information, clinical symptoms, laboratory tests, pulmonary function and imaging characteristics, modified British Medical Research Council dyspnea scale (mMRC) score, bronchiectasis severity index (BSI), FACED scores, bronchiectasis imaging Reiff score and acute exacerbation events in the past year were compared among the three groups. The risk factors for acute exacerbation hospitalization of bronchiectasis in the three groups were analyzed. Data analysis was performed using SPSS 25.0 and R 4.2.2 software. Results: The proportions of patients with high, medium, and low BEC were 22.22%, 48.77% and 29.01%, respectively. Among the three groups, the comorbidity of rhinitis, sinusitis, nasal polyps, atopic dermatitis, respiratory symptoms, mMRC and CAAT scores, BAS%, BAS count, serum IgE, induced sputum EOS%, FeNO, IL-4, IL-5, positive proportion of allergens, positive proportion of Pseudomonas aeruginosa(PA) in sputum culture, positive proportion of fungi, FEV1 improvement rate, BSI, Reiff score, the proportion of cylindrical bronchiectasis, the occurrence of acute exacerbations[86.11% (31/36) vs. 49.37% (39/79) vs. 72.34% (34/47), χ2=16.44,P<0.001] and hospitalizations[38.89%(14/36) vs. 22.78%(18/79) vs. 48.94%(23/47),χ2=9.49,P=0.009] were statistically significant among the three groups (P<0.05). The high BEC group had more severe clinical symptoms, a higher prevalence of nasal polyps, higher levels of type 2 inflammatory biomarkers, and a higher frequency of acute exacerbation, but lower rates of hospitalization for acute exacerbation hospitalization, lower BSI score, and less pulmonary imaging involvement. IgE(OR=1.002,95%CI:1.000-1.003,P=0.029) was a risk factor for acute exacerbation hospitalization in high BEC group. MMRC(OR=2.879,95%CI:1.345-6.162,P=0.006) and PA infection(OR=4.427,95%CI:1.129-17.358,P=0.033) were independent risk factors for acute exacerbation hospitalization in the medium BEC group. PA infection(OR=8.649,95%CI:1.932-38.724,P=0.005) was an independent risk factor for acute exacerbation hospitalization in the low BEC group(all P<0.05). Conclusions: BEC level can reveal the phenotypic differences of BEC bronchiectasis. High BEC bronchiectasis is associated with airway type 2 inflammation and allergic reaction, with severe clinical symptoms and frequent acute exacerbation, while low BEC bronchiectasis is associated with more PA infection and higher risk of exacerbation-related hospitalization. Identifying the phenotypic differences of BEC bronchiectasis may provide a basis for personalized treatment of bronchiectasis.