Leonie Biener, Hussein Morobeid, Carmen Pizarro, Daniel Kuetting, Georg Nickenig, Dirk Skowasch
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Treatment response was assessed after 7.8 ± 2.5 months based on acute exacerbations (AE), oral corticosteroid (OCS) therapy, Asthma Control Test (ACT), forced expiratory volume in 1 second (FEV1) and using the Biologics Asthma Response Score (BARS).</p><p><strong>Results: </strong>This study comprised 86 patients (mean age 56.1 ± 12.8 years; 54% female). Half (43, 50.0%) were never-smokers, half ex-smokers with an average of 26.9 ± 18.2 pack-years. Patients with ≥5% emphysema were more often ex-smokers (80% vs 41%, p=0.002), had poorer lung function (FEV1 median 1.3 [interquartile range: 1.0;1.6] vs 1.8[1-2;2.4] L, p=0.037), and more comorbid COPD (50% vs 21%, p=0.012). However, no significant differences were noted in treatment response regarding annualized AE rate (-2.5[-5;-1] vs -3.0[-5;-2] n/year, p=0.295) and OCS reduction (-4[-10;0] vs -5[-10;0] mg, p=0.691), ACT score (5[3;9] vs 4[0;9] points, p=0.579) or FEV1 improvement (0.03[-0.15;0.25] vs 0.23[-0.5;0.49] L, p=0.052), BARS (p=0.312), and remission rates (15.0% vs 19.7%, p=0.753).</p><p><strong>Conclusion: </strong>In patients with severe asthma, those with comorbid emphysema show similar treatment response to biologic therapy. 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引用次数: 0
摘要
背景:重症哮喘(SA)患者从生物制剂治疗中获益良多。然而,由于哮喘研究排除了吸烟≥10包年的患者,与吸烟相关的合并症的影响仍不清楚。我们的目的是在这项回顾性队列研究中考察肺气肿对哮喘生物治疗反应的影响:方法:使用计算机断层扫描检查肺气肿。方法:使用计算机断层扫描检查肺气肿,并根据肺气肿的数量(≥5% 或 结果)将 SA 患者分为两组:本研究包括 86 名患者(平均年龄 56.1 ± 12.8 岁;54% 为女性)。半数(43,50.0%)患者从不吸烟,半数为戒烟者,平均吸烟 26.9 ± 18.2 包年。肺气肿≥5%的患者多为前吸烟者(80% vs 41%,P=0.002),肺功能较差(FEV1 中位数为 1.3 [四分位数范围:1.0;1.6] vs 1.8[1-2;2.4] L,P=0.037),合并慢性阻塞性肺病的患者较多(50% vs 21%,P=0.012)。然而,在治疗反应方面,年化 AE 率(-2.5[-5;-1] vs -3.0[-5;-2] n/年,p=0.295)和 OCS 减少率(-4[-10;0] vs -5[-10;0] mg,p=0.691)、ACT 评分(-4[-10;0] vs -5[-10;0] mg,p=0.691)无明显差异。691)、ACT评分(5[3;9] vs 4[0;9]分,p=0.579)或FEV1改善(0.03[-0.15;0.25] vs 0.23[-0.5;0.49] L,p=0.052)、BARS(p=0.312)和缓解率(15.0% vs 19.7%,p=0.753):结论:在重症哮喘患者中,合并肺气肿的患者对生物制剂治疗的反应相似。结论:在重症哮喘患者中,合并肺气肿的患者对生物制剂治疗的反应相似,因此,合适的患者不应因合并肺气肿而拒绝接受生物制剂治疗。
The Influence of Emphysema on Treatment Response to Biologic Therapy in Severe Asthma.
Background: Patients with severe asthma (SA) benefit from biologic therapy substantially. However, the impact of smoking-related comorbidities remains unclear due to the exclusion of patients with ≥10 pack-years from asthma studies. Our aim was to examine the effects of emphysema on biologic treatment response in SA in this retrospective cohort study.
Methods: Pulmonary emphysema was examined using computed tomography. Patients with SA were included and divided into two groups based on emphysema quantity (≥5% or <5%). They received either anti-IgE (22.1%), anti-IL-5-(receptor) (52.3%), or anti-IL-4/IL-13 (25.6%) biologic therapy. Treatment response was assessed after 7.8 ± 2.5 months based on acute exacerbations (AE), oral corticosteroid (OCS) therapy, Asthma Control Test (ACT), forced expiratory volume in 1 second (FEV1) and using the Biologics Asthma Response Score (BARS).
Results: This study comprised 86 patients (mean age 56.1 ± 12.8 years; 54% female). Half (43, 50.0%) were never-smokers, half ex-smokers with an average of 26.9 ± 18.2 pack-years. Patients with ≥5% emphysema were more often ex-smokers (80% vs 41%, p=0.002), had poorer lung function (FEV1 median 1.3 [interquartile range: 1.0;1.6] vs 1.8[1-2;2.4] L, p=0.037), and more comorbid COPD (50% vs 21%, p=0.012). However, no significant differences were noted in treatment response regarding annualized AE rate (-2.5[-5;-1] vs -3.0[-5;-2] n/year, p=0.295) and OCS reduction (-4[-10;0] vs -5[-10;0] mg, p=0.691), ACT score (5[3;9] vs 4[0;9] points, p=0.579) or FEV1 improvement (0.03[-0.15;0.25] vs 0.23[-0.5;0.49] L, p=0.052), BARS (p=0.312), and remission rates (15.0% vs 19.7%, p=0.753).
Conclusion: In patients with severe asthma, those with comorbid emphysema show similar treatment response to biologic therapy. Therefore, suitable patients should not be denied biologics due to the presence of emphysema.
期刊介绍:
An international, peer-reviewed journal publishing original research, reports, editorials and commentaries on the following topics: Asthma; Pulmonary physiology; Asthma related clinical health; Clinical immunology and the immunological basis of disease; Pharmacological interventions and new therapies.
Although the main focus of the journal will be to publish research and clinical results in humans, preclinical, animal and in vitro studies will be published where they shed light on disease processes and potential new therapies.