Section of Pulmonary and Critical Care Medicine, University of New Mexico, Albuquerque, New Mexico, USA.
Department of Respiratory Medicine, Zaans Medical Center, Zaandam, The Netherlands.
Curr Opin Pulm Med. 2021 Jan;27(1):45-53. doi: 10.1097/MCP.0000000000000744.
Although respiratory viruses are common triggers of asthma exacerbation, it is unknown whether this also applies to infection with SARS-CoV-2. Indeed, patients with asthma and allergy appear underrepresented in large reports of COVID-19 cases worldwide. In this review, we evaluate existing literature on this topic and potential underlying mechanisms for any interrelationship between asthma and COVID-19.
Data from several preclinical and clinical reports suggest a lower susceptibility for COVID-19 in patients with underlying type 2 airway inflammation including asthma that may be related to a reduced expression of ACE2 and TMPRSS2 receptors for SARS-CoV-2. Corticosteroids further decrease expression of the ACE2 and TMPRSS2 receptors, hence may also have a protective effect against infection with SARS-CoV-2. In addition, some studies suggest that the reported improvement in asthma control and a reduction in asthma exacerbations during the COVID-19 pandemic may be related to improvement in adherence to controller therapy and reduced exposure to triggers, such as other respiratory viruses and air pollutants. Recent data point towards differential susceptibility for COVID-19 among asthma patients based on their phenotype and/or endotype. On the basis of existing evidence, continuation with controller therapies is recommended for all patients with asthma. For patients with severe uncontrolled asthma infected by SARS-CoV-2, adjustment of controllers and biologics should be based on a multidisciplinary decision.
Underrepresentation of SARS-CoV-2-infected patients with asthma and related allergic diseases may be based on potentially protective underlying mechanisms, such as type 2 airway inflammation, downregulation of ACE2/TMPRSS2 receptors, reduced exposures to triggers and improved adherence to controller medications. Although it is imperative that control should be maintained and asthma medications be continued in all patients, management of patients with severe uncontrolled asthma infected by SARS-CoV-2 including adjustment of controllers and biologics should be discussed on an individual basis.
虽然呼吸道病毒是哮喘加重的常见诱因，但尚不清楚这是否也适用于 SARS-CoV-2 感染。事实上，在全球范围内关于 COVID-19 病例的大型报告中，哮喘和过敏患者似乎代表性不足。在这篇综述中，我们评估了关于这一主题的现有文献以及哮喘和 COVID-19 之间任何相互关系的潜在潜在机制。
来自几项临床前和临床报告的数据表明，在患有潜在 2 型气道炎症的患者中，包括哮喘患者，COVID-19 的易感性较低，这可能与 ACE2 和 SARS-CoV-2 的 TMPRSS2 受体表达减少有关。皮质类固醇进一步降低 ACE2 和 TMPRSS2 受体的表达，因此也可能对 SARS-CoV-2 感染具有保护作用。此外，一些研究表明，在 COVID-19 大流行期间报告的哮喘控制改善和哮喘恶化减少可能与控制治疗的依从性提高以及减少接触其他呼吸道病毒和空气污染物等诱因有关。最近的数据表明，基于哮喘患者的表型和/或内型，他们对 COVID-19 的易感性存在差异。根据现有证据，建议所有哮喘患者继续使用控制器疗法。对于感染 SARS-CoV-2 的严重未控制的哮喘患者，应根据多学科决策调整控制器和生物制剂。
哮喘和相关过敏性疾病的 SARS-CoV-2 感染患者代表性不足可能基于潜在的保护机制，例如 2 型气道炎症、ACE2/TMPRSS2 受体下调、减少接触触发因素和提高对控制器药物的依从性。尽管在所有患者中保持控制和继续使用哮喘药物是至关重要的，但应根据个体情况讨论感染 SARS-CoV-2 的严重未控制的哮喘患者的管理，包括调整控制器和生物制剂。
