Astma w okresie infekcji, ze szczególnym uwzględnieniem pandemii COVID-19

For almost a year now, we have been living during the COVID-19 pandemic. In November 2019, an increasing number of patients were diagnosed with severe interstitial pneumonia in Wuhan (China). A new coronavirus, previously unknown in humans, SARS-CoV-2, turned out to be an etiological factor. The new virus called SARS-CoV-2 is closely related to the β-coronavirus found in bats. The first cases of the new disease have highlighted a similar clinical course of interstitial pneumonias previously found in China and the Middle East (SARS and MERS). The SARS-CoV and MERS-CoV viruses turned out to be etiological factors. Man has no natural immunity against these newly discovered viruses. As soon as the virus has passed from its natural environment (animals) to man, the transmission rate of the infection has accelerated. Most often the infection occurs in tightly closed, poorly ventilated rooms, which are clusters of large groups of people. With the exhaled aerosol formed in the airways of the infected person (sneezing, talking, singing, laughing, coughing) the virus enters the airways of subsequent people. This observation allowed to develop methods to reduce subsequent infections to a minimum. Pandemic COVID-19 raised many questions about the treatment of asthma/ COPD patients and the need to modify their treatment. Due to the similarity of symptoms, questions arose about the diagnosis and differentiation of COVID-19 from asthma/COPD. It is unclear whether patients with asthma/COPD are at increased risk of SARS-CoV-2 infection. It has not been shown in previous analyses that allergic diseases, asthma or COPD are factors in the development of infection caused by SARS-CoV-2. However, the turbulent course of SARS-CoV-2 infection and the cytokine storm syndrome (CSS) caused by this infection, which is characterized by elevated inflammatory markers (e.g., CRP, ferritin) and acquired immunodeficiency (lymphopenia with T-cell reduction) raise concerns about exacerbation of allergic inflammation in the airways. Moreover, disruption of the coagulation cascade in CSS may lead to coagulopathy with elevated D-dimers and fibrin metabolism disorders (generalized severe endovascular disease), which is reflected in the analyzed hematological parameters of COVID-19 patients. Increased lesions in the lung parenchyma may be caused by progressive disorders of the coagulation system, but also changes in small vessels occurring not only in the lungs, but also in the vessels of the kidneys, heart and brain. Older age and coexisting diseases for patients in this age group – heart disease, hypertension, chronic obstructive pulmonary disease (COPD), asthma, diabetes mellitus and obesity are risk factors for the more severe course of COVID-19. However, there is controversy about the influence of asthma and COPD on the course of COVID-19. Current recommendations of the CDC (Centers for Disease Control and Prevention – USA) state that patients with moderate to severe asthma may be more likely to develop a more severe disease if they are infected with SARS-CoV-2. It should be remembered that children are the least exposed to SARS-CoV-2 infection due to lower ACE-2 and TMPRSS2 receptor expression in the airways compared to adults. The basis of control therapy for asthma is inhalation steroids. Steroids interact directly with the respiratory epithelium, contributing to the reduction of inflammatory reactions through the growth of anti-inflammatory cytokines. An important element in SARS-CoV-2 infection are ACE-2 receptors present on the surface of respiratory epithelial cells. There are fewer of these receptors in allergic asthma, which means that SARS-CoV-2 viruses have less ability to connect to these cells. Preclinical studies have also shown that some substances used to treat asthma reduce the replication of SARS-CoV-2 in respiratory epithelial cells. Inhalational steroids reduce the severity of SARS-CoV-2 infection in COPD patients. It has also been shown that medications – glycopyronium, formoterol and triple combination drug containing budesonide, formoterol and glycopyronium inhibit coronavirus replication and reduce the synthesis of proinflammatory cytokines. Similar observations have been made in the case of rhinovirus infections. Not only asthma patients but also COPD patients should not interrupt their treatment with inhalation drugs, especially steroids during the SARS-CoV-2 pandemic. In COPD long-acting bronchodilators (β-mimetics – formoterol, salmeterol, cholinolytics – glycopyronium, tiotropium) are the first line of therapy. The addition of inhalation glucocorticosteroid in patients with frequent exacerbations during these exacerbations, followed by the introduction of oral corticosteroids and antibiotics, should be a natural effect in the course of SARS-CoV-2 infection. All safety rules should be observed when using drugs in nebulization. There are no indications to replace nebulization with pMDI. In patients treated with DPI, multi-dose inhalers should be used, safer than single dose (capsule) ones.