Asthma or eosinophilic granulomatosis with polyangiitis: a case-based review

Asthma or eosinophilic granulomatosis with polyangiitis: a case-based review | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case report Asthma or eosinophilic granulomatosis with polyangiitis: a case-based review Pu Wang, Ying Liu, MeiQi Shao, Da Chen This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-2118285/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background: Eosinophilic granulomatosis with polyangiitis (EGPA) is a small-vessel necrotizing vasculitis. Its most common clinical manifestations are asthma; ear, nose, and throat involvement; and lung involvement. As EGPA has similar features to asthma, most patients with this disease seek medical treatment for the first time with wheezing symptoms and, thus, may be regarded as having asthma. Case presentation: This report discusses an EGPA case regarded as recurrent asthma for 3 years. The patient underwent thoracic computed tomography (CT) 6 times in recent years, which recorded dynamic changes in an EGPA patient’s lungs for the first time. We initiated treatment with methylprednisolone and amethopterin. The patient’s symptoms rapidly improved, and some abnormal imaging manifestations on chest CT disappeared one month after the treatment. Conclusions: Consequently, early diagnosis and treatment are needed because the progression of the disease may be prohibited, and imaging manifestations on chest CT of EGPA may be reversible. Furthermore, to diagnose patients with asthma more reliably and precisely, we discuss the differential diagnosis between EGPA and asthma. Thirdly, imaging manifestations on chest CT could be regarded as an evaluation index to evaluate the therapeutic effect in patients with EGPA. Finally, low-dose CS can alleviate the symptoms of EGPA. EGPA asthma differential diagnosis CT Figures Figure 1 Background Eosinophilic granulomatosis with polyangiitis (EGPA), previously known as Churg–Strauss syndrome, was first illustrated by Churg and Strauss in 1951[ 1 ]. According to the 2012-revised Chapel Hill classification, EGPA is a small-vessel necrotizing vasculitis belonging to the antineutrophil cytoplasm antibody (ANCA)-associated vasculitis (AAV) group, which also includes granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA)[ 2 ]. EGPA is characterized by granulomatous and eosinophil-rich inflammation and systemic necrotizing vasculitis affecting small- to medium-sized vessels[ 3 ]. It has a low global incidence (1.22 cases per million person-years) and prevalence (15.27 cases per million individuals). Further, a meta-analysis has reported an incidence of 1.07 cases per million person-years and a prevalence of 12.13 cases per million individuals in European countries. Although the incidence and prevalence values for EGPA differed between countries, incidence estimates were less than 4 cases per million person-years, and prevalence estimates were less than 31 cases per million individuals in all studies[ 4 ]. Asthma; ear, nose, and throat (ENT) involvement; and lung involvement are the most common clinical manifestations. As EGPA has similar features to asthma, most patients with this disease seek medical treatment for the first time with wheezing symptoms, and a considerable number of patients may be regarded as having asthma. Currently, specific diagnostic criteria for EGPA diagnosis and management are insufficient, making distinguishing between EGPA and asthma difficult. The diagnosis of EGPA mainly depends on consensus guidelines. Here, we report a case of EGPA in a patient treated for asthma for 3 years. His examination results in the early years did not meet the consensus guidelines for EGPA; thus, he was not diagnosed with EGPA until 2021. In these 4 years, the patient underwent thoracic computed tomography (CT) 6 times, which recorded dynamic changes in an EGPA patient’s lungs for the first time. Case Presentation On June 16, 2021, a 64-year-old man who presented with cough, expectoration, and wheezing visited the hospital to seek medical treatment in the Department of Pneumology. His medical history, which could be dated back to 2018, was notable for bronchiectasis, pneumonia, asthma, sinusitis, and recurrent respiratory virus infection. CT imaging revealed microscopic nodules below the pleura of the left tongue, mild expansion of multiple bronchi in both lungs with infection, and multiple blurred patchy shadows, which may be more severe than his chest CT imaging in the past years (Fig. 1 ). Consequently, the patient was treated with levofloxacin, piperacillin-tazobactam, bromhexine, methylprednisolone, budesonide, doxofylline, salmeterol ticasone, montelukast, and mometasone furoate. Nine days later, his cough, expectoration, and wheezing improved. Four months later, on October 22, 2021, the patient’s symptoms returned, which led him to seek treatment in the Department of General Medicine in the same hospital. Additionally, he presented with an episode of low-grade fever after using anti-inflammatory drugs, which revealed multiple microscopic nodules and ground-glass nodules in both lungs, mild expansion of multiple bronchi in both lungs with infection, and ground-glass opacities in the lower lobe of the right lung (Fig. 1 ). Upon re-evaluation, patchy blood spots can be observed on the anterolateral skin of the distal left lower limb, with surrounding subcutaneous hemorrhagic spots. A few subcutaneous haemorrhagic spots were observed in the distal right lower limb. Moreover, ANCA examination yielded a positive result. Additional results from the inspection are summarized in Table 1. Discussions And Conclusions We finally confirmed EGPA in the patient because his clinical course adhered to the items in the Japanese Ministry of Health and Welfare diagnostic criteria for “allergic granulomatosis with polyangiitis/Churg–Strauss syndrome,” which is now known as EGPA[ 5 ]. The following criteria were met: bronchial asthma, allergic rhinitis, eosinophilia, fever, and purpura. Treatment with methylprednisolone (48 mg/day) and amethopterin (10 mg weekly) was initiated. His symptoms improved, and some abnormal imaging manifestations on the chest CT disappeared within one month (Fig. 1 ). Differential diagnosis Conventionally, differential diagnosis of EGPA primarily focused on vasculitic disorders such as GPA and MPA; however, based on this case report, there is no doubt that asthma should also be considered for differential diagnosis. Asthma is a common chronic inflammatory disease of the airways with symptoms including cough, wheeze, shortness of breath, and chest tightness[ 6 ], which presently impacts more than 300 million individuals worldwide; roughly 250,000 asthma-related deaths are reported annually[7; 8]. Notably, the prevalence of asthma is increasing rapidly in developing countries like China[ 9 ]. Both EGPA and asthma, which can be concluded as “adult-onset eosinophilic airway diseases,” are characterized by prominent peripheral blood eosinophilia. Eosinophils contain granules that are toxic to bronchial epithelial cells and play a vital role in the symptoms of asthma[ 60 ]. Hence, similar pathogenesis makes distinguishing between these two diseases difficult. In fact, whether asthma is a symptom or disease should be considered for each patient with asthma. Mechanisms/pathophysiology The exact aetiology and pathogenesis underlying the development of EGPA remains unknown[ 10 ]. EGPA has features of eosinophil infiltration and ANCA-induced endothelial damage, thus it is classified among the small-vessel vasculitides associated with ANCAs and hypereosinophilic syndromes (HESs)[11; 12]. Clinical manifestations of EGPA tend to fall into one of two major disease subsets dominated by vasculitic and eosinophilic manifestations, and ANCA can be used to differentiate between these two subsets. One genome-wide association study (GWAS) examining EGPA demonstrated that EGPA is comprised of two genetically distinct subtypes: MPO-ANCA + EGPA and ANCA – EGPA, which align with observed clinical differences among patients[13; 14]. Mendelian randomization revealed an increased risk of eosinophilia underlying susceptibility to EGPA. Meanwhile, it has been suggested that various of environmental factors such as allergens, infections, vaccinations, and medications are potential triggers of EGPA[15; 16]. To some extent, there are shared genetic associations which influence both eosinophil numbers and asthma[ 10 ]. Asthma symptoms have strong associations with airway inflammation, which is characterized by the infiltration and activation of immune cells including dendritic cells, eosinophils, neutrophils, lymphocytes, innate lymphoid cells, and mast cells, which gradually leads to mucus production, remodelling of the airway wall, bronchial hyperresponsiveness (BHR), and airway obstruction. Currently, asthma phenotypes are usually classified into type 2 or non-type 2 asthma based on its mechanistic pathogenetic processes[ 17 ]. Non-type 2 asthma, which is usually associated with obesity, aging, and smoking, is characterized by infiltration of Th1cells, Th17 cells, and neutrophils, the presence of type I interferons, and NLRP3 inflammasome activation[6; 18; 19]. Type 2 asthma is usually observed in the clinic as early-onset allergic asthma, late-onset eosinophilic asthma, or exercise-induced asthma, accompanied by recurrent and chronic rhinosinusitis, allergies to common aeroallergens, high eosinophil numbers in the airways, increased periostin, and high exhaled nitric oxide[20; 21]. Additionally, asthma is characterized by variable airflow obstruction, airway inflammation, and remodelling[ 22 ]. In a study of bronchoalveolar lavage fluid (BALF) in patients with EGPA and bronchial asthma, patients with EGPA had a much stronger Th2-type response compared to those with bronchial asthma [ 23 ]. Clinical presentation EGPA is considered to be an idiopathic condition[ 24 ]; the mean age at onset is 38 to 54 years[25; 26]. As a type of AAV, EGPAs present with manifestations relating to small vessel vasculitic lesions and organ dysfunction. Asthma is a near-universal feature often present for years before the onset of eosinophilia and eosinophilic tissue inflammation, and it is difficult to control even after EGPA treatment [ 10 ]. The presence or absence of ANCA in patients distinguish between EGPA’s two subtypes. Compared with the ANCA-negative subset that features myocardial involvement, lung infiltrates, and gastrointestinal symptoms, ANCA-positive patients are more likely to display peripheral neuropathy, glomerulonephritis, and purpura (which are due to small-vessel vasculitis) [13; 14; 27]. In general, asthma symptoms, eosinophilia greater than 10%, mononeuropathy (including multiplex) or polyneuropathy, non-fixed pulmonary infiltrates on CT, paranasal sinus abnormalities, and biopsy containing a blood vessel with extravascular eosinophils are cardinal characteristics of EGPA[ 59 ]. The symptoms of asthma are non-specific, inclusive of episodic wheezing, dyspnoea, chest tightness, and cough[28; 29]. Expiratory wheezing which may be heard on auscultation is the most noteworthy characteristic of asthma. No gold standard exists for diagnosis of asthma, and diagnosis is typically made using a two-pronged approach, including a careful review of medical history to include review of the nature of symptoms, timing, triggers, and response to treatment[ 30 ] in addition to objective measurements of variable expiratory airflow limitation, forced expiratory volume in 1 second (FEV 1 ), and forced vital capacity (FVC)[ 9 ]. Examination Histopathology of EGPA has revealed necrotizing small-vessel vasculitis and an abundance of eosinophils. More accurately, eosinophilic infiltrates (but no necrosis) are present in tissues or blood vessel walls in the early stages of EGPA. In later stages of the disease, the epithelioid cells within granulomas are surrounded by eosinophils and necrosis is present. Blood tests may show anaemia and eosinophilia as well as increases in C-reactive protein (CRP), lactate dehydrogenase (LDH), creatine kinase (CK), rheumatoid factor (RF), and platelets. In practice, the degree of eosinophilia elevation is typically at least 30% at the onset of vasculitis. A marked growth in total serum IgE level may be found in two-thirds of cases; meanwhile, the positivity rate of MPO-ANCA (P-ANCA) is only present in 30–40% of cases[ 31 ]. In addition, > 75% of patients with EGPA have been reported to have pulmonary parenchymal lesions on imaging, including GGO, peribronchial or centrilobular nodules, and bronchial wall thickening.[61; 63] Sputum eosinophilia is the most useful biomarker for asthma diagnosis[ 32 ]. Although there is no standardized cut-off, an asthma diagnosis may be considered with a blood eosinophil count more than 300 cells/µL or sputum eosinophilia increases over 1–2% of the normal range[ 33 ]. Pulmonary function tests such as FEV1, FVC, FEV 1 /FVC% and peak expiratory flow (PEF) are also necessary to make an asthma diagnosis. Accounting for reversible airflow obstruction, guidelines such as the Global Initiative for Asthma (GINA) suggest that a bronchial dilation test (BDT) should be completed to assess airway hyperresponsiveness for suspected asthma cases without contraindications[ 34 ]. A 20% decrease in FEV 1 after challenge with a standard dose of methacholine defines the positive result of bronchial provocation test (BPT)[ 30 ]. Following the use of a bronchodilator, an increase in FEV 1 of more than 12% that is greater than 200 mL above the normal range is an indicator of airflow obstruction reversibility[35; 36]. However, a negative test does not rule out asthma. Although it is present in many other conditions, airway hyperresponsiveness is a key feature of asthma. Lastly, a chest CT can be used to visualize airway wall thickness and obstruction of airways by mucus, which may contribute towards an asthma diagnosis[37; 38]. Treatment Treatment strategies for EGPA vary according to disease manifestations and severity. Treatment regimens may consist of corticosteroids (CS), immunosuppressants, intravenous immunoglobulins, plasma exchanges, and targeted biotherapies[ 39 ]. There is no doubt that concomitant manifestations of asthma should be managed aggressively. Locally administered treatments can often alleviate asthma and ENT manifestations. As for systemic therapies, corticosteroids are considered first-line treatment for EGPA. Immunosuppressive drugs such as cyclophosphamide function indirectly by reducing high glucocorticoid requirements[ 40 ]; these are typically recommended as a combination treatment, especially in severe cases with poor response to CS treatment and in patients with a poor prognosis[ 31 ]. Treatments targeting cytokines, such as humanized monoclonal antibodies mepolizumab and reslizumab, are additional therapeutic options that bind to and block the function of circulating IL-5, preventing binding between IL-5 and its receptor, which has demonstrated effects on airways and allergic manifestations[31; 41]. A randomized clinical trial illustrated that mepolizumab was useful in the majority of patients with asthma and chronic sinusitis due to its ability to maintain sustained remission, reduce relapse rates, and substantially reduce the dosage or duration of glucocorticoid therapy[ 42 ]. A study showed a 64% reduction in the corticosteroid dose after mepolizumab therapy[ 43 ]. Notably, rituximab is usually not considered as the first choice for treatment because its efficacy is less well established for ANCA – patients. Furthermore, patients with asthma and chronic sinusitis frequently experience relapses despite continuous use of rituximab[ 44 ]. Treatment strategies for asthma include environmental control, inhaled glucocorticoids (ICS), long-acting β-agonists (LABA), leukotriene antagonists, anticholinergics, and targeted biologic therapies[ 45 ]. These treatments have varying mechanisms of action which impact their suitability for different treatment scenarios. For patients experiencing acute stage asthma, the first actionable step is to distance the patient from known allergens. ICS may improve disease control and reduce asthma exacerbations by reducing the number of airway eosinophils[46; 47; 48; 49]. However, if ICS alone is not effective, the addition of a LABA such as formoterol may have significant benefits[ 50 ]. Leukotriene antagonists are best for treating asthma exacerbations in children[51; 52], and the anticholinergic tiotropium could reduce the frequency of asthma exacerbations[ 53 ]. The most widely used targeted biologic therapies include anti-IgEs, such as omalizumab, and anti-IL-5s, such as mepolizumab and reslizumab. Omalizumab is a humanized monoclonal antibody directed against IgE that has the ability to reduce the risk of asthma exacerbations in allergic asthmatic patients[54; 55; 56; 57; 58]. Since IL-5 leads to airway eosinophilic inflammation, anti-IL-5 agents are generally reserved as maintenance therapies for patients with uncontrolled persistent eosinophilic asthma. According to this Case Although the patient in this case report first developed wheezing in 2018, they did not meet the diagnostic criteria for EGPA based on initial examination. The patient was aware of his 3-year history of asthma, however, his EGPA status during this period remained in question. The development of EGPA on chest CT has not yet been reported. Here, we report a case of a patient with EGPA who underwent thoracic CT six times in 4 years and had dynamic changes on CT (Fig. 1 ), which included the premorbid period of the disease, the period of the disease, and the period after the treatment. According to his follow-up visits, varying degrees of absorption of the lesion were observed on the patient’s chest CT. Consequently, we consider that the imaging manifestations of EGPA on chest CT might be reversible. Meanwhile, early diagnosis and treatment may prevent disease progression. Furthermore, imaging manifestations on chest CT could be regarded as an evaluation index to evaluate the therapeutic effect in patients with EGPA. Asthma exacerbations are widely treated with inhaled CS. To relieve the recurring asthma symptoms, we administered intermittent short-term CS treatment to our patient. There are hormones available to ease the symptoms of EGPA; however, hormone treatment alone is insufficient to prevent recurrent symptoms in our patient. We considered the controversial notion that maintenance therapy is justified once remission is achieved. Ultimately, we adhered to the 2016 European Alliance of Associations for Rheumatology guidelines for AAVs to advise a combination of glucocorticoids and either methotrexate or mycophenolate mofetil[ 62 ]. To date, the patient remains in good condition, and re-examinations were normal. EGPA has shifted from being a disease with high mortality to a chronic condition requiring lifelong management by specialists. However, despite this substantial progress, additional collaborative studies and continued interactions between basic and clinical researchers are needed to develop a gold standard for EGPA diagnosis and treatment. The patient was finally diagnosed with EGPA after treatment for asthma for 3 years; therefore, EGPA should be considered a differential diagnosis in patients with asthma. To some extent, the abnormal manifestations on thoracic CT gradually returned to normal. We further speculated that the imaging manifestations on chest CT of EGPA might be reversible. Meanwhile, early diagnosis and treatment may prevent disease progression. Furthermore, imaging manifestations on chest CT could be regarded as an evaluation index to evaluate the therapeutic effect in patients with EGPA. Finally, low-dose CS is available to ease the symptoms of EGPA although it would be better to use a combination of glucocorticoids and either methotrexate or mycophenolate mofetil to control disease relapse. Abbreviations Eosinophilic granulomatosis with polyangiitis (EGPA) Antineutrophil cytoplasm antibody (ANCA)-associated vasculitis (AAV) Granulomatosis with polyangiitis (GPA) Microscopic polyangiitis (MPA) Ear, nose, and throat (ENT) Computed tomography (CT) Hypereosinophilic syndromes (hess) Genome-wide association study (GWAS) Bronchial hyperresponsiveness (BHR) Bronchoalveolar lavage fluid (BALF) Forced expiratory volume in 1 second (FEV1) Forced vital capacity (FVC) C-reactive protein (CRP) Lactate dehydrogenase (LDH) Creatine kinase (CK) Rheumatoid factor (RF) Positivity rate of MPO-ANCA (P-ANCA) Peak expiratory flow (PEF) Global Initiative for Asthma (GINA) Bronchial dilation test (BDT) Bronchial provocation test (BPT) Corticosteroids (CS) Inhaled glucocorticoids (ICS) Long-acting β-agonists (LABA) Declarations Ethics approval and consent to participate: All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, as revised in 2000. Informed consent was obtained from all patients for being included in the study. Consent for publication: Informed consent was obtained from the patient for publication of their data. Availability of data and materials: The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request. Competing interests: The authors declare that they have no competing interests Funding: Not applicable Authors' contributions: DC and PW contributed the central idea, analysed most of the data, and wrote the initial draft of the paper. YL and MQS contributed to refining the ideas, carrying out additional analyses and finalizing this paper. Acknowledgements: Not applicable References Churg J, Strauss L. Allergic granulomatosis, allergic angiitis, and periarteritis nodosa. Am J Pathol. 1951;27:277-301. 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Walker S, Monteil M, Phelan K, Lasserson TJ, Walters EH. Anti-IgE for chronic asthma in adults and children. Cochrane Database Syst Rev. 2006 Apr 19;(2):CD003559. Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, et al. The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33:160-72. Yanagisawa S, Ichinose M. Definition and diagnosis of asthma-COPD overlap (ACO). Allergol Int. 2018;67:172-8. Kim YK, Lee KS, Chung MP, Han J, Chong S, Chung MJ, Yi CA, Kim HY. Pulmonary involvement in Churg-Strauss syndrome: an analysis of CT, clinical, and pathologic findings. Eur Radiol. 2007;17:3157-65. Yates M, Watts RA, Bajema IM, Cid MC, Crestani B, Hauser T, et al. EULAR/ERA-EDTA recommendations for the management of ANCA-associated vasculitis. Ann Rheum Dis. 2016;75:1583-94. Sanchez F, Gutierrez JM, Kha LC, Jimenez-Juan L, Cool C, Vargas D, et al. Pathological entities that may affect the lungs and the myocardium. Evaluation with chest CT and cardiac MR. Clin Imaging. 2021;70:124-35. Table Table 1 is available in the Supplementary Files section Supplementary Files Table.xlsx Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-2118285","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case report","associatedPublications":[],"authors":[{"id":140964017,"identity":"51ced43a-8c77-4763-baac-65296dda58a4","order_by":0,"name":"Pu Wang","email":"","orcid":"","institution":"Fourth Affiliated Hospital of China Medical University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Pu","middleName":"","lastName":"Wang","suffix":""},{"id":140964018,"identity":"60a7c513-60f4-4ccf-bff6-ae1e2a165c9b","order_by":1,"name":"Ying Liu","email":"","orcid":"","institution":"Fourth Affiliated Hospital of China Medical University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Ying","middleName":"","lastName":"Liu","suffix":""},{"id":140964019,"identity":"eeb64996-c86b-437b-ac65-20ef1e58002e","order_by":2,"name":"MeiQi Shao","email":"","orcid":"","institution":"Fourth Affiliated Hospital of China Medical University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"MeiQi","middleName":"","lastName":"Shao","suffix":""},{"id":140964021,"identity":"e974016a-95d6-40f4-9689-8629c392ee00","order_by":3,"name":"Da Chen","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA1ElEQVRIiWNgGAWjYDACCSDmYbDhYWNvPnDgQwXxWtLk+HmOJR6ccYZ4LYeNJWf4GB/mbSFCB//s5mMP3tQwJ264wfPhAG8Dgzy/2AECltw5lm445xhb4obbvRsOSO5gMJw5OwG/FgOJHDNpHjaexA13zm44YHiGIcHgNkEt+d+kef5JAB2W8+BAYhtRWnLYpHnbDIDez2E4cJAYLRI30swk5/YlgALZ4GDDGQnCfuGfkfxM4s23/6CofPz5T4WNPL80AS0YtpKmfBSMglEwCkYBdgAAG8RJtCyXYRwAAAAASUVORK5CYII=","orcid":"","institution":"","correspondingAuthor":true,"submittingAuthor":false,"prefix":"","firstName":"Da","middleName":"","lastName":"Chen","suffix":""}],"badges":[],"createdAt":"2022-09-30 01:32:42","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-2118285/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-2118285/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":27321877,"identity":"acae0053-00fe-4216-a082-1a5a875e590c","added_by":"auto","created_at":"2022-10-04 14:05:20","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":818810,"visible":true,"origin":"","legend":"\u003cp\u003eSee image above for figure legend.\u003c/p\u003e","description":"","filename":"Figure1.png","url":"https://assets-eu.researchsquare.com/files/rs-2118285/v1/85c7711e8013bb9533dca6c9.png"},{"id":40332285,"identity":"e5d033a7-79b2-419f-bb53-2cb72f2f8ad5","added_by":"auto","created_at":"2023-07-20 18:07:06","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":860278,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-2118285/v1/f577a38a-b025-4fb9-b460-a02297a817c6.pdf"},{"id":27321876,"identity":"fc7ee1bd-79e8-47f4-918c-dbcc3b72318c","added_by":"auto","created_at":"2022-10-04 14:05:19","extension":"xlsx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":11554,"visible":true,"origin":"","legend":"","description":"","filename":"Table.xlsx","url":"https://assets-eu.researchsquare.com/files/rs-2118285/v1/573c98b734b8a8493f6fd674.xlsx"}],"financialInterests":"","formattedTitle":"Asthma or eosinophilic granulomatosis with polyangiitis: a case-based review","fulltext":[{"header":"Background","content":"\u003cp\u003eEosinophilic granulomatosis with polyangiitis (EGPA), previously known as Churg\u0026ndash;Strauss syndrome, was first illustrated by Churg and Strauss in 1951[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. According to the 2012-revised Chapel Hill classification, EGPA is a small-vessel necrotizing vasculitis belonging to the antineutrophil cytoplasm antibody (ANCA)-associated vasculitis (AAV) group, which also includes granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA)[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. EGPA is characterized by granulomatous and eosinophil-rich inflammation and systemic necrotizing vasculitis affecting small- to medium-sized vessels[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. It has a low global incidence (1.22 cases per million person-years) and prevalence (15.27 cases per million individuals). Further, a meta-analysis has reported an incidence of 1.07 cases per million person-years and a prevalence of 12.13 cases per million individuals in European countries. Although the incidence and prevalence values for EGPA differed between countries, incidence estimates were less than 4 cases per million person-years, and prevalence estimates were less than 31 cases per million individuals in all studies[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. Asthma; ear, nose, and throat (ENT) involvement; and lung involvement are the most common clinical manifestations. As EGPA has similar features to asthma, most patients with this disease seek medical treatment for the first time with wheezing symptoms, and a considerable number of patients may be regarded as having asthma. Currently, specific diagnostic criteria for EGPA diagnosis and management are insufficient, making distinguishing between EGPA and asthma difficult. The diagnosis of EGPA mainly depends on consensus guidelines. Here, we report a case of EGPA in a patient treated for asthma for 3 years. His examination results in the early years did not meet the consensus guidelines for EGPA; thus, he was not diagnosed with EGPA until 2021. In these 4 years, the patient underwent thoracic computed tomography (CT) 6 times, which recorded dynamic changes in an EGPA patient\u0026rsquo;s lungs for the first time.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eOn June 16, 2021, a 64-year-old man who presented with cough, expectoration, and wheezing visited the hospital to seek medical treatment in the Department of Pneumology. His medical history, which could be dated back to 2018, was notable for bronchiectasis, pneumonia, asthma, sinusitis, and recurrent respiratory virus infection. CT imaging revealed microscopic nodules below the pleura of the left tongue, mild expansion of multiple bronchi in both lungs with infection, and multiple blurred patchy shadows, which may be more severe than his chest CT imaging in the past years (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). Consequently, the patient was treated with levofloxacin, piperacillin-tazobactam, bromhexine, methylprednisolone, budesonide, doxofylline, salmeterol ticasone, montelukast, and mometasone furoate. Nine days later, his cough, expectoration, and wheezing improved.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eFour months later, on October 22, 2021, the patient\u0026rsquo;s symptoms returned, which led him to seek treatment in the Department of General Medicine in the same hospital. Additionally, he presented with an episode of low-grade fever after using anti-inflammatory drugs, which revealed multiple microscopic nodules and ground-glass nodules in both lungs, mild expansion of multiple bronchi in both lungs with infection, and ground-glass opacities in the lower lobe of the right lung (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). Upon re-evaluation, patchy blood spots can be observed on the anterolateral skin of the distal left lower limb, with surrounding subcutaneous hemorrhagic spots. A few subcutaneous haemorrhagic spots were observed in the distal right lower limb. Moreover, ANCA examination yielded a positive result. Additional results from the inspection are summarized in Table\u0026nbsp;1.\u003c/p\u003e"},{"header":"Discussions And Conclusions","content":"\u003cp\u003eWe finally confirmed EGPA in the patient because his clinical course adhered to the items in the Japanese Ministry of Health and Welfare diagnostic criteria for \u0026ldquo;allergic granulomatosis with polyangiitis/Churg\u0026ndash;Strauss syndrome,\u0026rdquo; which is now known as EGPA[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. The following criteria were met: bronchial asthma, allergic rhinitis, eosinophilia, fever, and purpura. Treatment with methylprednisolone (48 mg/day) and amethopterin (10 mg weekly) was initiated. His symptoms improved, and some abnormal imaging manifestations on the chest CT disappeared within one month (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e \u003cdiv id=\"Sec4\" class=\"Section2\"\u003e \u003ch2\u003eDifferential diagnosis\u003c/h2\u003e \u003cp\u003eConventionally, differential diagnosis of EGPA primarily focused on vasculitic disorders such as GPA and MPA; however, based on this case report, there is no doubt that asthma should also be considered for differential diagnosis.\u003c/p\u003e \u003cp\u003eAsthma is a common chronic inflammatory disease of the airways with symptoms including cough, wheeze, shortness of breath, and chest tightness[\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e], which presently impacts more than 300\u0026nbsp;million individuals worldwide; roughly 250,000 asthma-related deaths are reported annually[7; 8]. Notably, the prevalence of asthma is increasing rapidly in developing countries like China[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eBoth EGPA and asthma, which can be concluded as \u0026ldquo;adult-onset eosinophilic airway diseases,\u0026rdquo; are characterized by prominent peripheral blood eosinophilia. Eosinophils contain granules that are toxic to bronchial epithelial cells and play a vital role in the symptoms of asthma[\u003cspan citationid=\"CR60\" class=\"CitationRef\"\u003e60\u003c/span\u003e]. Hence, similar pathogenesis makes distinguishing between these two diseases difficult. In fact, whether asthma is a symptom or disease should be considered for each patient with asthma.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec5\" class=\"Section2\"\u003e \u003ch2\u003eMechanisms/pathophysiology\u003c/h2\u003e \u003cp\u003eThe exact aetiology and pathogenesis underlying the development of EGPA remains unknown[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. EGPA has features of eosinophil infiltration and ANCA-induced endothelial damage, thus it is classified among the small-vessel vasculitides associated with ANCAs and hypereosinophilic syndromes (HESs)[11; 12]. Clinical manifestations of EGPA tend to fall into one of two major disease subsets dominated by vasculitic and eosinophilic manifestations, and ANCA can be used to differentiate between these two subsets. One genome-wide association study (GWAS) examining EGPA demonstrated that EGPA is comprised of two genetically distinct subtypes: MPO-ANCA\u003csup\u003e+\u003c/sup\u003e EGPA and ANCA\u003csup\u003e\u0026ndash;\u003c/sup\u003eEGPA, which align with observed clinical differences among patients[13; 14]. Mendelian randomization revealed an increased risk of eosinophilia underlying susceptibility to EGPA. Meanwhile, it has been suggested that various of environmental factors such as allergens, infections, vaccinations, and medications are potential triggers of EGPA[15; 16]. To some extent, there are shared genetic associations which influence both eosinophil numbers and asthma[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eAsthma symptoms have strong associations with airway inflammation, which is characterized by the infiltration and activation of immune cells including dendritic cells, eosinophils, neutrophils, lymphocytes, innate lymphoid cells, and mast cells, which gradually leads to mucus production, remodelling of the airway wall, bronchial hyperresponsiveness (BHR), and airway obstruction. Currently, asthma phenotypes are usually classified into type 2 or non-type 2 asthma based on its mechanistic pathogenetic processes[\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e]. Non-type 2 asthma, which is usually associated with obesity, aging, and smoking, is characterized by infiltration of Th1cells, Th17 cells, and neutrophils, the presence of type I interferons, and NLRP3 inflammasome activation[6; 18; 19]. Type 2 asthma is usually observed in the clinic as early-onset allergic asthma, late-onset eosinophilic asthma, or exercise-induced asthma, accompanied by recurrent and chronic rhinosinusitis, allergies to common aeroallergens, high eosinophil numbers in the airways, increased periostin, and high exhaled nitric oxide[20; 21]. Additionally, asthma is characterized by variable airflow obstruction, airway inflammation, and remodelling[\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eIn a study of bronchoalveolar lavage fluid (BALF) in patients with EGPA and bronchial asthma, patients with EGPA had a much stronger Th2-type response compared to those with bronchial asthma [\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e].\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec6\" class=\"Section2\"\u003e \u003ch2\u003eClinical presentation\u003c/h2\u003e \u003cp\u003eEGPA is considered to be an idiopathic condition[\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e]; the mean age at onset is 38 to 54 years[25; 26]. As a type of AAV, EGPAs present with manifestations relating to small vessel vasculitic lesions and organ dysfunction. Asthma is a near-universal feature often present for years before the onset of eosinophilia and eosinophilic tissue inflammation, and it is difficult to control even after EGPA treatment [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. The presence or absence of ANCA in patients distinguish between EGPA\u0026rsquo;s two subtypes. Compared with the ANCA-negative subset that features myocardial involvement, lung infiltrates, and gastrointestinal symptoms, ANCA-positive patients are more likely to display peripheral neuropathy, glomerulonephritis, and purpura (which are due to small-vessel vasculitis) [13; 14; 27]. In general, asthma symptoms, eosinophilia greater than 10%, mononeuropathy (including multiplex) or polyneuropathy, non-fixed pulmonary infiltrates on CT, paranasal sinus abnormalities, and biopsy containing a blood vessel with extravascular eosinophils are cardinal characteristics of EGPA[\u003cspan citationid=\"CR59\" class=\"CitationRef\"\u003e59\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThe symptoms of asthma are non-specific, inclusive of episodic wheezing, dyspnoea, chest tightness, and cough[28; 29]. Expiratory wheezing which may be heard on auscultation is the most noteworthy characteristic of asthma. No gold standard exists for diagnosis of asthma, and diagnosis is typically made using a two-pronged approach, including a careful review of medical history to include review of the nature of symptoms, timing, triggers, and response to treatment[\u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e] in addition to objective measurements of variable expiratory airflow limitation, forced expiratory volume in 1 second (FEV\u003csub\u003e1\u003c/sub\u003e), and forced vital capacity (FVC)[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e].\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec7\" class=\"Section2\"\u003e \u003ch2\u003eExamination\u003c/h2\u003e \u003cp\u003eHistopathology of EGPA has revealed necrotizing small-vessel vasculitis and an abundance of eosinophils. More accurately, eosinophilic infiltrates (but no necrosis) are present in tissues or blood vessel walls in the early stages of EGPA. In later stages of the disease, the epithelioid cells within granulomas are surrounded by eosinophils and necrosis is present. Blood tests may show anaemia and eosinophilia as well as increases in C-reactive protein (CRP), lactate dehydrogenase (LDH), creatine kinase (CK), rheumatoid factor (RF), and platelets. In practice, the degree of eosinophilia elevation is typically at least 30% at the onset of vasculitis. A marked growth in total serum IgE level may be found in two-thirds of cases; meanwhile, the positivity rate of MPO-ANCA (P-ANCA) is only present in 30\u0026ndash;40% of cases[\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e]. In addition, \u0026gt;\u0026thinsp;75% of patients with EGPA have been reported to have pulmonary parenchymal lesions on imaging, including GGO, peribronchial or centrilobular nodules, and bronchial wall thickening.[61; 63]\u003c/p\u003e \u003cp\u003eSputum eosinophilia is the most useful biomarker for asthma diagnosis[\u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e]. Although there is no standardized cut-off, an asthma diagnosis may be considered with a blood eosinophil count more than 300 cells/\u0026micro;L or sputum eosinophilia increases over 1\u0026ndash;2% of the normal range[\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e]. Pulmonary function tests such as FEV1, FVC, FEV\u003csub\u003e1\u003c/sub\u003e/FVC% and peak expiratory flow (PEF) are also necessary to make an asthma diagnosis. Accounting for reversible airflow obstruction, guidelines such as the Global Initiative for Asthma (GINA) suggest that a bronchial dilation test (BDT) should be completed to assess airway hyperresponsiveness for suspected asthma cases without contraindications[\u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e]. A 20% decrease in FEV\u003csub\u003e1\u003c/sub\u003e after challenge with a standard dose of methacholine defines the positive result of bronchial provocation test (BPT)[\u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e]. Following the use of a bronchodilator, an increase in FEV\u003csub\u003e1\u003c/sub\u003e of more than 12% that is greater than 200 mL above the normal range is an indicator of airflow obstruction reversibility[35; 36]. However, a negative test does not rule out asthma. Although it is present in many other conditions, airway hyperresponsiveness is a key feature of asthma. Lastly, a chest CT can be used to visualize airway wall thickness and obstruction of airways by mucus, which may contribute towards an asthma diagnosis[37; 38].\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003eTreatment\u003c/h2\u003e \u003cp\u003eTreatment strategies for EGPA vary according to disease manifestations and severity. Treatment regimens may consist of corticosteroids (CS), immunosuppressants, intravenous immunoglobulins, plasma exchanges, and targeted biotherapies[\u003cspan citationid=\"CR39\" class=\"CitationRef\"\u003e39\u003c/span\u003e]. There is no doubt that concomitant manifestations of asthma should be managed aggressively. Locally administered treatments can often alleviate asthma and ENT manifestations. As for systemic therapies, corticosteroids are considered first-line treatment for EGPA. Immunosuppressive drugs such as cyclophosphamide function indirectly by reducing high glucocorticoid requirements[\u003cspan citationid=\"CR40\" class=\"CitationRef\"\u003e40\u003c/span\u003e]; these are typically recommended as a combination treatment, especially in severe cases with poor response to CS treatment and in patients with a poor prognosis[\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e]. Treatments targeting cytokines, such as humanized monoclonal antibodies mepolizumab and reslizumab, are additional therapeutic options that bind to and block the function of circulating IL-5, preventing binding between IL-5 and its receptor, which has demonstrated effects on airways and allergic manifestations[31; 41]. A randomized clinical trial illustrated that mepolizumab was useful in the majority of patients with asthma and chronic sinusitis due to its ability to maintain sustained remission, reduce relapse rates, and substantially reduce the dosage or duration of glucocorticoid therapy[\u003cspan citationid=\"CR42\" class=\"CitationRef\"\u003e42\u003c/span\u003e]. A study showed a 64% reduction in the corticosteroid dose after mepolizumab therapy[\u003cspan citationid=\"CR43\" class=\"CitationRef\"\u003e43\u003c/span\u003e]. Notably, rituximab is usually not considered as the first choice for treatment because its efficacy is less well established for ANCA\u003csup\u003e\u0026ndash;\u003c/sup\u003e patients. Furthermore, patients with asthma and chronic sinusitis frequently experience relapses despite continuous use of rituximab[\u003cspan citationid=\"CR44\" class=\"CitationRef\"\u003e44\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eTreatment strategies for asthma include environmental control, inhaled glucocorticoids (ICS), long-acting β-agonists (LABA), leukotriene antagonists, anticholinergics, and targeted biologic therapies[\u003cspan citationid=\"CR45\" class=\"CitationRef\"\u003e45\u003c/span\u003e]. These treatments have varying mechanisms of action which impact their suitability for different treatment scenarios. For patients experiencing acute stage asthma, the first actionable step is to distance the patient from known allergens. ICS may improve disease control and reduce asthma exacerbations by reducing the number of airway eosinophils[46; 47; 48; 49]. However, if ICS alone is not effective, the addition of a LABA such as formoterol may have significant benefits[\u003cspan citationid=\"CR50\" class=\"CitationRef\"\u003e50\u003c/span\u003e]. Leukotriene antagonists are best for treating asthma exacerbations in children[51; 52], and the anticholinergic tiotropium could reduce the frequency of asthma exacerbations[\u003cspan citationid=\"CR53\" class=\"CitationRef\"\u003e53\u003c/span\u003e]. The most widely used targeted biologic therapies include anti-IgEs, such as omalizumab, and anti-IL-5s, such as mepolizumab and reslizumab. Omalizumab is a humanized monoclonal antibody directed against IgE that has the ability to reduce the risk of asthma exacerbations in allergic asthmatic patients[54; 55; 56; 57; 58]. Since IL-5 leads to airway eosinophilic inflammation, anti-IL-5 agents are generally reserved as maintenance therapies for patients with uncontrolled persistent eosinophilic asthma.\u003c/p\u003e \u003cp\u003eAccording to this Case\u003c/p\u003e \u003cp\u003eAlthough the patient in this case report first developed wheezing in 2018, they did not meet the diagnostic criteria for EGPA based on initial examination. The patient was aware of his 3-year history of asthma, however, his EGPA status during this period remained in question.\u003c/p\u003e \u003cp\u003eThe development of EGPA on chest CT has not yet been reported. Here, we report a case of a patient with EGPA who underwent thoracic CT six times in 4 years and had dynamic changes on CT (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e), which included the premorbid period of the disease, the period of the disease, and the period after the treatment. According to his follow-up visits, varying degrees of absorption of the lesion were observed on the patient\u0026rsquo;s chest CT. Consequently, we consider that the imaging manifestations of EGPA on chest CT might be reversible. Meanwhile, early diagnosis and treatment may prevent disease progression. Furthermore, imaging manifestations on chest CT could be regarded as an evaluation index to evaluate the therapeutic effect in patients with EGPA.\u003c/p\u003e \u003cp\u003eAsthma exacerbations are widely treated with inhaled CS. To relieve the recurring asthma symptoms, we administered intermittent short-term CS treatment to our patient. There are hormones available to ease the symptoms of EGPA; however, hormone treatment alone is insufficient to prevent recurrent symptoms in our patient. We considered the controversial notion that maintenance therapy is justified once remission is achieved. Ultimately, we adhered to the 2016 European Alliance of Associations for Rheumatology guidelines for AAVs to advise a combination of glucocorticoids and either methotrexate or mycophenolate mofetil[\u003cspan citationid=\"CR62\" class=\"CitationRef\"\u003e62\u003c/span\u003e]. To date, the patient remains in good condition, and re-examinations were normal.\u003c/p\u003e \u003cp\u003eEGPA has shifted from being a disease with high mortality to a chronic condition requiring lifelong management by specialists. However, despite this substantial progress, additional collaborative studies and continued interactions between basic and clinical researchers are needed to develop a gold standard for EGPA diagnosis and treatment.\u003c/p\u003e \u003cp\u003eThe patient was finally diagnosed with EGPA after treatment for asthma for 3 years; therefore, EGPA should be considered a differential diagnosis in patients with asthma. To some extent, the abnormal manifestations on thoracic CT gradually returned to normal. We further speculated that the imaging manifestations on chest CT of EGPA might be reversible. Meanwhile, early diagnosis and treatment may prevent disease progression. Furthermore, imaging manifestations on chest CT could be regarded as an evaluation index to evaluate the therapeutic effect in patients with EGPA. Finally, low-dose CS is available to ease the symptoms of EGPA although it would be better to use a combination of glucocorticoids and either methotrexate or mycophenolate mofetil to control disease relapse.\u003c/p\u003e \u003c/div\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eEosinophilic granulomatosis with polyangiitis (EGPA)\u003c/p\u003e\n\u003cp\u003eAntineutrophil cytoplasm antibody (ANCA)-associated vasculitis (AAV)\u003c/p\u003e\n\u003cp\u003eGranulomatosis with polyangiitis (GPA)\u003c/p\u003e\n\u003cp\u003eMicroscopic polyangiitis (MPA)\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eEar, nose, and throat (ENT)\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eComputed tomography (CT)\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eHypereosinophilic syndromes (hess)\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eGenome-wide association study (GWAS)\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eBronchial hyperresponsiveness (BHR)\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eBronchoalveolar lavage fluid (BALF)\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eForced expiratory volume in 1 second (FEV1)\u003c/p\u003e\n\u003cp\u003eForced vital capacity (FVC)\u003c/p\u003e\n\u003cp\u003eC-reactive protein (CRP)\u003c/p\u003e\n\u003cp\u003eLactate dehydrogenase (LDH)\u003c/p\u003e\n\u003cp\u003eCreatine kinase (CK)\u003c/p\u003e\n\u003cp\u003eRheumatoid factor (RF)\u003c/p\u003e\n\u003cp\u003ePositivity rate of MPO-ANCA (P-ANCA)\u0026nbsp;\u003c/p\u003e\n\u003cp\u003ePeak expiratory flow (PEF)\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eGlobal Initiative for Asthma (GINA)\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eBronchial dilation test (BDT)\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eBronchial provocation test (BPT)\u003c/p\u003e\n\u003cp\u003eCorticosteroids (CS)\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eInhaled glucocorticoids (ICS)\u003c/p\u003e\n\u003cp\u003eLong-acting \u0026beta;-agonists (LABA)\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003eEthics approval and consent to participate: All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, as revised in 2000. Informed consent was obtained from all patients for being included in the study.\u003c/p\u003e\n\u003cp\u003eConsent for publication: Informed consent was obtained from the patient for publication of their data.\u003c/p\u003e\n\u003cp\u003eAvailability of data and materials: The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.\u003c/p\u003e\n\u003cp\u003eCompeting interests: The authors declare that they have no competing interests\u003c/p\u003e\n\u003cp\u003eFunding:\u0026nbsp;Not applicable\u003c/p\u003e\n\u003cp\u003eAuthors\u0026apos; contributions: DC and PW contributed the central idea, analysed most of the data, and wrote the initial draft of the paper. YL and MQS contributed to refining the ideas, carrying out additional analyses and finalizing this paper.\u003c/p\u003e\n\u003cp\u003eAcknowledgements: Not applicable\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n \u003cli\u003eChurg J, Strauss L. Allergic granulomatosis, allergic angiitis, and periarteritis nodosa. Am J Pathol. 1951;27:277-301.\u003c/li\u003e\n \u003cli\u003eJennette JC, Falk RJ, Bacon PA, Basu N, Cid MC, Ferrario F, et al. 2012 revised International Chapel Hill Consensus Conference Nomenclature of Vasculitides. Arthritis Rheum. 2013;65:1-11.\u003c/li\u003e\n \u003cli\u003eFagni F, Bello F, Emmi G. Eosinophilic Granulomatosis With Polyangiitis: Dissecting the Pathophysiology. Front Med (Lausanne). 2021;8:627776.\u003c/li\u003e\n \u003cli\u003eJakes RW, Kwon N, Nordstrom B, Goulding R, Fahrbach K, Tarpey J, Van Dyke MK. Burden of illness associated with eosinophilic granulomatosis with polyangiitis: a systematic literature review and meta-analysis. 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The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33:160-72.\u003c/li\u003e\n \u003cli\u003eYanagisawa S, Ichinose M. Definition and diagnosis of asthma-COPD overlap (ACO). Allergol Int. 2018;67:172-8.\u003c/li\u003e\n \u003cli\u003eKim YK, Lee KS, Chung MP, Han J, Chong S, Chung MJ, Yi CA, Kim HY. Pulmonary involvement in Churg-Strauss syndrome: an analysis of CT, clinical, and pathologic findings. Eur Radiol. 2007;17:3157-65.\u003c/li\u003e\n \u003cli\u003eYates M, Watts RA, Bajema IM, Cid MC, Crestani B, Hauser T, et al. EULAR/ERA-EDTA recommendations for the management of ANCA-associated vasculitis. Ann Rheum Dis. 2016;75:1583-94.\u003c/li\u003e\n \u003cli\u003eSanchez F, Gutierrez JM, Kha LC, Jimenez-Juan L, Cool C, Vargas D, et al. Pathological entities that may affect the lungs and the myocardium. Evaluation with chest CT and cardiac MR. Clin Imaging. 2021;70:124-35.\u003c/li\u003e\n\u003c/ol\u003e"},{"header":"Table","content":"\u003cp\u003eTable 1 is available in the Supplementary Files section\u003c/p\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":true,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"EGPA, asthma, differential diagnosis, CT","lastPublishedDoi":"10.21203/rs.3.rs-2118285/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-2118285/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground: \u003c/strong\u003eEosinophilic granulomatosis with polyangiitis (EGPA) is a small-vessel necrotizing vasculitis. Its most common clinical manifestations are asthma; ear, nose, and throat involvement; and lung involvement. As EGPA has similar features to asthma, most patients with this disease seek medical treatment for the first time with wheezing symptoms and, thus, may be regarded as having asthma.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase presentation: \u003c/strong\u003eThis report discusses an EGPA case regarded as recurrent asthma for 3 years. The patient underwent thoracic computed tomography (CT) 6 times in recent years, which recorded dynamic changes in an EGPA patient’s lungs for the first time. We initiated treatment with methylprednisolone and amethopterin. The patient’s symptoms rapidly improved, and some abnormal imaging manifestations on chest CT disappeared one month after the treatment.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusions:\u003c/strong\u003e Consequently, early diagnosis and treatment are needed because the progression of the disease may be prohibited, and imaging manifestations on chest CT of EGPA may be reversible. Furthermore, to diagnose patients with asthma more reliably and precisely, we discuss the differential diagnosis between EGPA and asthma. Thirdly, imaging manifestations on chest CT could be regarded as an evaluation index to evaluate the therapeutic effect in patients with EGPA. Finally, low-dose CS can alleviate the symptoms of EGPA.\u003c/p\u003e","manuscriptTitle":"Asthma or eosinophilic granulomatosis with polyangiitis: a case-based review","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2022-10-04 14:05:18","doi":"10.21203/rs.3.rs-2118285/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"dfafe3a9-e6b6-4e2b-bb71-f2354847cf40","owner":[],"postedDate":"October 4th, 2022","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2023-07-20T18:06:54+00:00","versionOfRecord":[],"versionCreatedAt":"2022-10-04 14:05:18","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-2118285","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-2118285","identity":"rs-2118285","version":["v1"]},"buildId":"7rjqhiLT3MXkJMwkYKINL","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}