Finger-in-Glove Appearance of Allergic Bronchopulmonary Aspergillosis in a Chronic Obstructive Pulmonary Disease Patient Without Asthma or Cystic Fibrosis: A Case Report and Literature Review

Finger-in-Glove Appearance of Allergic Bronchopulmonary Aspergillosis in a Chronic Obstructive Pulmonary Disease Patient Without Asthma or Cystic Fibrosis: A Case Report and Literature 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 Finger-in-Glove Appearance of Allergic Bronchopulmonary Aspergillosis in a Chronic Obstructive Pulmonary Disease Patient Without Asthma or Cystic Fibrosis: A Case Report and Literature Review Maulik K. Lathiya, Antonios N. Charokopos, Bansi P. Savaliya, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6115782/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 Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity reaction to Aspergillus species, commonly observed in patients with asthma or cystic fibrosis. However, its occurrence in individuals with chronic obstructive pulmonary disease (COPD) is rare and not well-documented. Radiological findings such as the "finger-in-glove" sign on computed tomography (CT) scans can aid in diagnosis, but a high index of suspicion is required in atypical cases. ABPA can contribute to mucoid impaction, leading to progressive pulmonary dysfunction if left untreated. Case Presentation We report a unique case of ABPA in a patient with COPD who had no prior history of asthma or cystic fibrosis. The patient presented with worsening respiratory symptoms, and imaging studies revealed mucoid impaction with the characteristic "finger-in-glove" sign. Laboratory findings included peripheral eosinophilia and elevated serum IgE, supporting the diagnosis of ABPA. Management involved antifungal therapy and corticosteroids, followed by a tapering regimen, with prophylactic treatment for pneumocystis pneumonia (PCP) to prevent opportunistic infections. Follow-up pulmonary function tests demonstrated a moderate decline in diffusion capacity, necessitating continued monitoring for potential early interstitial lung disease (ILD) or pulmonary hypertension. Conclusions This case highlights the importance of considering ABPA in patients with COPD who present with mucoid impaction, even in the absence of traditional risk factors. A thorough differential diagnosis of eosinophilia in pulmonary disease is crucial to distinguish between hypersensitivity reactions and malignant myeloproliferative disorders, ensuring appropriate treatment strategies. Clinicians should maintain a high level of awareness for ABPA in COPD patients to facilitate timely diagnosis and management. Allergic bronchopulmonary aspergillosis (ABPA) chronic obstructive pulmonary disease (COPD) aspergillus fumigatus finger-in-glove sign Figures Figure 1 Figure 2 Figure 3 Introduction Mucoid impaction or airway filling with mucoid secretions are frequent findings on computed tomography (CT) and chest X-rays. If mucus impaction occurs in the large airways, the condition is classically manifested by tubular or branching opacities that resemble fingers, known as the “finger-in-glove” sign. Although the finger-in-glove sign is rare and prominently identified on CT of the thorax, it is highly specific to cases of allergic bronchopulmonary aspergillosis (ABPA). However, “inspissated” mucus that accumulates within the airways, known as mucus plugs, is common in plastic bronchitis, asthma, and ABPA. [ 1 ] Furthermore, mucus impaction is one of the diagnostic criteria for ABPA. Multiple diagnostic criteria including those from 1977, 2013, 2016, and a newly proposed criteria in 2020 have been recommended for ABPA, all of which have identified asthma as one of the main components for ABPA diagnosis. However, several patients do not meet these criteria. [ 2 , 3 ] We present a case of ABPA in a chronic obstructive pulmonary disease (COPD) patient without asthma or cystic fibrosis (CF) with the classic and more enhanced finger-in-glove appearance on CT scan that fulfils the criteria of mild COPD. Case Presentation A 77-year-old male with COPD, having a history of smoking, prostate cancer, bronchiectasis, colon adenocarcinoma with metastasis to the lung with post wedge resection in 2014, and fibrotic changes due to underlying interstitial lung disease (with no history of asthma and cystic fibrosis) presented to the emergency department for evaluation. His symptoms included worsening cough and shortness of breath due to pneumonia, which had been refractory to levofloxacin treatment, initiated two days earlier. Additionally, he reported an episode of choking on a pill, which he managed to retrieve after some difficulty. At presentation, he denied having fever or chills, chest pain, back pain, abdominal pain, nausea, vomiting, diarrhea, or urinary symptoms. Vital signs were unremarkable with a temperature of 36.6°C, a respiratory rate of 24 breaths per minute, a blood pressure of 138/83 mm Hg, and a pulse of 86 bpm. Physical examination revealed adventitious sounds at the bases but no expiratory wheezes. Lung sounds decreased in both lung bases, with no neurological, urinary, or gastrointestinal symptoms. During evaluation in the emergency room, chest X-ray showed a mass-like region of consolidation in the medial aspect of the left upper lobe, extending to the pulmonary hilum. This raised the suspicion of an underlying malignancy or mass, prompting further investigation using a CT scan. The CT scan confirmed dilated, unopacified bronchi throughout the left upper lobe, consistent with the chest X-ray findings. This raised the possibility of a mucus plug, foreign body, or malignancy (Fig. 1 ). Laboratory results included a CBC showing a hemoglobin level of 12.3 g/L and mild leukocytosis (10.5/µL), with a differential count of neutrophils (6.53), lymphocytes (0.84), monocytes (0.72), eosinophils (2.32), and basophils (0.11). Electrolyte and renal parameters were normal. Lactate levels were normal at 1.0, C-reactive protein levels were < 3 mg/dL, and procalcitonin levels were 0.07 ng/mL. A bronchoscopy was recommended after consulting the pulmonary medicine. During bronchoscopy, mild, thick, and impacted secretions were observed in the left bronchial tree and a lymph node biopsy was performed (Fig. 2 ). The mucus plug was evacuated and sent for microscopic examination and culture (Fig. 3 ). The findings were concerning for ABPA, as secretions showed eosinophilia, > 3.75 index for Aspergillus antigen and a fungal culture positive for Aspergillus fumigatus complex. Additionally, an esophagogram with fluoroscopy for swallowing function, speech, and occupational therapy was performed, and both findings were normal. Endobronchial ultrasound performed during bronchoscopy revealed extensive inflammation, with numerous eosinophils and scant fragments of inflamed and reactive bronchial mucosa. Fungal hyphae, consistent with Aspergillus , were identified within the exudates. A. fumigatus IgG AB levels were within the normal reference limits at 54.2 mg/dL (reference range: <102 mg/dL), with the IgE levels of 4.71 kU/L, and total IgE levels of 424 kU/L (reference range: <214 kU/L). Pulmonary function tests were conducted to confirm the diagnosis of COPD by adhering to standard protocols, including spirometry and post-bronchodilator testing. This revealed the presence of irreversible or partially reversible airflow limitation, indicated by a < 0.7 post-bronchodilator ratio of FEV1/FVC or a < LLN value of FEV1/FVC. The GOLD staging system was employed based on the percentage of predicted FEV1 for patient age and height. In our case, spirometry results post-bronchodilation showed a post-FEV1 of 2.4 L and a post-FVC of 3.78 L, resulting in an FEV1/FVC ratio percentage of 64.81%, thus meeting the GOLD criteria for COPD diagnosis (< 70%). The post-FEV1 level of 2.45 L specifically aligns with GOLD 1 criteria for “Mild COPD” (FEV1 ≥ 80% predicted). Subsequent physical examination revealed bilateral crepitus at the base of the lungs. Additionally, an X-ray conducted two weeks prior to the visit, prompted by a chronic cough, revealed mild interstitial opacities in the lower lungs and patchy airspace opacities. The patient was treated with voriconazole and a high-dose of prednisolone for two weeks (followed by a tapering regimen), and trimethoprim-sulfamethoxazole for Pneumocystis pneumonia prophylaxis. Additional tests including total IgE, A. fumigatus specific IgE, hypersensitivity pneumonia panel, direct microscopy (including Gram staining and acid-fast staining), and cultures (bacterial, fungal, and mycobacterial) were performed. At the follow-up, the patient showed continued improvement and decreased IgE levels. Due to persistent eosinophilia, the patient was followed-up in the oncology clinic. Bone marrow biopsy revealed 30% cellularity with trilineage hematopoietic maturation, including increased eosinophils. Peripheral blood showed slight normochromic and normocytic anemia as well as absolute eosinophilia. Concurrent molecular and cytogenetic studies performed at the Mayo Clinic, Rochester, were negative for KIT mutations, abnormalities associated with eosinophilia, and a normal karyotype. Serum tryptase levels were within normal limits. The oncology department concluded that there was no end-organ damage based on history and physical examination. Eosinophilia was reactive to ABPA and improved with treatment. Imaging revealed no splenomegaly or lymphadenopathy. Concerns regarding the constitutional symptoms remain unknown. No cytopenia was observed and normal LDH levels of 204 U/L (range: 122–222 U/L) were observed. Following another bronchoscopy, the Aspergillus antigen index of the patient was interpreted as negative, with a value < 0.5. Pulmonary function tests revealed a moderate decline in diffusion capacity and no signs of airflow obstruction. Early COPD, early interstitial lung disease, and pulmonary vascular diseases, such as pulmonary hypertension, were among the differential diagnoses. A clinical correlation was recommended. Written informed consent was obtained from the patient to share details and related images of the case for publication. Discussion Mucus is a complex mixture of various components including mucin glycoproteins, water, ions, proteins, and lipids. The composition of mucus differs, depending on the environmental and pathophysiological conditions. Normally, when mucoid impaction is identified on a plain chest radiograph, the next step in the diagnostic evaluation is a chest CT scan. Clues that may aid in the differential diagnosis of mucoid impaction include hilar adenopathy and an endobronchial or perihilar mass that may indicate a neoplastic cause, with diffuse or multifocal bronchiectasis suggesting an underlying immune deficiency or systemic disease (e.g., CF, primary ciliary dyskinesia). Central bronchiectasis and high-attenuation mucus (HAM) are suggestive of ABPA. To date, there is no definitive test or agreement on the diagnostic criteria for confirming ABPA. Some clinical practice guidelines for the diagnosis and treatment of ABPA, such as those developed by the International Society for Human & Animal Mycology (ISHAM) working group, are available; however, the criteria for diagnosis vary across guidelines (10) . Some typical follow-up findings that support ABPA diagnosis include peripheral eosinophilia, elevated total serum IgE and anti- A. fumigatus IgE, bronchoscopy revealing mucoid impaction demonstrating hyphae, eosinophilia, Aspergillus -specific IgE and IgA, positive Aspergillus skin test, pulmonary infiltrates, bronchiectasis changes, and/or finger-in-glove opacity on radiologic evaluation. [ 4 , 8 ] Additional serologic or genetic testing may help confirm the underlying diagnosis. However, some diseases appear similar on CT scans, including plastic bronchitis, asthma, Aspergillus tracheobronchitis, hyper-IgE syndrome, lipoid and chronic eosinophilic pneumonia, and pulmonary alveolar proteinosis. [ 5 ] In such cases, bronchoscopy is recommended for further diagnostic evaluation (e.g., assessing an endobronchial lesion) or treatment (e.g., removal of a foreign body) [ 6 ] . In our case, the patient presented with a history of smoking and pill aspiration, with CT scan findings revealing a new, isolated mucoid impaction characterized by a finger-in-glove shaped opacity. This was discovered incidentally, with no known risk factors for its more common causes, such as ABPA and neoplasm. Similar cases have been reported in the past, where ABPA was discovered in patients with COPD who first exhibited bronchiectasis and mucoid impaction. Despite not having asthma or cystic fibrosis, the patient had chronic inflammation and reduced mucociliary clearance, which likely made it easier for Aspergillus to colonize. Radiologic signs such as central bronchiectasis and high-attenuation mucus were important diagnostic indicators, and bronchoscopy along with microbiological analysis confirmed the presence of Aspergillus (9) . These cases demonstrate how important it is to rule out ABPA as a potential cause of mucoid impaction in COPD patients. This will ensure timely diagnosis and appropriate corticosteroid and antifungal therapy to halt the disease's progression. Additionally, the evaluation of mucoid impaction is typically based on its presentation on CT images, including tubular branching, ovoid opacities, and other additional findings. High attenuation and branching are characteristic features of ABPA on CT scans, in contrast to the mucoid impaction associated with other disorders, where radiographically, lower-attenuation mucus fills the airways [ 5 ] . In this case, the patient presented with a history of pill aspiration and worsening cough, which is highly suggestive of the underlying cause of the impacted mucus discovered on the CT scan. In addition to ABPA, the differential diagnoses of highly-attenuated mucoid impaction include endobronchial lesions, inhalation of foreign bodies, bronchial atresia, and bronchiectasis due to any cause. [ 1 ] Therefore, it is essential to differentiate ABPA from other causes of mucoid impaction, because ABPA treatment requires the use of corticosteroids and antifungal agents, whereas other conditions may require different treatment approaches. [ 1 ] Thus, we considered bronchoscopy to evaluate thick mucus impaction to identify whether it was an aspirated pill or impacted mucus. Upon evaluation, it was discovered to be Aspergillus , which was later confirmed by laboratory findings. ABPA is a pulmonary disorder caused by hypersensitivity to A. fumigatus that primarily complicates the course of asthma and CF. It is caused by host immune reactions against A. fumigatus which colonizes the airways of patients with asthma and CF. In asthma and CF, impaired mucociliary clearance normally allows Aspergillus to germinate in the bronchial tree. However, defects in immunity can persist and lead to the activation of Th2 CD4 + T-cells and cytokines, such as interleukin (IL)-5 (mediating eosinophilic airway inflammation) and IL-8 (mediating neutrophil chemotaxis). Instead of a Th1 CD4 + T-cell response against Aspergillus , bronchial wall damage and mucus hypersecretion lead to Aspergillus infection in the bronchial tree [2, 6]. Similarly, the underlying pathogenesis of COPD involves extensive exposure to noxious stimuli, increased oxidative stress (most commonly due to cigarette smoke), and increased release of reactive oxygen species by inflammatory cells. This activates CD8 + T-cells and mediates inflammation, promoting goblet cell proliferation and hypertrophy, mucus hypersecretion, and ciliary function impairment, resulting in chronic cough. Therefore, the environment that facilitates Aspergillus growth and leads to ABPA in COPD appears to be similar to that of asthma. However, ABPA is infrequently diagnosed in the context of post-tuberculosis fibro-cavitary disease [ 2 , 7 ] . In this case, the patient had a history of COPD instead of asthma or CF, which may be considered the underlying cause of ABPA exacerbation. Thus, this case presented an atypical manifestation of ABPA within the spectrum of pulmonary disorders commonly encountered in the United States, suggesting the inclusion of ABPA in the list of differential diagnoses for patients with COPD. Although ABPA predominantly complicates asthma and cystic fibrosis, its occurrence in conjunction with COPD is rare. Furthermore, evaluation of eosinophilia raises the possibility of an underlying hematological malignancy. The eosinophil count, however, was 10.6 upon admission. The following day, it decreased to 6.5, and before discharge, it decreased to 5.0, with the current levels being 1.4. However, the pattern of eosinophilia observed in this case, characterized by a gradual decrease in the eosinophil count over time, suggests a non-malignant etiology. Long-term myeloproliferative illnesses seem unlikely, given this pattern of eosinophilia. Overall, this case underscores the importance of considering ABPA in the differential diagnosis of COPD patients presenting with mucoid impaction, the complexity of the patient’s medical history, including interstitial lung disease, bronchiectasis, COPD, and prior malignancy, posed challenges in diagnosing ABPA. The absence of asthma or cystic fibrosis, along with reactive eosinophilia, made symptom attribution difficult. This case underscores the need to consider ABPA in COPD patients with mucoid impaction and highlights the necessity for alternative diagnostic criteria in atypical cases. Concomitant conditions may influence disease progression and treatment response, though their exact role remains unclear. Future research should explore the pathophysiological mechanisms underlying ABPA in COPD without asthma, assess its prevalence in this population, and investigate the long-term impact on pulmonary function to improve diagnostic and therapeutic strategies. Declarations Funding None. Author Contributions Maulik K. Lathiya, Bansi P. Savaliya contributed to the conceptualization, writing, original draft preparation, graphics, and reviewing; Charokopos Antonios and Cristian Madrid contributed to reviewing and editing. All authors read and approved the final manuscript. Conflicts of Interest None. Data Available Statement No, this manuscript does not have any research data outside the submitted manuscript file. Acknowledgements We thank Drew J. Persson and Zaug Paj Her from the University of Minnesota for editing a draft of this manuscript. Ethics approval This study was approved by the ethics committee of Mayo Clinic. Written informed consent was obtained from the patient for the publication of this case report and any accompanying figure. Consent to participate and consent for publication Written informed consent was obtained from the patient for the publication of this case report and any accompanying figures. Competing interests None. References Agarwal, R., A.N. Aggarwal, and D. Gupta, High-attenuation mucus in allergic bronchopulmonary aspergillosis: another cause of diffuse high-attenuation pulmonary abnormality. AJR Am J Roentgenol, 2006. 186(3): p. 904. Agarwal, R., et al., Developments in the diagnosis and treatment of allergic bronchopulmonary aspergillosis. Expert Rev Respir Med, 2016. 10(12): p. 1317-1334. Asano, K., et al., New clinical diagnostic criteria for allergic bronchopulmonary aspergillosis/mycosis and its validation. J Allergy Clin Immunol, 2021. 147(4): p. 1261-1268.e5. Agarwal R, Sehgal IS, Muthu V, et al. Revised ISHAM-ABPA working group clinical practice guidelines for diagnosing, classifying and treating allergic bronchopulmonary aspergillosis/mycoses. Eur Respir J. 2024;63(4):2400061. Published 2024 Apr 4. doi:10.1183/13993003.00061-2024 Panchabhai, T.S., et al., Plugs of the Air Passages: A Clinicopathologic Review. Chest, 2016. 150(5): p. 1141-1157. Martinez, S., et al., Mucoid impactions: finger-in-glove sign and other CT and radiographic features. Radiographics, 2008. 28(5): p. 1369-82. Agarwal, R., R. Srinivas, and S.K. Jindal, Allergic bronchopulmonary aspergillosis complicating chronic obstructive pulmonary disease. Mycoses, 2008. 51(1): p. 83-5. Sisodia, J. and Bajaj T. Allergic Bronchopulmonary Aspergillosis. [Updated 2023 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542329/ Mir E, Shah A. Allergic bronchopulmonary aspergillosis in a patient with chronic obstructive pulmonary disease. Prim Care Respir J. 2012 Mar;21(1):111-4. doi: 10.4104/pcrj.2012.00001. PMID: 22222946; PMCID: PMC6547891. Agarwal R, Sehgal IS, Muthu V, et al. Revised ISHAM-ABPA working group clinical practice guidelines for diagnosing, classifying and treating allergic bronchopulmonary aspergillosis/mycoses. Eur Respir J. 2024;63(4):2400061. Published 2024 Apr 4. doi:10.1183/13993003.00061-2024 Additional Declarations No competing interests reported. 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-6115782","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":439410233,"identity":"ce861ab3-461a-4c8a-b752-fe741e3e2738","order_by":0,"name":"Maulik K. Lathiya","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAABA0lEQVRIie3RMUvDQBTA8RcC6RKJY7r4Gd4UEKX9IF0uHNSlB05ZHOyUqeCaSb+C/QavBJrlSNaDLimFTA4dMyjYi4IuuWYUvP9078GPOzgAm+0PhgAeMH0gcIjR7ffeMxH3i1wTwInMBxLdVBOgfAAZVdt6n04gKiRSLatZkHGCY5L3E5+PME45RHKBxNROZGrOnKw0EOBeGKcuRKTJcSeWaoHuRWogwUGTR8DqTZNSvGjyYSJhd0sOqLqHkXjVxDGSQxSysvBRNffEJBdr2bDNqrzrJdOnuBm3ycMVVny9b7cT8VzwTd0mN72ky/HA/5ku2emDzvb+ewgGAJvNZvtXfQJKNGSsXvckLQAAAABJRU5ErkJggg==","orcid":"","institution":"Mayo Clinic","correspondingAuthor":true,"prefix":"","firstName":"Maulik","middleName":"K.","lastName":"Lathiya","suffix":""},{"id":439410234,"identity":"f37d3d0e-0e36-4299-b60d-5ecbf4dc0da0","order_by":1,"name":"Antonios N. Charokopos","email":"","orcid":"","institution":"Mayo Clinic Health System","correspondingAuthor":false,"prefix":"","firstName":"Antonios","middleName":"N.","lastName":"Charokopos","suffix":""},{"id":439410235,"identity":"725eb034-356f-4239-91ea-05ef0b9aa9ff","order_by":2,"name":"Bansi P. Savaliya","email":"","orcid":"","institution":"Mayo Clinic","correspondingAuthor":false,"prefix":"","firstName":"Bansi","middleName":"P.","lastName":"Savaliya","suffix":""},{"id":439410237,"identity":"d6553b62-875e-49b9-8a05-c6b0a9867ab4","order_by":3,"name":"Cristian I. Madrid","email":"","orcid":"","institution":"Mayo Clinic Health System","correspondingAuthor":false,"prefix":"","firstName":"Cristian","middleName":"I.","lastName":"Madrid","suffix":""}],"badges":[],"createdAt":"2025-02-26 19:38:05","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-6115782/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6115782/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":81013047,"identity":"951e9839-0ec7-42a6-88d3-86af4031f585","added_by":"auto","created_at":"2025-04-21 08:32:51","extension":"jpg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":57072,"visible":true,"origin":"","legend":"\u003cp\u003eBefore bronchoscopy, classic finger-in-glove appearance of dilated un opacified bronchi throughout the left upper lobe seen on computed tomography scan of the chest in (A) axial (orange arrows), (B) coronal (red arrows), and (C) lateral (sagittal) view (yellow arrows).\u003c/p\u003e","description":"","filename":"1.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6115782/v1/52c2b0d8588b97e8dec249a1.jpg"},{"id":81013049,"identity":"f0fa23eb-a5d4-4572-9eaf-43aca0445a2a","added_by":"auto","created_at":"2025-04-21 08:32:51","extension":"jpg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":50329,"visible":true,"origin":"","legend":"\u003cp\u003eBronchoscopic view of partial obstruction of the left bronchial tree by large mucoid cast in the patient with chronic obstructive pulmonary disease.\u003c/p\u003e","description":"","filename":"2.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6115782/v1/443553e0af52a402b2ba90ea.jpg"},{"id":81013050,"identity":"281f0b93-8a18-4376-92d4-e5e4064ceace","added_by":"auto","created_at":"2025-04-21 08:32:51","extension":"jpg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":52872,"visible":true,"origin":"","legend":"\u003cp\u003eComputed tomography scan of the chest status post bronchoscopic clearance of mucus plug in left upper bronchial tree seen in (A) axial (orange arrows), (B) coronal (red arrows), and (C) sagittal view (yellow arrows).\u003c/p\u003e","description":"","filename":"3.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6115782/v1/11383d45208c0e09467a7238.jpg"},{"id":102904840,"identity":"baba1727-c407-4b94-956f-36a1c600e36f","added_by":"auto","created_at":"2026-02-18 08:57:54","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":557869,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6115782/v1/4d2dd6aa-d8f6-4b49-b6bf-beb8e9e4bb8c.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Finger-in-Glove Appearance of Allergic Bronchopulmonary Aspergillosis in a Chronic Obstructive Pulmonary Disease Patient Without Asthma or Cystic Fibrosis: A Case Report and Literature Review","fulltext":[{"header":"Introduction","content":"\u003cp\u003eMucoid impaction or airway filling with mucoid secretions are frequent findings on computed tomography (CT) and chest X-rays. If mucus impaction occurs in the large airways, the condition is classically manifested by tubular or branching opacities that resemble fingers, known as the \u0026ldquo;finger-in-glove\u0026rdquo; sign. Although the finger-in-glove sign is rare and prominently identified on CT of the thorax, it is highly specific to cases of allergic bronchopulmonary aspergillosis (ABPA). However, \u0026ldquo;inspissated\u0026rdquo; mucus that accumulates within the airways, known as mucus plugs, is common in plastic bronchitis, asthma, and ABPA.\u003csup\u003e[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]\u003c/sup\u003e Furthermore, mucus impaction is one of the diagnostic criteria for ABPA. Multiple diagnostic criteria including those from 1977, 2013, 2016, and a newly proposed criteria in 2020 have been recommended for ABPA, all of which have identified asthma as one of the main components for ABPA diagnosis. However, several patients do not meet these criteria.\u003csup\u003e[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]\u003c/sup\u003e We present a case of ABPA in a chronic obstructive pulmonary disease (COPD) patient without asthma or cystic fibrosis (CF) with the classic and more enhanced finger-in-glove appearance on CT scan that fulfils the criteria of mild COPD.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eA 77-year-old male with COPD, having a history of smoking, prostate cancer, bronchiectasis, colon adenocarcinoma with metastasis to the lung with post wedge resection in 2014, and fibrotic changes due to underlying interstitial lung disease (with no history of asthma and cystic fibrosis) presented to the emergency department for evaluation. His symptoms included worsening cough and shortness of breath due to pneumonia, which had been refractory to levofloxacin treatment, initiated two days earlier. Additionally, he reported an episode of choking on a pill, which he managed to retrieve after some difficulty. At presentation, he denied having fever or chills, chest pain, back pain, abdominal pain, nausea, vomiting, diarrhea, or urinary symptoms. Vital signs were unremarkable with a temperature of 36.6\u0026deg;C, a respiratory rate of 24 breaths per minute, a blood pressure of 138/83 mm Hg, and a pulse of 86 bpm. Physical examination revealed adventitious sounds at the bases but no expiratory wheezes. Lung sounds decreased in both lung bases, with no neurological, urinary, or gastrointestinal symptoms.\u003c/p\u003e \u003cp\u003eDuring evaluation in the emergency room, chest X-ray showed a mass-like region of consolidation in the medial aspect of the left upper lobe, extending to the pulmonary hilum. This raised the suspicion of an underlying malignancy or mass, prompting further investigation using a CT scan. The CT scan confirmed dilated, unopacified bronchi throughout the left upper lobe, consistent with the chest X-ray findings. This raised the possibility of a mucus plug, foreign body, or malignancy (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). Laboratory results included a CBC showing a hemoglobin level of 12.3 g/L and mild leukocytosis (10.5/\u0026micro;L), with a differential count of neutrophils (6.53), lymphocytes (0.84), monocytes (0.72), eosinophils (2.32), and basophils (0.11). Electrolyte and renal parameters were normal. Lactate levels were normal at 1.0, C-reactive protein levels were \u0026lt;\u0026thinsp;3 mg/dL, and procalcitonin levels were 0.07 ng/mL.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eA bronchoscopy was recommended after consulting the pulmonary medicine. During bronchoscopy, mild, thick, and impacted secretions were observed in the left bronchial tree and a lymph node biopsy was performed (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). The mucus plug was evacuated and sent for microscopic examination and culture (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e). The findings were concerning for ABPA, as secretions showed eosinophilia, \u0026gt;\u0026thinsp;3.75 index for \u003cem\u003eAspergillus\u003c/em\u003e antigen and a fungal culture positive for \u003cem\u003eAspergillus fumigatus\u003c/em\u003e complex. Additionally, an esophagogram with fluoroscopy for swallowing function, speech, and occupational therapy was performed, and both findings were normal. Endobronchial ultrasound performed during bronchoscopy revealed extensive inflammation, with numerous eosinophils and scant fragments of inflamed and reactive bronchial mucosa. Fungal hyphae, consistent with \u003cem\u003eAspergillus\u003c/em\u003e, were identified within the exudates. \u003cem\u003eA. fumigatus\u003c/em\u003e IgG AB levels were within the normal reference limits at 54.2 mg/dL (reference range: \u0026lt;102 mg/dL), with the IgE levels of 4.71 kU/L, and total IgE levels of 424 kU/L (reference range: \u0026lt;214 kU/L). Pulmonary function tests were conducted to confirm the diagnosis of COPD by adhering to standard protocols, including spirometry and post-bronchodilator testing. This revealed the presence of irreversible or partially reversible airflow limitation, indicated by a\u0026thinsp;\u0026lt;\u0026thinsp;0.7 post-bronchodilator ratio of FEV1/FVC or a\u0026thinsp;\u0026lt;\u0026thinsp;LLN value of FEV1/FVC. The GOLD staging system was employed based on the percentage of predicted FEV1 for patient age and height. In our case, spirometry results post-bronchodilation showed a post-FEV1 of 2.4 L and a post-FVC of 3.78 L, resulting in an FEV1/FVC ratio percentage of 64.81%, thus meeting the GOLD criteria for COPD diagnosis (\u0026lt;\u0026thinsp;70%). The post-FEV1 level of 2.45 L specifically aligns with GOLD 1 criteria for \u0026ldquo;Mild COPD\u0026rdquo; (FEV1\u0026thinsp;\u0026ge;\u0026thinsp;80% predicted). Subsequent physical examination revealed bilateral crepitus at the base of the lungs. Additionally, an X-ray conducted two weeks prior to the visit, prompted by a chronic cough, revealed mild interstitial opacities in the lower lungs and patchy airspace opacities.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eThe patient was treated with voriconazole and a high-dose of prednisolone for two weeks (followed by a tapering regimen), and trimethoprim-sulfamethoxazole for \u003cem\u003ePneumocystis\u003c/em\u003e pneumonia prophylaxis. Additional tests including total IgE, \u003cem\u003eA. fumigatus\u003c/em\u003e specific IgE, hypersensitivity pneumonia panel, direct microscopy (including Gram staining and acid-fast staining), and cultures (bacterial, fungal, and mycobacterial) were performed. At the follow-up, the patient showed continued improvement and decreased IgE levels. Due to persistent eosinophilia, the patient was followed-up in the oncology clinic. Bone marrow biopsy revealed 30% cellularity with trilineage hematopoietic maturation, including increased eosinophils. Peripheral blood showed slight normochromic and normocytic anemia as well as absolute eosinophilia. Concurrent molecular and cytogenetic studies performed at the Mayo Clinic, Rochester, were negative for KIT mutations, abnormalities associated with eosinophilia, and a normal karyotype. Serum tryptase levels were within normal limits. The oncology department concluded that there was no end-organ damage based on history and physical examination. Eosinophilia was reactive to ABPA and improved with treatment. Imaging revealed no splenomegaly or lymphadenopathy. Concerns regarding the constitutional symptoms remain unknown. No cytopenia was observed and normal LDH levels of 204 U/L (range: 122\u0026ndash;222 U/L) were observed. Following another bronchoscopy, the \u003cem\u003eAspergillus\u003c/em\u003e antigen index of the patient was interpreted as negative, with a value\u0026thinsp;\u0026lt;\u0026thinsp;0.5. Pulmonary function tests revealed a moderate decline in diffusion capacity and no signs of airflow obstruction. Early COPD, early interstitial lung disease, and pulmonary vascular diseases, such as pulmonary hypertension, were among the differential diagnoses. A clinical correlation was recommended.\u003c/p\u003e \u003cp\u003eWritten informed consent was obtained from the patient to share details and related images of the case for publication.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eMucus is a complex mixture of various components including mucin glycoproteins, water, ions, proteins, and lipids. The composition of mucus differs, depending on the environmental and pathophysiological conditions. Normally, when mucoid impaction is identified on a plain chest radiograph, the next step in the diagnostic evaluation is a chest CT scan. Clues that may aid in the differential diagnosis of mucoid impaction include hilar adenopathy and an endobronchial or perihilar mass that may indicate a neoplastic cause, with diffuse or multifocal bronchiectasis suggesting an underlying immune deficiency or systemic disease (e.g., CF, primary ciliary dyskinesia). Central bronchiectasis and high-attenuation mucus (HAM) are suggestive of ABPA. To date, there is no definitive test or agreement on the diagnostic criteria for confirming ABPA. Some clinical practice guidelines for the diagnosis and treatment of ABPA, such as those developed by the International Society for Human \u0026amp; Animal Mycology (ISHAM) working group, are available; however, the criteria for diagnosis vary across guidelines \u003csup\u003e(10)\u003c/sup\u003e. Some typical follow-up findings that support ABPA diagnosis include peripheral eosinophilia, elevated total serum IgE and anti-\u003cem\u003eA. fumigatus\u003c/em\u003e IgE, bronchoscopy revealing mucoid impaction demonstrating hyphae, eosinophilia, \u003cem\u003eAspergillus\u003c/em\u003e-specific IgE and IgA, positive \u003cem\u003eAspergillus\u003c/em\u003e skin test, pulmonary infiltrates, bronchiectasis changes, and/or finger-in-glove opacity on radiologic evaluation.\u003csup\u003e[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]\u003c/sup\u003e Additional serologic or genetic testing may help confirm the underlying diagnosis. However, some diseases appear similar on CT scans, including plastic bronchitis, asthma, \u003cem\u003eAspergillus\u003c/em\u003e tracheobronchitis, hyper-IgE syndrome, lipoid and chronic eosinophilic pneumonia, and pulmonary alveolar proteinosis.\u003csup\u003e[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]\u003c/sup\u003e In such cases, bronchoscopy is recommended for further diagnostic evaluation (e.g., assessing an endobronchial lesion) or treatment (e.g., removal of a foreign body) \u003csup\u003e[\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eIn our case, the patient presented with a history of smoking and pill aspiration, with CT scan findings revealing a new, isolated mucoid impaction characterized by a finger-in-glove shaped opacity. This was discovered incidentally, with no known risk factors for its more common causes, such as ABPA and neoplasm. Similar cases have been reported in the past, where ABPA was discovered in patients with COPD who first exhibited bronchiectasis and mucoid impaction. Despite not having asthma or cystic fibrosis, the patient had chronic inflammation and reduced mucociliary clearance, which likely made it easier for Aspergillus to colonize. Radiologic signs such as central bronchiectasis and high-attenuation mucus were important diagnostic indicators, and bronchoscopy along with microbiological analysis confirmed the presence of Aspergillus \u003csup\u003e(9)\u003c/sup\u003e. These cases demonstrate how important it is to rule out ABPA as a potential cause of mucoid impaction in COPD patients. This will ensure timely diagnosis and appropriate corticosteroid and antifungal therapy to halt the disease's progression.\u003c/p\u003e \u003cp\u003eAdditionally, the evaluation of mucoid impaction is typically based on its presentation on CT images, including tubular branching, ovoid opacities, and other additional findings. High attenuation and branching are characteristic features of ABPA on CT scans, in contrast to the mucoid impaction associated with other disorders, where radiographically, lower-attenuation mucus fills the airways \u003csup\u003e[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]\u003c/sup\u003e. In this case, the patient presented with a history of pill aspiration and worsening cough, which is highly suggestive of the underlying cause of the impacted mucus discovered on the CT scan. In addition to ABPA, the differential diagnoses of highly-attenuated mucoid impaction include endobronchial lesions, inhalation of foreign bodies, bronchial atresia, and bronchiectasis due to any cause.\u003csup\u003e[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]\u003c/sup\u003e Therefore, it is essential to differentiate ABPA from other causes of mucoid impaction, because ABPA treatment requires the use of corticosteroids and antifungal agents, whereas other conditions may require different treatment approaches.\u003csup\u003e[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]\u003c/sup\u003e Thus, we considered bronchoscopy to evaluate thick mucus impaction to identify whether it was an aspirated pill or impacted mucus. Upon evaluation, it was discovered to be \u003cem\u003eAspergillus\u003c/em\u003e, which was later confirmed by laboratory findings.\u003c/p\u003e \u003cp\u003eABPA is a pulmonary disorder caused by hypersensitivity to \u003cem\u003eA. fumigatus\u003c/em\u003e that primarily complicates the course of asthma and CF. It is caused by host immune reactions against \u003cem\u003eA. fumigatus\u003c/em\u003e which colonizes the airways of patients with asthma and CF. In asthma and CF, impaired mucociliary clearance normally allows \u003cem\u003eAspergillus\u003c/em\u003e to germinate in the bronchial tree. However, defects in immunity can persist and lead to the activation of Th2 CD4\u0026thinsp;+\u0026thinsp;T-cells and cytokines, such as interleukin (IL)-5 (mediating eosinophilic airway inflammation) and IL-8 (mediating neutrophil chemotaxis). Instead of a Th1 CD4\u0026thinsp;+\u0026thinsp;T-cell response against \u003cem\u003eAspergillus\u003c/em\u003e, bronchial wall damage and mucus hypersecretion lead to \u003cem\u003eAspergillus\u003c/em\u003e infection in the bronchial tree [2, 6].\u003c/p\u003e \u003cp\u003eSimilarly, the underlying pathogenesis of COPD involves extensive exposure to noxious stimuli, increased oxidative stress (most commonly due to cigarette smoke), and increased release of reactive oxygen species by inflammatory cells. This activates CD8\u0026thinsp;+\u0026thinsp;T-cells and mediates inflammation, promoting goblet cell proliferation and hypertrophy, mucus hypersecretion, and ciliary function impairment, resulting in chronic cough. Therefore, the environment that facilitates \u003cem\u003eAspergillus\u003c/em\u003e growth and leads to ABPA in COPD appears to be similar to that of asthma. However, ABPA is infrequently diagnosed in the context of post-tuberculosis fibro-cavitary disease \u003csup\u003e[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]\u003c/sup\u003e. In this case, the patient had a history of COPD instead of asthma or CF, which may be considered the underlying cause of ABPA exacerbation. Thus, this case presented an atypical manifestation of ABPA within the spectrum of pulmonary disorders commonly encountered in the United States, suggesting the inclusion of ABPA in the list of differential diagnoses for patients with COPD. Although ABPA predominantly complicates asthma and cystic fibrosis, its occurrence in conjunction with COPD is rare.\u003c/p\u003e \u003cp\u003eFurthermore, evaluation of eosinophilia raises the possibility of an underlying hematological malignancy. The eosinophil count, however, was 10.6 upon admission. The following day, it decreased to 6.5, and before discharge, it decreased to 5.0, with the current levels being 1.4. However, the pattern of eosinophilia observed in this case, characterized by a gradual decrease in the eosinophil count over time, suggests a non-malignant etiology. Long-term myeloproliferative illnesses seem unlikely, given this pattern of eosinophilia.\u003c/p\u003e \u003cp\u003eOverall, this case underscores the importance of considering ABPA in the differential diagnosis of COPD patients presenting with mucoid impaction, the complexity of the patient\u0026rsquo;s medical history, including interstitial lung disease, bronchiectasis, COPD, and prior malignancy, posed challenges in diagnosing ABPA. The absence of asthma or cystic fibrosis, along with reactive eosinophilia, made symptom attribution difficult. This case underscores the need to consider ABPA in COPD patients with mucoid impaction and highlights the necessity for alternative diagnostic criteria in atypical cases. Concomitant conditions may influence disease progression and treatment response, though their exact role remains unclear.\u003c/p\u003e \u003cp\u003eFuture research should explore the pathophysiological mechanisms underlying ABPA in COPD without asthma, assess its prevalence in this population, and investigate the long-term impact on pulmonary function to improve diagnostic and therapeutic strategies.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor Contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eMaulik K. Lathiya, Bansi P. Savaliya contributed to the conceptualization, writing, original draft preparation, graphics, and reviewing; Charokopos Antonios and Cristian Madrid contributed to reviewing and editing. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConflicts of Interest\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData Available Statement\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNo, this manuscript does not have any research data outside the submitted manuscript file.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe thank Drew J. Persson and Zaug Paj Her from the University of Minnesota for editing a draft of this manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics approval\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study was approved by the ethics committee of Mayo Clinic. Written informed consent was obtained from the patient for the publication of this case report and any accompanying figure.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent to participate and consent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient for the publication of this case report and any accompanying figures.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eAgarwal, R., A.N. Aggarwal, and D. Gupta, High-attenuation mucus in allergic bronchopulmonary aspergillosis: another cause of diffuse high-attenuation pulmonary abnormality. AJR Am J Roentgenol, 2006. 186(3): p. 904. \u003c/li\u003e\n\u003cli\u003eAgarwal, R., et al., Developments in the diagnosis and treatment of allergic bronchopulmonary aspergillosis. Expert Rev Respir Med, 2016. 10(12): p. 1317-1334. \u003c/li\u003e\n\u003cli\u003eAsano, K., et al., New clinical diagnostic criteria for allergic bronchopulmonary aspergillosis/mycosis and its validation. J Allergy Clin Immunol, 2021. 147(4): p. 1261-1268.e5. \u003c/li\u003e\n\u003cli\u003eAgarwal R, Sehgal IS, Muthu V, et al. Revised ISHAM-ABPA working group clinical practice guidelines for diagnosing, classifying and treating allergic bronchopulmonary aspergillosis/mycoses. Eur Respir J. 2024;63(4):2400061. Published 2024 Apr 4. doi:10.1183/13993003.00061-2024\u003c/li\u003e\n\u003cli\u003ePanchabhai, T.S., et al., Plugs of the Air Passages: A Clinicopathologic Review. Chest, 2016. 150(5): p. 1141-1157. \u003c/li\u003e\n\u003cli\u003eMartinez, S., et al., Mucoid impactions: finger-in-glove sign and other CT and radiographic features. Radiographics, 2008. 28(5): p. 1369-82. \u003c/li\u003e\n\u003cli\u003eAgarwal, R., R. Srinivas, and S.K. Jindal, Allergic bronchopulmonary aspergillosis complicating chronic obstructive pulmonary disease. Mycoses, 2008. 51(1): p. 83-5.\u003c/li\u003e\n\u003cli\u003eSisodia, J. and Bajaj T. Allergic Bronchopulmonary Aspergillosis. [Updated 2023 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542329/\u003c/li\u003e\n\u003cli\u003eMir E, Shah A. Allergic bronchopulmonary aspergillosis in a patient with chronic obstructive pulmonary disease. Prim Care Respir J. 2012 Mar;21(1):111-4. doi: 10.4104/pcrj.2012.00001. PMID: 22222946; PMCID: PMC6547891.\u003c/li\u003e\n\u003cli\u003eAgarwal R, Sehgal IS, Muthu V, et al. Revised ISHAM-ABPA working group clinical practice guidelines for diagnosing, classifying and treating allergic bronchopulmonary aspergillosis/mycoses. Eur Respir J. 2024;63(4):2400061. Published 2024 Apr 4. doi:10.1183/13993003.00061-2024\u003c/li\u003e\n\u003c/ol\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":false,"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":"Allergic bronchopulmonary aspergillosis (ABPA), chronic obstructive pulmonary disease (COPD), aspergillus fumigatus, finger-in-glove sign","lastPublishedDoi":"10.21203/rs.3.rs-6115782/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6115782/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eBackground\u003c/p\u003e\n\u003cp\u003eAllergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity reaction to \u003cem\u003eAspergillus\u003c/em\u003especies, commonly observed in patients with asthma or cystic fibrosis. However, its occurrence in individuals with chronic obstructive pulmonary disease (COPD) is rare and not well-documented. Radiological findings such as the \"finger-in-glove\" sign on computed tomography (CT) scans can aid in diagnosis, but a high index of suspicion is required in atypical cases. ABPA can contribute to mucoid impaction, leading to progressive pulmonary dysfunction if left untreated.\u003c/p\u003e\n\u003cp\u003eCase Presentation\u003c/p\u003e\n\u003cp\u003eWe report a unique case of ABPA in a patient with COPD who had no prior history of asthma or cystic fibrosis. The patient presented with worsening respiratory symptoms, and imaging studies revealed mucoid impaction with the characteristic \"finger-in-glove\" sign. Laboratory findings included peripheral eosinophilia and elevated serum IgE, supporting the diagnosis of ABPA. Management involved antifungal therapy and corticosteroids, followed by a tapering regimen, with prophylactic treatment for pneumocystis pneumonia (PCP) to prevent opportunistic infections. Follow-up pulmonary function tests demonstrated a moderate decline in diffusion capacity, necessitating continued monitoring for potential early interstitial lung disease (ILD) or pulmonary hypertension.\u003c/p\u003e\n\u003cp\u003eConclusions\u003c/p\u003e\n\u003cp\u003eThis case highlights the importance of considering ABPA in patients with COPD who present with mucoid impaction, even in the absence of traditional risk factors. A thorough differential diagnosis of eosinophilia in pulmonary disease is crucial to distinguish between hypersensitivity reactions and malignant myeloproliferative\u003c/p\u003e\n\u003cp\u003edisorders, ensuring appropriate treatment strategies. Clinicians should maintain a high level of awareness for ABPA in COPD patients to facilitate timely diagnosis and management.\u003c/p\u003e","manuscriptTitle":"Finger-in-Glove Appearance of Allergic Bronchopulmonary Aspergillosis in a Chronic Obstructive Pulmonary Disease Patient Without Asthma or Cystic Fibrosis: A Case Report and Literature Review","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-04-21 08:32:46","doi":"10.21203/rs.3.rs-6115782/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":"e0d76b34-4adb-463e-b6ec-738a8bbe776f","owner":[],"postedDate":"April 21st, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-02-18T08:56:56+00:00","versionOfRecord":[],"versionCreatedAt":"2025-04-21 08:32:46","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-6115782","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6115782","identity":"rs-6115782","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}