Diagnosis and management of acute eosinophilic pneumonia masquerading as malignancy and community-acquired pneumonia in an elderly male: a case report

Introduction

Acute eosinophilic pneumonia (AEP) is an acute inflammatory lung disorder characterized by fever, diffuse pulmonary infiltrates, hypoxemia, and a prominent increase in eosinophils in bronchoalveolar lavage fluid (BALF) or lung tissue (1,2). AEP is a rare entity with an estimated incidence of approximately 9.1 cases per 100,000 persons (3), affecting predominantly adults. Although its etiology is frequently idiopathic, it may also be drug-induced or associated with various environmental exposures, including cigarette smoking, dust inhalation, mold exposure, and humid environments, with the exposure duration ranging from hours to several weeks prior to symptom onset (4). Its clinical manifestations, such as fever, cough, and dyspnea, often overlap with those of community-acquired pneumonia (CAP), leading to frequent misdiagnosis and unnecessary antibiotic use.

The diagnostic challenge is compounded in elderly patients, who frequently have multiple comorbidities that can obscure the clinical picture. Furthermore, the radiographic presentation of AEP, which can include lymphadenopathy and pleural effusions, may mimic lymphoma or metastatic diseases, prompting extensive and invasive oncological workups. We report a case of a 75-year-old male with multiple comorbidities whose AEP presented a profound diagnostic challenge, initially masquerading as both CAP and lung malignancy. This case highlights the critical importance of considering AEP in the differential diagnosis of atypical pneumonias, the utility of a multidisciplinary team (MDT) in complex cases, and the need for timely intervention with corticosteroids. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-356/rc).

Case presentation

A 75-year-old male was admitted to the respiratory department with a fortnight history (approximately 2 weeks) of intermittent fever, profuse sweating, fatigue, and dry cough without sputum production. One day before symptom onset, he had taken a prolonged hot bath in a humid bathroom environment, representing a potential environmental exposure trigger. Before admission, he underwent routine blood tests at a local hospital, which revealed elevated white blood cell count and C-reactive protein (CRP) level, and he had received antipyretic and anti-infective treatments. He denied subjective dyspnea; however, he reported reduced exercise tolerance. His past medical history included hypertension, type 2 diabetes mellitus, and a recent cerebral infarction with residual right-hand weakness.

On admission, his vital signs were: temperature 38.2 ℃, blood pressure 138/82 mmHg, heart rate 92 beats/min, respiratory rate 22 breaths/min, and oxygen saturation of 90% measured by pulse oximetry on room air. Supplemental oxygen at 2 L/min via nasal cannula was initiated. Arterial blood gas analysis performed while receiving oxygen at 2 L/min revealed a PaO₂ of 75 mmHg, corresponding to an oxygenation index of approximately 258, indicating mild type I hypoxemic respiratory failure. Physical examination showed no evidence of severe tachypnea, respiratory distress, rash, or peripheral lymphadenopathy. He was treated with cefoperazone-sulbactam (2 g every 8 hours) and moxifloxacin (0.4 g once daily) for CAP. Laboratory findings revealed leukocytosis [16.37×10⁹/L; reference range, (3.5–9.5)×10⁹/L] with marked eosinophilia [6.53×10⁹/L, 39.9%; reference range, (0.02–0.52)×10⁹/L]. Inflammatory markers were elevated, including CRP 67.15 mg/L (reference <10 mg/L) and interleukin-6 (IL-6) 46.70 pg/mL (reference <7 pg/mL). Total immunoglobulin E (IgE) was 886.80 IU/mL (reference <100 IU/mL). Hemoglobin A1c (HbA1c) was 8.2% (reference range, 4.0–6.0%). A chest contrast-enhanced computed tomography (CECT) scan revealed bilateral pulmonary infiltrates, pleural effusions, and enlarged mediastinal lymph nodes (Figure 1), raising strong suspicion for malignancy. Nasopharyngeal swab was positive for Klebsiella pneumoniae and Streptococcus pneumoniae, but blood and BALF microbial cultures and targeted next generation sequencing tests were negative. Bronchoalveolar lavage (BAL) fluid analysis demonstrated 40% eosinophils. Following MDT consultation, AEP was highly suspected. Prior to pathological confirmation, empirical intravenous methylprednisolone (40 mg/day) was initiated immediately after MDT consultation, given a high clinical suspicion of AEP, while cefoperazone-sulbactam (2 g every 8 hours) and moxifloxacin (0.4 g once daily) were continued. Subsequently, CT-guided percutaneous lung biopsy was performed. Histopathology showed interstitial fibrous tissue hyperplasia with scattered eosinophilic infiltration and no evidence of malignancy (Figure 2), confirming the diagnosis of AEP. Of note, the biopsy was obtained on day 24 after symptom onset, following antibiotic and corticosteroid treatment, which may account for the absence of typical diffuse alveolar damage. After discharge, the patient continued to receive oral prednisone therapy at an initial dose of 25 mg daily, with a sequential reduction of 5 mg per week, and the treatment was discontinued after 1 month of administration. The clinical symptoms and radiological findings improved rapidly; chest CT (Figure 3) demonstrated marked resolution of pulmonary infiltrates and pleural effusion, and the peripheral blood eosinophil count normalized to 0.24×10⁹/L. No recurrence was observed during the 3-month follow-up period. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was reviewed and approved by the Ethics Review Board of The First Affiliated Hospital of Henan Medical University (approval No. EC-025-324). Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Figure 1 Axial chest CECT demonstrates diffuse bilateral pulmonary infiltrates (curved arrow), peripheral parenchymal consolidation (thick solid arrow), prominent mediastinal lymphadenopathy (thin sharp arrow), right hilar mass, and right pleural effusion. (A-C) Lung window images, and (D-F) mediastinal window images. CECT, contrast-enhanced computed tomography.

Figure 2 The pathological manifestations of transbronchial lung biopsy specimens (hematoxylin and eosin stain) show that eosinophilic infiltration is indicated by black arrows.

Figure 3 Follow-up axial chest CT scans at the same level demonstrated marked resolution of pulmonary infiltrates, consolidated lesions (thick solid arrow), mediastinal lymphadenopathy (thin sharp arrow), and pleural effusion. (A-C) Lung windows view and (D-F) mediastinal windows view. CT, computed tomography.

Discussion

This case illustrates three critical challenges in diagnosing AEP in the elderly: (I) the absence of classic symptoms like dyspnea; (II) the presence of comorbidities that steer the diagnostic focus toward CAP; and (III) a radiographic presentation that convincingly mimics malignancy (3).

The patient had a normal eosinophil count before admission, followed by a significant increase in peripheral blood eosinophils after admission, which was consistent with the temporal evolution of AEP (5). However, this important clue was not initially appreciated due to his advanced age and multiple comorbidities.

The definitive diagnosis of AEP requires marked eosinophilic infiltration in BALF or peripheral blood, characteristic radiological findings, and exclusion of alternative diagnoses. In this case, BALF eosinophils accounted for 40%, and the peripheral eosinophil count reached 6.53×10⁹/L, fulfilling key laboratory criteria for AEP (3).

However, the initial imaging presentation, characterized by bilateral pulmonary infiltrates. Although prominent mediastinal lymphadenopathy raised suspicion for malignancy, lymph node enlargement has been reported in AEP, particularly in subacute or elderly cases (6). The nodes were discrete and homogeneously enhancing, and biopsy ruled out malignancy and vasculitis. This diagnostic dilemma is not uncommon, as the typical radiological features of AEP, including diffuse ground-glass opacities, interlobular septal thickening, and pleural effusions, exhibit significant overlap with conditions such as organizing pneumonia, lymphoma, and pulmonary malignancies (7). This prompted a necessary but extensive oncological workup. Our experience aligns with literature suggesting that while lymphadenopathy is reported in AEP, its prominence can be misleading. Unlike lung malignancy, which typically demonstrates an insidious onset and progressive clinical course, AEP is characterized by an acute or subacute presentation and a rapid, often dramatic response to corticosteroid therapy. Recognizing this distinction is essential, as early identification of AEP can prevent unnecessary invasive oncological investigations and delays in appropriate treatment. The MDT consultation was instrumental in this scenario, allowing radiologists to point out features less typical of malignancy (e.g., discrete, homogeneously enhancing nodes) and guiding the decision to pursue a tissue diagnosis via CT-guided biopsy rather than more invasive surgical mediastinal staging. The biopsy provided the definitive evidence required to rule out cancer and confirm AEP, underscoring its value in complex and atypical presentations (7,8).

The patient showed a dramatic response to corticosteroids, which is a hallmark of AEP. A stepwise tapering regimen was implemented, and no relapse occurred during follow-up, which contrasts with the high relapse rate typically observed in CEP. The management of steroid therapy in an elderly diabetic patient requires careful balancing. We opted for a moderate dose (40 mg/day methylprednisolone) with close glycemic monitoring, which proved effective and safe. This approach facilitated a successful outcome without precipitating adverse metabolic events.

Conclusions

AEP should be considered in elderly patients presenting with acute or subacute febrile respiratory illness and pulmonary infiltrates, even when imaging mimics malignancy. Prominent lymphadenopathy should not exclude AEP, and a multidisciplinary approach with lung biopsy may be essential for definitive diagnosis.

Acknowledgments

The authors thank the interventional pulmonology team and respiratory endoscopy nursing staff at The First Affiliated Hospital of Henan Medical University for their expert clinical support and assistance during patient management and bronchoscopic procedures.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-356/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-356/prf

Funding: This work was supported by the Higher Education Research Project of Henan Higher Education Society (No. 2025SXHLX110).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-356/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was reviewed and approved by the Ethics Review Board of The First Affiliated Hospital of Henan Medical University (approval No. EC-025-324). Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. De Giacomi F, Vassallo R, Yi ES, et al. Acute Eosinophilic Pneumonia. Causes, Diagnosis, and Management. Am J Respir Crit Care Med 2018;197:728-36. [Crossref] [PubMed]
2. Carbone RG, Puppo F, Mattar E, et al. Acute and chronic eosinophilic pneumonia: an overview. Front Med (Lausanne) 2024;11:1355247. [Crossref] [PubMed]
3. Suzuki Y, Suda T. Eosinophilic pneumonia: A review of the previous literature, causes, diagnosis, and management. Allergol Int 2019;68:413-9. [Crossref] [PubMed]
4. Akaba T, Kimura Y, Kondo M, et al. Clinical characteristics and outcomes of acute eosinophilic pneumonia: A nationwide descriptive study. World Allergy Organ J 2025;18:101139. [Crossref] [PubMed]
5. Jhun BW, Kim SJ, Kim K, et al. Clinical implications of initial peripheral eosinophilia in acute eosinophilic pneumonia. Respirology 2014;19:1059-65. [Crossref] [PubMed]
6. Price M, Gilman MD, Carter BW, et al. Imaging of Eosinophilic Lung Diseases. Radiol Clin North Am 2016;54:1151-64. [Crossref] [PubMed]
7. Cottin V. Eosinophilic Lung Diseases. Immunol Allergy Clin North Am 2023;43:289-322. [Crossref] [PubMed]
8. Ren HQ, Zhao Q, Jiang J, et al. Acute Eosinophilic Pneumonia Masquerading as a Lung Abscess. Clin Lab 2023;69. [Crossref] [PubMed]