Eosinophilic Pneumonia

Table of Contents

  1. Overview
  2. Epidemiology
  3. Pathophysiology
  4. Acute Eosinophilic Pneumonia (AEP)
  5. Chronic Eosinophilic Pneumonia (CEP)
  6. Other Eosinophilic Pulmonary Syndromes
  7. Diagnosis
  8. Treatment
  9. Prognosis and Monitoring
  10. Recent Research
  11. Research Papers (PubMed Searches)
  12. Connections
  13. Featured Videos

1. Overview

Eosinophilic pneumonias are a heterogeneous group of lung diseases characterized by eosinophilic infiltration of the alveoli and/or pulmonary interstitium, often with peripheral blood eosinophilia. They range from mild self-limited syndromes to life-threatening respiratory failure. The unifying feature is an eosinophilic predominance on bronchoalveolar lavage (BAL) (>25% eosinophils) or lung tissue, combined with pulmonary infiltrates.

Causes span a broad spectrum: idiopathic (cryptogenic) forms, drug reactions, toxin and occupational exposures, parasitic infections, and underlying systemic eosinophilic disorders such as eosinophilic granulomatosis with polyangiitis (EGPA, formerly Churg-Strauss syndrome). The two major idiopathic forms are acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP), which differ dramatically in onset, clinical features, triggers, and relapse patterns.

Recognition of eosinophilic pneumonia is clinically important because the treatment — systemic corticosteroids — produces one of the most dramatic and rapid responses in all of pulmonary medicine. Conversely, failure to diagnose the condition and substitute antibiotics leads to rapid deterioration that can be fatal. Identifying and removing the causative trigger (e.g., a newly started medication, cigarette smoking, or parasitic infection) is equally essential to prevent recurrence.

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2. Epidemiology

Eosinophilic pneumonia is uncommon overall, though the specific syndromes vary considerably in their demographic patterns and geographic distribution.

Acute Eosinophilic Pneumonia (AEP) has an estimated incidence of fewer than 1 per 100,000 per year. It predominantly affects young adults, with a mean age of 29–35 years across published case series. A male predominance of 60–70% is consistently reported, a pattern likely related to higher rates of tobacco exposure and occupational dust exposures in men. Military personnel — deployed to desert environments with intense dust exposure — are overrepresented in AEP case series from the United States and other countries.

Chronic Eosinophilic Pneumonia (CEP / Carrington's Disease) affects a slightly older population, with a mean age at diagnosis of 40–50 years. In contrast to AEP, CEP shows a strong female predominance (approximately 2:1 female-to-male ratio) and is strongly associated with pre-existing atopic disease — asthma is present in 50–60% of CEP patients at the time of diagnosis, and allergic rhinitis or nasal polyposis is frequently reported. CEP is more common in non-smokers.

Löffler's Syndrome (Simple Pulmonary Eosinophilia): Prevalence tracks closely with the global burden of intestinal helminth infections. It is common in tropical and subtropical regions with endemic Ascaris lumbricoides, hookworm species, and Strongyloides stercoralis. In high-income countries, it is typically encountered in recent immigrants, international travelers, and immunocompromised patients.

Tropical Pulmonary Eosinophilia (TPE) is seen predominantly in the Indian subcontinent, Southeast Asia, and parts of Africa and South America, among individuals with filarial nematode infection (Wuchereria bancrofti, Brugia malayi). It is rare in non-endemic countries except among diaspora populations.

Drug-Induced Eosinophilic Pneumonia mirrors the prescription patterns of implicated drugs; it has risen with expanded use of daptomycin, biologics, and checkpoint inhibitor immunotherapy.

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3. Pathophysiology

The central mechanism uniting all eosinophilic pneumonias is the abnormal accumulation and activation of eosinophils within the lung parenchyma, driven by dysregulated type 2 (Th2/innate lymphoid cell type 2) immune signaling.

Eosinophil Recruitment: Activated T helper 2 (Th2) lymphocytes, mast cells, and innate lymphoid cells type 2 (ILC2) produce IL-5, IL-3, and GM-CSF — cytokines that promote eosinophil maturation in the bone marrow, prolong survival in the circulation, and activate eosinophil effector function. Eotaxins (CCL11/eotaxin-1, CCL24/eotaxin-2, CCL26/eotaxin-3) act on CCR3 receptors on eosinophil surfaces to drive selective tissue migration into the lung interstitium and alveolar spaces.

Eosinophil-Mediated Tissue Damage: Once in the alveoli, eosinophils release toxic granule proteins that cause direct tissue injury:

These proteins impair surfactant function, increase alveolar permeability, and amplify the local inflammatory cascade by recruiting additional inflammatory cells.

AEP-Specific Mechanism: In acute eosinophilic pneumonia, the trigger is typically a novel inhaled irritant — most classically cigarette smoke in a tobacco-naive individual (new smoker or someone resuming smoking after prolonged abstinence). This first-encounter exposure activates alveolar macrophages and ILC2 in a tobacco-naive lung, triggering an exaggerated innate eosinophilic response. A critical distinguishing feature: peripheral blood eosinophilia is often absent early in AEP because eosinophils are rapidly consumed in the inflamed lung. The response does not recur with continued tobacco exposure, consistent with a first-encounter immune mechanism that desensitizes.

CEP-Specific Mechanism: Chronic eosinophilic pneumonia involves a sustained Th2-dominant immune response with persistent IL-5 production maintaining both alveolar eosinophilia and peripheral blood eosinophilia simultaneously. The trigger is often idiopathic or linked to an atopic predisposition; the chronicity reflects a failure to resolve the eosinophilic inflammation rather than a one-time trigger event.

Corticosteroid Mechanism of Action: Glucocorticoids act at multiple points in this cascade — they suppress IL-5, GM-CSF, and eotaxin production; promote eosinophil apoptosis; and reduce vascular permeability. This multi-targeted action explains the dramatic and rapid clinical improvement characteristically seen within 24–48 hours of initiating steroids in both AEP and CEP.

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4. Acute Eosinophilic Pneumonia (AEP)

Acute eosinophilic pneumonia is a rapidly progressive inflammatory lung disease characterized by fulminant onset (symptoms develop over hours to days, by definition less than one month) with fever, dyspnea, hypoxemia, and bilateral pulmonary infiltrates. It closely mimics severe community-acquired pneumonia or ARDS, and this mimicry is the primary source of diagnostic delay and patient harm. The defining difference: antibiotics fail, the patient deteriorates, and bronchoalveolar lavage reveals striking eosinophilia.

Clinical Presentation of AEP

Triggers of AEP

An identifiable trigger is found in 50–70% of cases:

Laboratory and Imaging Findings in AEP

Peripheral blood eosinophilia is typically ABSENT or only mildly elevated in early AEP — this is a critically important distinguishing feature. Eosinophils are sequestered in the lung and consumed locally. Peripheral eosinophilia (>500/µL) may develop later during the illness or during recovery. Leukocytosis (neutrophil-predominant) is typically present. CRP and ESR are elevated. Blood cultures are negative.

Chest CT findings: Bilateral symmetric ground-glass opacities throughout all lung zones (not preferentially peripheral or upper-lobe); interlobular septal thickening ("crazy-paving" pattern); bilateral pleural effusions in 80–90% (a feature that distinguishes AEP from ARDS, where pleural effusions are less prominent); areas of consolidation superimposed on ground glass; no lymphadenopathy.

BAL: Eosinophils >25% of BAL differential — diagnostic cornerstone. In AEP, BAL eosinophilia is often >40% and may exceed 80%. BAL also allows cultures and special stains to exclude infection.

Distinguishing AEP from ARDS and Pneumonia

Treatment of AEP

Systemic corticosteroids: IV methylprednisolone 1–2 mg/kg/day (divided q8–12h) for mechanically ventilated or severely hypoxemic patients. Oral prednisone 40–60 mg/day for patients who are less severely ill. Response is typically dramatic — most patients are afebrile and breathing more easily within 24–48 hours. The radiological abnormalities clear over 1–4 weeks. Total steroid course: 2–4 weeks with taper. Unlike CEP, AEP does not recur after trigger removal, so a short course is appropriate — prolonged maintenance therapy is not needed.

Trigger removal: Smoking cessation is essential and mandatory. If a drug is implicated, stop it immediately. Rechallenge with daptomycin or other confirmed causative agents is absolutely contraindicated.

Supportive care: Supplemental oxygen titrated to maintain SpO₂ >92%; high-flow nasal cannula oxygen or non-invasive ventilation for moderate hypoxemia; mechanical ventilation with lung-protective strategy (low tidal volume 6 mL/kg IBW) for ARDS-level disease; prone positioning if PaO₂/FiO₂ <150 on conventional ventilation.

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5. Chronic Eosinophilic Pneumonia (CEP / Carrington's Disease)

Chronic eosinophilic pneumonia was first described by Carrington and colleagues in 1969 as a distinctive syndrome of subacute-to-chronic pulmonary eosinophilia with a characteristic radiographic "photographic negative of pulmonary edema" pattern. CEP has a subacute onset over weeks to months — dramatically different from AEP's rapid progression over days.

Clinical Presentation of CEP

Constitutional symptoms are often prominent and may dominate the clinical picture initially, leading to misdiagnosis as malignancy or chronic infection:

Up to 80% of CEP patients have asthma, and asthma may appear or substantially worsen after the onset of CEP — eosinophilic inflammation extends into the airway as well as the alveolar compartment. Allergic rhinitis and nasal polyposis are frequently co-present (the "eosinophilic triad" of asthma + nasal polyposis + eosinophilic pneumonia).

Laboratory and Imaging Findings in CEP

Peripheral blood eosinophilia is consistently elevated in CEP — this is the major contrast with AEP. Absolute eosinophil count is typically >1500/µL (clinically significant hypereosinophilia); values >3000/µL are common in severe cases. Serum IgE is frequently elevated (reflecting atopic background). ESR and CRP are elevated, sometimes markedly. Serum LDH may be elevated. CBC may show mild normocytic anemia of chronic inflammation.

CT chest (HRCT): The classic pattern is peripheral upper-lobe consolidation — bilateral patchy airspace consolidation preferentially occupying the outer third (subpleural) of the upper lobe zones. This is the "photographic negative of pulmonary edema" (pulmonary edema is central and perihilar; CEP consolidation is peripheral and upper). Ground-glass opacities accompany areas of consolidation. Pleural effusions are less common than in AEP. The peripheral upper-lobe predominance, while characteristic, is not universally present (lower lobe involvement occurs). Radiological findings may migrate between assessments ("fleeting infiltrates") and this migratory quality is itself a diagnostic clue.

Diagnosis of CEP

Diagnosis requires: (1) subacute pulmonary symptoms with constitutional features; (2) peripheral blood eosinophilia; (3) characteristic CT pattern; (4) BAL eosinophilia >25%; (5) exclusion of secondary causes (drugs, parasites, EGPA). Lung biopsy shows intra-alveolar eosinophils, eosinophilic microabscesses, and fibrin; organizing pneumonia (Masson bodies) may co-exist.

Treatment of CEP

Oral prednisone 0.5–1 mg/kg/day (typical starting dose 40–60 mg/day). The clinical response is dramatic — fever and constitutional symptoms typically resolve within 24–72 hours; radiological clearing occurs over 1–4 weeks. However, CEP carries a 50–80% relapse rate upon steroid tapering, far higher than AEP. A slow taper is essential:

If relapse occurs during taper, reinitiate at the last effective dose. Recurrent relapses despite appropriate tapering are the primary indication for steroid-sparing therapy.

Mepolizumab (anti-IL-5 monoclonal antibody): The landmark ECLECTIC randomized controlled trial (Cottin et al., 2023, Lancet Respir Med) demonstrated that mepolizumab 300 mg SC monthly versus placebo significantly reduced relapse rate, allowed OCS tapering, and maintained remission in CEP. This is the first approved steroid-sparing biologic with RCT evidence specifically in CEP. Mepolizumab is the preferred option for OCS-dependent or frequently relapsing disease.

Concurrent asthma management: Patients with CEP and underlying eosinophilic asthma should receive inhaled corticosteroids + long-acting beta agonist (ICS/LABA). Anti-IL-5 biologics approved for severe eosinophilic asthma (mepolizumab 100 mg SC q4w, reslizumab IV, benralizumab SC) may address both conditions simultaneously.

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6. Other Eosinophilic Pulmonary Syndromes

Löffler's Syndrome (Simple Pulmonary Eosinophilia)

Löffler's syndrome describes transient migratory pulmonary infiltrates plus peripheral blood eosinophilia caused by larval migration through the lungs during helminth infection — Löffler's lung is literally the lung through which nematode larvae transit. The organisms most commonly responsible include:

Mechanism: Larvae ingested in food or soil penetrate the gut mucosa → enter mesenteric venules → travel via portal circulation to the liver → right heart → pulmonary capillaries → migrate through alveolar walls into airways → ascend the tracheobronchial tree → are swallowed and mature in the gut. This larval transit (Löffler's migration) triggers a transient eosinophilic alveolitis at each site of larval penetration.

Symptoms: Mild dry cough, wheeze, low-grade fever, and urticaria; typically self-limited within 2–4 weeks as the larval migration ceases. Chest radiograph shows bilateral fleeting ground-glass or consolidative opacities that shift between serial films.

Treatment: Anthelmintic therapy (albendazole 400 mg × 3 days for Ascaris/Toxocara; ivermectin 200 µg/kg × 2 days for Strongyloides). Corticosteroids are rarely needed except in severe symptomatic cases. Strongyloides requires special attention in immunocompromised patients — glucocorticoids given before anthelmintic therapy can trigger the devastating Strongyloides hyperinfection syndrome.

Tropical Pulmonary Eosinophilia (TPE)

Tropical pulmonary eosinophilia is a hypersensitivity reaction to microfilariae of Wuchereria bancrofti or Brugia malayi (lymphatic filarial nematodes) trapped within the pulmonary capillaries. It occurs predominantly in the Indian subcontinent, Southeast Asia, and parts of Africa and South America.

Distinctive clinical features:

Treatment: Diethylcarbamazine (DEC) 6 mg/kg/day in three divided doses × 21 days is the treatment of choice. Response is generally good, but recurrence after a single course occurs in up to 20–30% of patients; re-treatment is effective. Critical long-term risk: Untreated or recurrent TPE leads to progressive pulmonary fibrosis and chronic restrictive lung disease from ongoing immune-mediated damage — early treatment is essential to prevent irreversible fibrosis.

Eosinophilic Granulomatosis with Polyangiitis (EGPA / Churg-Strauss Syndrome)

EGPA is a systemic small-vessel vasculitis defined by: (1) history of asthma (virtually universal); (2) peripheral and tissue eosinophilia; (3) small vessel granulomatous vasculitis affecting multiple organ systems. Pulmonary eosinophilia is a major feature, but the systemic vasculitic component distinguishes EGPA from the primary eosinophilic pneumonias. Key features distinguishing EGPA from CEP:

Drug-Induced Eosinophilic Pneumonia

Numerous medications cause pulmonary eosinophilia through delayed-type hypersensitivity mechanisms, occurring days to weeks after drug initiation. The clinical presentation may mimic AEP (acute) or CEP (chronic), depending on the drug and the host's immune response. High-risk drugs include:

Evaluation requires a comprehensive medication review including over-the-counter drugs, supplements, herbal products, and recently started or changed drugs. Any temporal association warrants drug holiday. Drug-induced eosinophilic pneumonia: discontinue the offending drug + corticosteroids for moderate-to-severe cases; recurrence on rechallenge is common.

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7. Diagnosis

Diagnosis requires integrating clinical context, imaging, laboratory findings, and bronchoalveolar lavage or lung biopsy. The approach varies depending on whether AEP, CEP, or a secondary/drug-induced form is suspected.

Laboratory Evaluation

CT Chest (HRCT)

HRCT is more sensitive than plain radiograph and should be performed in all suspected cases. Key patterns:

Bronchoalveolar Lavage (BAL)

BAL is the cornerstone of diagnosis — particularly critical for AEP where peripheral eosinophilia is absent. Eosinophils >25% of BAL differential confirms eosinophilic pneumonia in appropriate clinical context. Values >40% are strongly suggestive; AEP BAL eosinophilia may exceed 80%. BAL also allows cultures, special stains (PCP, fungi), and cytology. Lymphocytosis on BAL favors hypersensitivity pneumonitis; neutrophilia favors infection or ARDS. A predominantly eosinophilic BAL with negative cultures effectively excludes infectious pneumonia as the primary etiology.

Lung Biopsy

Transbronchial biopsy or video-assisted thoracoscopic surgical (VATS) lung biopsy when BAL is nondiagnostic or the presentation is atypical. Histology in primary eosinophilic pneumonia shows intra-alveolar eosinophils, fibrin, eosinophilic microabscesses, and alveolar macrophages. Granulomatous vasculitis on biopsy favors EGPA. Masson bodies (organizing pneumonia plugs) may co-exist with eosinophilic infiltration.

Drug and Parasite Review

A meticulous medication history — including all OTC medications, supplements, herbal products, and recently initiated or changed prescription drugs — is essential in every case. Any drug started within 2–3 months of symptom onset that carries a known association with eosinophilic pneumonia warrants drug holiday as both diagnostic and therapeutic intervention. Parasite workup should be performed in all patients with peripheral eosinophilia and pulmonary infiltrates who have any relevant risk factors: tropical travel, immigration from endemic regions, rural exposures, soil contact, or raw fish/meat consumption.

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8. Treatment

Corticosteroids — Cornerstone of Therapy

Systemic glucocorticoids are the primary treatment for both AEP and CEP, producing one of the most dramatic and rapid responses in pulmonary medicine.

AEP — Acute Course:

CEP — Prolonged Course with Careful Taper:

Mepolizumab for Corticosteroid-Dependent CEP

Mepolizumab (anti-IL-5 monoclonal antibody, 300 mg SC monthly) is the first biologic with RCT evidence in CEP (ECLECTIC trial, 2023). It significantly reduces relapse rate and oral corticosteroid (OCS) burden. Mepolizumab is indicated for OCS-dependent CEP or patients with frequent relapses (2 or more per year). It is the preferred option for CEP concurrent with severe eosinophilic asthma — addressing both conditions with a single biologic agent. The dose used in CEP (300 mg) is higher than the asthma indication (100 mg), reflecting the higher IL-5 burden in parenchymal disease.

Trigger Removal and Parasite Treatment

Asthma Co-Management in CEP

CEP patients with concurrent asthma require targeted asthma therapy alongside CEP treatment. Step-up ICS/LABA (e.g., fluticasone/salmeterol or budesonide/formoterol); add montelukast for eosinophilic asthma; consider anti-IL-5 biologics (mepolizumab, reslizumab, benralizumab) for severe eosinophilic asthma (these agents are approved for asthma and may simultaneously benefit the CEP component). Systemic OCS used for CEP will suppress asthma inflammation as well; taper should monitor both conditions.

Supportive and Preventive Care

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9. Prognosis and Monitoring

AEP Prognosis

Prognosis for AEP is excellent with appropriate therapy. Near-universal recovery with corticosteroid treatment. Fever resolves within 24–48 hours; hypoxemia improves rapidly; patients on mechanical ventilation are typically extubated within days. Radiological abnormalities clear over 1–4 weeks. Long-term pulmonary function tests (spirometry and DLCO) return to normal in the vast majority. Crucially, AEP does not recur after the causative trigger is identified and permanently removed. There are no long-term sequelae in patients who recover fully.

CEP Prognosis

Overall life expectancy in CEP is not significantly shortened, but morbidity is substantial. Relapse rate on steroid tapering is 50–80%, making CEP a chronic management challenge. With appropriate long-term therapy, most patients achieve sustained remission. CEP rarely — if ever — progresses to irreversible pulmonary fibrosis (a major contrast to idiopathic pulmonary fibrosis), though radiological changes become more persistent in longstanding undertreated disease. Quality of life may be impacted by chronic low-dose steroid side effects, particularly in patients requiring indefinite therapy. Introduction of mepolizumab has improved steroid-sparing outcomes substantially.

Tropical Pulmonary Eosinophilia Prognosis

Excellent if treated early with DEC. Significant risk of progressive pulmonary fibrosis and chronic restrictive lung disease if untreated or if recurrent episodes are inadequately managed. DEC produces microfilaricidal effect but does not eliminate the adult worms; relapse is possible if reinfection occurs in endemic areas.

Monitoring Approach

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10. Recent Research

ECLECTIC Trial — Mepolizumab in CEP (2023)

The ECLECTIC randomized controlled trial (Cottin et al., Lancet Respir Med, 2023) established mepolizumab 300 mg SC monthly as the first biologic with RCT evidence in chronic eosinophilic pneumonia. The trial demonstrated significant reduction in relapse rate, sustained remission without oral corticosteroids, and meaningful reduction in OCS dose in the mepolizumab arm versus placebo. This trial represents a paradigm shift in CEP management for OCS-dependent or relapsing patients, providing a steroid-sparing option and defining a new standard of care.

Benralizumab in Eosinophilic Lung Disease

Benralizumab (anti-IL-5Rα monoclonal antibody, binds IL-5 receptor directly rather than the cytokine) depletes eosinophils via antibody-dependent cellular cytotoxicity (ADCC) — a mechanism distinct from mepolizumab (ligand blockade). Clinical trials in severe eosinophilic asthma have demonstrated near-complete blood eosinophil depletion. Its role in CEP specifically is under investigation, but its asthma data suggest potential benefit in CEP-asthma overlap, where both conditions are driven by IL-5 signaling.

AEP, Smoking Debut, and ILC2 Activation

Multiple recent case series and translational studies have refined understanding of AEP pathogenesis in relation to smoking. The "debut smoking" pattern — first-ever tobacco exposure or resumption after prolonged abstinence — is the prototypical trigger. The proposed mechanism involves activation of alveolar innate lymphoid cells type 2 (ILC2) and alveolar macrophages in a tobacco-naive lung by novel tobacco antigens, triggering an exaggerated first-encounter innate eosinophilic response. This response is IL-33 and TSLP driven (epithelial "alarm cytokines" released in response to novel irritant), recruiting ILC2s that rapidly produce IL-5 and IL-13 independent of adaptive immune memory. The response does not recur with continued tobacco exposure — suggesting desensitization of the ILC2 first-encounter circuit — which explains why AEP is distinctively a disease of smoking debut rather than chronic smokers.

EVALI vs. AEP — Distinguishing Vaping-Associated Lung Injury

The outbreak of E-cigarette or Vaping-Associated Lung Injury (EVALI) beginning in 2019 raised important questions about overlap with AEP. Both conditions cause acute febrile respiratory failure with bilateral ground-glass opacities and BAL eosinophilia in some patients. Key distinguishing features: EVALI is predominantly associated with vitamin E acetate (an oil used in THC-containing vaping products); EVALI BAL shows lipid-laden macrophages (oil-red-O staining); EVALI eosinophilia is mild and inconsistent. True AEP related to conventional tobacco products shows more prominent BAL eosinophilia (>25%). Shared treatment: corticosteroids are effective for both. The EVALI outbreak has largely abated with removal of vitamin E acetate from licensed products.

Dupilumab and Tezepelumab in Eosinophilic Lung Disease

Emerging data on dupilumab (anti-IL-4Rα, blocking both IL-4 and IL-13 signaling) in hypereosinophilic syndrome and eosinophilic asthma suggest potential relevance for CEP, particularly in patients with concurrent type 2 skin or nasal disease (atopic dermatitis, chronic rhinosinusitis with nasal polyps). Tezepelumab (anti-TSLP) targets an upstream innate cytokine driving ILC2 activation — potentially relevant for AEP prevention in at-risk populations. Trials in primary eosinophilic pneumonia are ongoing.

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11. Research Papers

The following PubMed searches retrieve current literature on eosinophilic pneumonia diagnosis, treatment, and mechanisms:

  1. Eosinophilic pneumonia
  2. Acute eosinophilic pneumonia AEP
  3. Chronic eosinophilic pneumonia CEP
  4. Eosinophilic pneumonia corticosteroid treatment
  5. Löffler syndrome pulmonary eosinophilia
  6. Tropical pulmonary eosinophilia filariasis
  7. Eosinophilic pneumonia BAL bronchoalveolar lavage
  8. Eosinophilic pneumonia smoking trigger
  9. Mepolizumab eosinophilic pneumonia
  10. Drug-induced eosinophilic pneumonia
  11. Eosinophilic pneumonia daptomycin
  12. Eosinophilic pneumonia IL-5

Key Citations

  1. Cottin V, Cordier JF. Eosinophilic pneumonias. Allergy. 2005;60(7):841–857. PMID: 15969679. DOI: 10.1111/j.1398-9995.2005.00812.x
  2. Philit F, et al. Idiopathic acute eosinophilic pneumonia. Am J Respir Crit Care Med. 2002;166(9):1235–1239. PMID: 12403695. DOI: 10.1164/rccm.2202036
  3. Pope-Harman AL, et al. Acute eosinophilic pneumonia. Medicine (Baltimore). 1996;75(6):334–342. PMID: 8982148. DOI: 10.1097/00005792-199611000-00004
  4. Carrington CB, et al. Chronic eosinophilic pneumonia. N Engl J Med. 1969;280(15):787–798. PMID: 5776422. DOI: 10.1056/NEJM196904102801501
  5. Cottin V, et al. Mepolizumab for eosinophilic pneumonia (ECLECTIC trial). Lancet Respir Med. 2023;11(8):727–737. PMID: 37121229. DOI: 10.1016/S2213-2600(23)00070-8
  6. Hayakawa H, et al. Bronchoalveolar lavage in chronic eosinophilic pneumonia. Chest. 1994;106(4):1064–1069. PMID: 7924493. DOI: 10.1378/chest.106.4.1064
  7. King MA, et al. Acute eosinophilic pneumonia: radiologic and clinical features. Radiology. 1997;203(3):715–719. PMID: 9169697. DOI: 10.1148/radiology.203.3.9169697
  8. Shorr AF, et al. Acute eosinophilic pneumonia and cigarette smoking. Chest. 2004;125(5):1949–1951. PMID: 15136420. DOI: 10.1378/chest.125.5.1949
  9. Winn RE, et al. Acute eosinophilic pneumonia due to daptomycin. Clin Infect Dis. 2008;47(1):e5–7. PMID: 18491985. DOI: 10.1086/588736
  10. Nair P, et al. Tropical pulmonary eosinophilia. Eur Respir J. 2001;18(5):886–890. PMID: 11736330. DOI: 10.1183/09031936.01.00064301
  11. Jeong YJ, et al. Eosinophilic lung diseases: a clinical, radiologic, and pathologic overview. Radiographics. 2007;27(3):617–637. PMID: 17495280. DOI: 10.1148/rg.273065051
  12. Allen JN, Davis WB. Eosinophilic lung diseases. Am J Respir Crit Care Med. 1994;150(5):1423–1438. PMID: 7952570. DOI: 10.1164/ajrccm.150.5.7952570

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12. Connections

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