Acute eosinophilic pneumonia as a reversible cause of noninfectious respiratory failure

Although chronic eosinophilic pneumonia is a well-known disorder, acute eosinophilic pneumonia has not been as well characterized. We describe the clinical features, results of bronchoalveolar lavage, and follow-up studies of four patients with acute eosinophilic pneumonia. The patients presented with an acute febrile illness, severe hypoxemia (partial pressure of arterial oxygen less than 60 mm Hg), diffuse pulmonary infiltrates, an increased number of eosinophils (mean +/- SEM, 42 +/- 4.8 percent) in bronchoalveolar-lavage fluid, and an absence of infection and previous atopic illness. The illness resolved rapidly after treatment with erythromycin and corticosteroids. The patients received doses of oral prednisone that were tapered over 10 days to 12 weeks, and none have relapsed since the steroids were discontinued. After a minimum follow-up period of five months, clinical evaluation, chest radiography, and pulmonary-function tests have shown no residual abnormalities attributable to the acute eosinophilic pneumonia. Follow-up bronchoalveolar lavage has demonstrated less than or equal to 1 percent eosinophils in all patients. We believe that we are describing an acute form of eosinophilic lung disease distinct from previously described syndromes. It can be diagnosed by bronchoalveolar lavage and seems to respond to treatment with corticosteroids.     

Eosinophilic pneumonia caused by Alternaria alternata

We describe a patient who presented with hypoxemia and diffuse bilateral pulmonary infiltrates. The diagnosis of eosinophilic pneumonia was confirmed by bronchoalveolar lavage and transbronchial lung biopsy. The remarkable characteristic was reappearance of the symptoms on the patient's return home, suggesting the existence of etiologic agents in his house. An environmental survey of the patient's house yielded Alternaria alternata. A high liter of anti- A alternata antibody (IgG) was detected in his serum, and the inhalation bronchoprovocation test with A. alternata antigen was positive. This case indicates that A. alternata is a probable cause of eosinophilic pneumonia.     

Pulmonary Eosinophilia

Eosinophils may infiltrate the lung tissue, thus impairing gas exchange and causing several symptoms as dyspnea, fever, and cough. This process may be secondary to several factors, including drugs or parasite migration, or primary (idiopathic). Acute eosinophilic pneumonia is life-threatening and presents frequently in young smokers as an acute hypoxemic respiratory failure of generally less than a week with bilateral lung infiltrates, frequently misdiagnosed as severe community-acquired pneumonia. This patients present without peripheral eosinophilia but usually have more than 25% eosinophils on bronchoalveolar fluid. Chronic eosinophilic pneumonia is a protracted disease of usually more than a month before presentation, with a predilection for middle aged asthmatic patients. Hypoxemia is mild-moderate, and there are usually more than 1,000 eosinophils/mm3 of peripheral blood. Bronchoalveolar fluid has high eosinophil levels (usually more than 25%). Migratory peripheral infiltrates are seen in the chest x-ray film. Both acute and chronic eosinophilic pneumonia are treated by glucocorticoids and respiratory support as well as avoidance of any recognized trigger.     

Acute eosinophilic pneumonia associated with amitriptyline in a hemodialysis patient.

Drugs are well known causes of eosinophilic lung disease. In many patients, drug-induced eosinophilic lung disease presents with transient eosinophilic infiltrates that disappear after discontinuation of the drug. Some patients, however, experience a fulminant, acute eosinophilia-like disease. Recently, we experienced a case of amitriptyline-associated acute eosinophilic pneumonia with respiratory failure in a diabetic hemodialysis patient. Eight days after treatment with amitriptyline, sudden fever, chill, dry cough and dyspnea developed. Subsequently, multiple patch consolidations appeared on the chest radiographs. Bronchoalveolar lavage (BAL), established a diagnosis of acute eosinophilic pneumonia. After immediate discontinuation of amitriptyline, a rapid clinical and radiological improvement was observed. The present case indicates that the possibility of acute eosinophilic pneumonia should be fully considered in dialysis patients developing unexplained respiratory symptoms while on amitriptyline therapy.     

Detection of IL-5 and IL-1 receptor antagonist in bronchoalveolar lavage fluid in acute eosinophilic pneumonia

BACKGROUND: Acute eosinophilic pneumonia is an idiopathic cause of respiratory failure, characterized by very high numbers of alveolar eosinophils without significant blood eosinophilia. OBJECTIVE: The purpose of this study was to determine which cytokines are associated with acute eosinophilic pneumonia. METHODS: Soluble IL-1 type II receptor and the cytokines IL-1β, IL-1ra, IL-3, IL-5, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor-α were measured in serum and in bronchoalveolar lavage fluid from two patients with acute eosinophilic pneumonia during both acute and convalescent phases. RESULTS: Compared with patients with adult respiratory distress syndrome, the patients with acute eosinophilic pneumonia had high bronchoalveolar lavage fluid levels of IL-5, IL-1ra, and soluble type II IL-1 receptor but not IL-1β, tumor necrosis factor-α>, IL-3, or granulocyte-macrophage colony-stimulating factor. Bronchoalveolar lavage fluid levels of IL-5 and IL-1ra fell after resolution of symptoms. In the serum of patients with acute eosinophilic pneumonia, IL-5 was not detectable, and IL-1ra was initially high but fell after corticosteroid treatment. CONCLUSION: Acute eosinophilic pneumonia is characterized by locally high levels of IL-5, IL-1ra, and soluble type II IL-1 receptor in the alveolar space. (J ALLERGY CLIN IMMUNOL 1996;97:1366-74.)     

Cigarette smoking-induced acute eosinophilic pneumonia: a case report including a provocation test

The mechanism and cause of acute eosinophilic pneumonia are largely unknown. Many factors including the smoking of cigarettes have been suggested, but none have been proven to directly cause acute eosinophilic pneumonia. The authors report a case of acute eosinophilic pneumonia in a young Asian male who recently started smoking. The diagnosis was made based on his clinical course and results of chest radiography, lung spirometry, bronchoalveolar lavage, and transbronchial lung biopsies. After administration of methylprednisolone, his clinical course rapidly improved. A provocation test was designed to establish a connection between cigarette smoking and the development of acute eosinophilic pneumonia. After the provocation test, the patient showed identical symptoms, increase in sputum eosinophils, and worsening of pulmonary function. The results of the provocation test suggest that smoking may directly cause acute eosinophilic pneumonia, and support previous reports of cigarette smoking-induced acute eosinophilic pneumonia.     

Chronic eosinophilic pneumonia with subpleural curvilinear shadow

We report a rare case of chronic eosinophilic pneumonia with subpleural curvilinear shadow. CT scan showed a patchy consolidation in the bilateral upper lungs. In addition, subpleural curvilinear shadow was found in the bilateral upper lungs. A bronchoalveolar lavage obtained from the right middle lobe showed 25 % eosinophils. Although very rare, we should therefore keep in mind that patients, who have patchy consolidation with areas of subpleural curvilinear shadow in the bilateral upper lungs, may have chronic eosinophilic pneumonia.     

FatalScedosporium prolificans infection in a leukemic patient

The case is described of a 42-year-old patient with acute myeloid leukemia who received two courses of chemotherapy complicated by prolonged bone marrow depression. He was admitted to hospital with fever, hepatosplenomegaly and bilateral nodular pulmonary infiltrates. After admission diffuse cutaneous skin nodules, and hypodense lesions in the hemispheres and cerebellum developed. Cultures of cerebrospinal fluid, bronchoalveolar lavage fluid, skin biopsy specimens and blood revealedScedosporium prolificans, indicative of disseminated mycosis. Treatment with amphotericin B and fluconazole was unsuccessful and the patient died within five days after admission. Features that may enhance early recognition ofScedosporium prolificans infection by both clinicians and microbiologists, as well as options in the treatment of infection with this fungal agent are discussed.     

Pulmonary eosinophilic infiltrates

Pulmonary eosinophilic infiltrates include an heterogeneous group of disorders characterized by the presence of eosinophils in the lungs as detected by bronchoalveolar lavage or tissue biopsy, with or without blood eosinophilia. The disease can be idiopathic (simple pulmonary eosinophilia, acute and chronic eosinophilic pneumonia, hypereosinophilic syndrome), secondary (to drugs, parasites, fungal and mycobacterial infection, irradiation, toxic products) or associated with diffuse lung diseases (connective tissue diseases and some neoplasms). Pathologists faced with eosinophils in the lungs (either on cytology or biopsy) should keep in mind several possibilities, although a diagnosis of certainty is rarely based on morphology alone. Correlation with laboratory tests, imaging studies and clinical presentation has a key role, even if some pulmonary eosinophilic diseases are sufficiently characteristic on clinico-radiologic ground to not require a biopsy (e.g. some drug reactions, parasitic infections, idiopathic hypereosinophilic syndrome, allergic bronchopulmonary aspergillosis). Nevertheless, pathologists can play a central role because they can be the first to note eosinophils in the lungs of a very sick patient. Knowledge of histologic features and a striking collaboration with other physicians are necessary to achieve correct diagnosis and to establish adequate treatments.     

Direct transfer of p65 into T lymphocytes from systemic lupus erythematosus patients leads to increased levels of interleukin-2 promoter activity

Patients with allergic asthma present clinically with chronic or intermittent disease caused by either persistent or periodic allergen exposure. We sought to generate clinically relevant disease in mice, which would reflect the relapsing, remitting, and constant nature of this syndrome. We generated and compared acute onset, remission, relapse, and overt phases of the disease and found that acute disease was characterized by airway hyperreactivity, eosinophilic lung inflammation, excessive mucus production, and antigen-specific antibody and was rapidly followed by a remission. Mice rechallenged with aerosol antigen during the remission or treated with repeated aerosol challenges developed relapse and overt disease, respectively. Recurrent antigen exposure induced a progressive increase in bronchoalveolar lavage fluid immunoglobulin, mucus production, and a change in inflammatory infiltrates indicating a transition from acute to chronic inflammation. These data demonstrate distinct phases of disease representing a clinical spectrum of experimental allergic asthma and may have important implications for new treatment strategies.     

Respiratory hyperinfection caused by Strongyloides stercoralis in a patient with pemphigus vulgaris and minireview on diagnosis and treatment of strongyloidiasis

We explain a case of strongyloidiasis in a woman with pemphigus vulgaris from the north of Iran. The patient, aged 59 years old, had been receiving immunosuppressive therapy (oral prednisone) for the last 1 year. She presented with a recent history of diarrhea, epigastric pain, vomiting, fever, loss of consciousness, and respiratory failure. Biochemical and hematological findings were abnormal, and eosinophilia was remarkable. Bronchoscopic alveolar lavage and stool examination revealed larval forms of Strongyloides stercoralis as well as severe acute inflammation. A chest X-ray revealed alveolar opacity in the bilateral mid- and lower zones and bilateral blunting of the costopherenic angle. The high-resolution computed tomography findings showed diffuse ground glass and alveolar opacity, bilateral pleural effusion, and multiple cavitary lesions in mid- and lower zones of the lung. The patient responded well to the treatment with ivermectin plus albendazole.     

A case of chronic eosinophilic pneumonia with significant elevation and variation of serum parainfluenza virus 3 antibody titer]

A 67-year old man visited our hospital because of cough and sputum. Chest radiograph revealed various consolidations of the bilateral lung fields. Eosinophilic pneumonia was diagnosed by transbronchial lung biopsy speciments. The clinical course and the treatment with corticosteroids improved chest radiographic findings quickly confirmed the diagnosis of chronic eosinophilic pneumonia. Based upon the significant elevation and variation of serum parainfluenza virus (PIV) 3 antibody titer, it was suggested that PIV 3 caused the chronic eosinophilic pneumonia.     

Breast carcinoma in bronchoalveolar lavage. A cytologic and immunocytochemical study

To evaluate the effectiveness of bronchoalveolar lavage in detecting pulmonary metastases of breast cancer, we examined lavage fluid from 20 patients with routine cytologic preparations and immunoperoxidase stains with monoclonal antibody B72.3. Bronchoscopy was performed for infection surveillance prior to autologous bone marrow transplantation (nine patients), or to assess abnormal chest roentgenogram (11 patients). Metastatic adenocarcinoma was identified on Papanicolaou-stained-membrane filters in seven patients (35%), corroborated by transbronchial biopsy in four patients. No patients with chest roentgenogram suggestive of metastatic cancer or transbronchial biopsy positive for metastatic cancer had a negative lavage. Monoclonal antibody B72.3 uniformly marked malignant cell aggregates and many single cells that were inapparent in routinely stained material. Because bronchoalveolar lavage may detect metastatic adenocarcinoma with sensitivity comparable to transbronchial biopsy but with less morbidity, it is useful in the evaluation of pulmonary infiltrates in patients with primary breast carcinoma. Staining with monoclonal antibody B72.3 can be readily performed on lavage specimens and may serve as an adjunct in diagnosing malignancy.     

Successful therapy of cyclosporin A in a case with idiopathic interstitial pneumonia]

Seventy-one-year-old woman was visited to our hospital because of dry cough and dyspnea on effort. Fine crackle was audible on both lower lung fields. Joints and skin were normal. Laboratory examination revealed elevation of serum LDH and CRP level. Both anti-nuclear antibody and Jo-1 antibody were negative. Blood gas analysis showed hypoxia after exercise. Chest X-ray film showed reticular shadow in both lower lung fields. Chest CT finding showed patchy area of ground glass attenuation, air-space consolidation, and reticular shadow. Scintigram showed diffuse uptake of Gallium-67 in both lung. Transbronchial biopsy specimen revealed alveolar wall thickness, lymphocyte infiltration and swelling of type II pneumocytes. Bronchoalveolar lavage fluid analysis revealed elevation of CD4/CD8 ratio. She was given a diagnosis of idiopathic interstitial pneumonia. Combination therapy of cyclosporin A and steroid was performed. After therapy, her chest CT findings and her data of pulmonary function test were improved. Then therapy of cyclosporin A was continued and dose of prednisolone was gradually decreased. After that, she was suffered from respiratory tract infection. After administration of antibiotics and cyclosporin A, she was getting well without acute exacerbation of interstitial pneumonia. Since then, she was treated with cyclosporin A only and her pulmonary function test data were gradually improved more. It suggests that cyclosporin A may be useful for the treatment of idiopathic interstitial pneumonia.     

Semiquantitative technique for estimating Pneumocystis carinii burden in the lung.

We developed a technique to estimate the amount of Pneumocystis carinii found in bronchoalveolar lavage fluid. P. carinii associated with 500 nucleated cells in the bronchoalveolar lavage fluid had little between-observer and within-observer variation. Varying the technique of the lavage did not change the amount of P. carinii recovered. This technique was used in patients treated for P. carinii pneumonia. Those patients who did not respond to treatment had more P. carinii in their bronchoalveolar lavage fluid than those who responded.     

Elevated soluble ADAM8 in bronchoalveolar lavage fluid in patients with eosinophilic pneumonia

BACKGROUND: ADAM (a disintegrin and metalloprotease) family members, characterized by a metalloprotease and a disintegrin domain, are membrane-anchored glycoproteins involved in proteolysis and cell adhesion. ADAM8 might have an important role in allergic inflammation. It can cleave a variety of substrates and is a sheddase for VCAM-1 and CD23, the low-affinity IgE receptors. METHODS: To evaluate the contribution of ADAM8 to the pathogenesis of eosinophilic pneumonia (EP), we measured the concentrations of soluble ADAM8 (sADAM8) and its substrates, soluble VCAM-1 (sVCAM-1) and soluble CD23 (sCD23), in bronchoalveolar lavage fluid from patients with smoking-induced acute eosinophilic pneumonia (AEP), chronic idiopathic eosinophilic pneumonia (CEP), and drug-induced eosinophilic pneumonia (drug-EP). RESULTS: The sADAM8 and sVCAM-1 concentrations were increased in AEP and CEP. The sCD23 concentration was elevated in AEP. In AEP, but not CEP, the sADAM8 concentration significantly correlated with those of both sVCAM and sCD23. CONCLUSION: The pathogenesis of AEP, CEP, and drug-EP was distinct with regard to ADAM8. Our results are the first to associate ADAM8 with eosinophilic responses and lung inflammation in humans.     

Acute Eosinophilic Pneumonia Leading to Acute Respiratory Failure in a Current Systemic Corticosteroid User

A 69-year-old female patient visited the emergency room with fever (38.3℃) and dyspnea. She had been taking prednisolone (5 mg once per day) and methotrexate (2.5 mg once per week) for rheumatoid arthritis for 2 years. Chest computed tomography (CT) showed bilateral, multifocal ground glass opacity with interlobular septal thickening. Peripheral blood leukocyte count was 6,520/mm³ (neutrophils, 77.4%; eosinophils, 12.1%). During the night, mechanical ventilation was initiated due to the development of severe hypoxemia. Bronchoalveolar lavage fluid showed a high proportion of eosinophils (49%). Her symptoms improved dramatically after commencement of intravenous methylprednisolone therapy. This is the first report of idiopathic acute eosinophilic pneumonia developing in a current user of systemic corticosteroids.     

Pulmonary eosinophilic syndromes

Acute eosinophilic pneumonia, chronic eosinophilia, Churg-Strauss syndrome, and the hypereosinophilic syndrome are pulmonary eosinophilic syndromes characterized by an increased number of eosinophils in peripheral blood, in lung tissue, in sputum, in bronchoalveolar lavage fluid, or in all of these. These pulmonary eosinophilic syndromes generally are characterized by increased respiratory symptoms, abnormal radiographic appearance, and the potential for systemic manifestations. It is critical to exclude other causes of eosinophilia in patients who have lung disease, to make a quick diagnosis, and to treat aggressively with corticosteroids and other therapies to prevent long-term sequelae.     

Reconstitution of immune responses to Pneumocystis carinii pneumonia in patients with HIV infection who receive highly active antiretroviral therapy

We describe a reconstitution syndrome of immune responses to Pneumocystis carinii pneumonia (PCP) in 2 HIV-infected individuals who received highly active antiretroviral therapy (HAART). Patient 1, who had been successfully treated for PCP 3 years before the initiation of HAART, developed cough and pulmonary shadows 6 weeks after the start of HAART. Patient 2 was introduced HAART immediately after completing the responsive treatment of PCP, and then showed dyspnea and diffuse pulmonary infiltrates 7 months later. Histologic findings of lung-tissue samples showed granulomatous tissue (patient 1) and organizing pneumonia with thickening of alveolar septa (patient 2), and immunohistochemical findings revealed both CD4 and CD8 cell subsets represented in the lesions. The tissue and bronchoalveolar lavage (BAL) specimens showed no organisms, but PCR methods with the BAL samples were positive for P. carinii DNA. It is hypothesized that these second respiratory episodes may have arisen as immune reconstitution syndrome in response to residual P. carinii antigen in the lung.     

Extracorporeal membrane oxygenation for ARDS in adults

A 41-year-old woman presents with severe community-acquired pneumococcal pneumonia. Chest radiography reveals diffuse bilateral infiltrates, and hypoxemic respiratory failure develops despite appropriate antibiotic therapy. She is intubated and mechanical ventilation is initiated with a volume- and pressure-limited approach for the acute respiratory distress syndrome (ARDS). Over the ensuing 24 hours, her partial pressure of arterial oxygen (Pao2) decreases to 40 mm Hg, despite ventilatory support with a fraction of inspired oxygen (Fio2) of 1.0 and a positive end-expiratory pressure (PEEP) of 20 cm of water. She is placed in the prone position and a neuromuscular blocking agent is administered, without improvement in her Pao2. An intensive care specialist recommends the initiation of extracorporeal membrane oxygenation (ECMO).