The eosinophilic pneumonias

Acute and chronic eosinophilic pneumonia can be distinguished by their clinical, laboratory, and radiographic features. Patients with both acute and chronic eosinophilic pneumonia present with cough, dyspnea, and fever. Patients with chronic eosinophilic pneumonia present subacutely over weeks to months but patients with acute eosinophilic pneumonia present within 5 days of symptom onset. Chest radiographs in chronic eosinophilic pneumonia show peripheral alveolar infiltrates. In contrast, radiographs in acute eosinophilic pneumonia show mixed interstitial and alveolar infiltrates, Kerley B lines, and pleural effusions. Both disorders are characterized by high percentages of bronchoalveolar lavage eosinophils, but high numbers of blood eosinophils accompanies only chronic eosinophilic pneumonia. The diagnosis of both disorders can usually be made based on clinical and radiographic findings; however, lung biopsy is occasionally necessary to distinguish the eosinophilic pneumonias from other eosinophilic lung diseases. In both conditions, patients will respond rapidly and completely to corticosteroids but patients with chronic eosinophilic pneumonia usually relapse if less than 6 months of treatment is given, whereas patients with acute eosinophilic pneumonia do not relapse after a brief course of treatment.     

Clinicopathological differences between acute and chronic eosinophilic pneumonia]

Considerable confusion exists regarding the proper classification of idiopathic eosinophilic pneumonia (IEP). In addition, there are no reports that reveal clinicopathological differences between the various eosinophilic pneumonias. A problem persists in describing what the essential histological differences are between the different types of IEP. In this context, we examined the histological findings of acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP) and contrasted them with the clinical features and radiological findings. Radiologically, ground glass opacity and interlobular septal thickening were characteristic of the AEP cases studied, while air space consolidation was seen in all CEP cases. Histologically, interstitial edema and fibrin deposition were prominent in the AEP cases. Type II cells were detached from the alveolar walls, though the basal lamina was predominantly intact. In CEP, in addition to cellular infiltration, there was prominent intraluminal fibrosis. Disruption of the basal lamina was observed and nests of intraluminal fibrosis were directly adjacent and connected to the alveolar walls. From these findings, we conclude that the histological differences between AEP and CEP are the severity of basal lamina damage, the amount of subsequent intraluminal fibrosis, and the severity of interstitial edema. Especially in AEP, interstitial edema is an essential histological finding and this finding explains the acute onset, and the radiographic findings, as well as the rapid and complete improvement noted in such cases.     

Clinicopathological differences between acute and chronic eosinophilic pneumonia

OBJECTIVE: Considerable confusion exists regarding the proper classification of idiopathic eosinophilic pneumonia (IEP). Furthermore, there are no reports describing the clinicopathological differences between the various forms of eosinophilic pneumonias. METHODOLOGY: The histological findings in acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP) were examined and the clinical and radiological features were contrasted with them. RESULTS: Radiologically, ground glass opacity and interlobular septal thickening were characteristic of the AEP cases, while air space consolidation was seen in all CEP cases. Histologically, interstitial oedema and fibrin deposition were prominent in the AEP cases. Type II cells were detached from the alveolar walls, although the basal lamina was predominantly intact. In CEP, in addition to cellular infiltration, there was prominent intraluminal fibrosis. Disruption of the basal lamina was observed and nests of intraluminal fibrosis were directly adjacent and connected to the alveolar walls. CONCLUSIONS: An essential histological difference between AEP and CEP is the severity of basal lamina damage and the amount of subsequent intraluminal fibrosis. In AEP particularly, these findings explain the radiographical findings, as well as the rapid and complete improvement noted in such cases.     

A case report and literature review of acute eosinophilic pneumonia

Although chronic eosinophilic pneumonia is a well-known disorder, acute eosinophilic pneumonia has not been as well described. We described the clinical features of two patients with acute eosinophilic pneumonia. The patients presented with an acute onset of high fever, severe hypoxemia and diffuse pulmonary infiltrates. Eosinophilic pneumonia was diagnosed by bronchoalveolar-lavage and confirmed by transbronchial lung biopsy. We believe that we have described an acute type of eosinophilic lung disorder which can not be applied to Crofton's classification of PIE, so we reviewed previously reported cases of acute eosinophilic pneumonia and tried to summarize their clinicopathological features. We also emphasized the existence of eosinophil infiltration into the bronchial wall in Acute Eosinophilic Pneumonia.     

急性纤维蛋白性机化性肺炎的临床病理特征

目的介绍一种新近定义的弥漫性急性肺损伤类型-急性纤维蛋白性机化性肺炎,以提高临床医生对其的认识方法分析南京市鼓楼医院确诊的1例患者以及国外有关文献的报道,总结其临床特征。结果急性纤维蛋白性机化性肺炎患者表现为急性或亚急性起病,主要临床表现为呼吸困难、咳嗽、咳痰,肺功能为限制性通气功能障碍和弥散降低,CT可见两肺斑片状实变影,主要病理表现为肺泡腔内可以看到特征性纤维蛋白球以及机化的疏松结缔组织,而没有DAD中的经典透明膜形成。结论急性纤维蛋白性机化性肺炎的病理组织学特点决定了它是一种不同于弥漫性肺泡损伤、机化性肺炎和嗜酸细胞性肺炎的新的肺损伤类型,但其是否为一个独特的疾病综合征有待进一步明确。     

急性嗜酸粒细胞性肺炎1例并文献复习

目的 探讨急性嗜酸性粒细胞肺炎的临床表现、诊断、治疗方法及预后.方法 结合我院收治的1例急性嗜酸粒细胞性肺炎的临床资料及国内外文献报道的病例进行综合分析.结果 患者18岁,青年男性,咳嗽、咯痰10余天,胸闷、胸痛8 d,加重伴发热4 d入院.胸部CT示双肺炎,双侧胸腔积液,抗感染治疗无效,病情进行性加重,胸水中找到嗜酸...     

Acute eosinophilic pneumonia induced by cigarette smoking]

The subject was a 24-year-old man who presented with acute fever, dry cough, and dyspnea. Chest X-ray films revealed diffuse infiltrates in both lungs. Bronchoalveolar lavage fluid specimens contained an increased number of eosinophils. Transbronchial lung biopsy specimens demonstrated the infiltration of eosinophils into alveolar walls and air spaces. These findings were consistent with acute eosinophilic pneumonia. The patient recovered without medical treatment. Eight days prior to admission, he had resumed smoking after 3 years of abstention. It was suggested that the cause of acute eosinophilic pneumonia in this case was associated with the resumption of smoking. To confirm that association, a smoking challenge test is usually necessary. However, similar symptoms also developed later, after the patient was passively exposed to cigarette smoke. Therefore, we concluded that smoking was probably the etiologic agent of his illness.     

Acute eosinophilic pneumonia with positive response to smoking challenge test, suggesting the involvement of health food]

A 17-year-old girl was admitted to our hospital because of acute febrile illness, progressive dyspnea and severe hypoxemia. Chest radiography and HRCT showed bilateral diffuse ground-glass opacities, consolidation, Kerley lines and pleural effusion. Analysis of bronchoalveolar lavage fluid showed 41.9% eosinophils, and a transbronchial lung biopsy revealed infiltration of eosinophils into the alveolar septa and mild alveolar septal edema. The patient's condition was improved immediately by corticosteroid therapy. She had begun smoking and taking health food (chitosan) 3 months before the admission. A smoking challenge test was positive and a drug-induced lymphocyte stimulation test for chitosan was positive. These findings suggested acute eosinophilic pneumonia caused by smoking and health food. The concentration of interleukin-5 (IL-5) in the serum and BALF/granulocyte colony-stimulating factor (G-CSF) in the serum on admission were very high, but decreased after the improvement. Therefore, it is likely that IL-5 and G-CSF are important in the onset of acute eosinophilic pneumonia.     

A case of eosinophilic pneumonia with acute progressive dyspnea and diffuse small nodular shadows on chest X-ray film

A 52-year-old man was admitted to our hospital with high-grade fever, dry cough and severe dyspnea. Chest X-ray films revealed diffuse small nodular shadows in all lung fields, prominently in the middle and lower lung fields. On examination, peripheral blood eosinophilic leukocytosis and severe hypoxemia were demonstrated. His clinical condition improved during five days after the admission without any therapy but oxygen inhalation. The abnormal shadows decreased in several days, and disappeared completely in thirty days. Bronchoalveolar lavage fluid revealed increased total cell counts, mostly with eosinophils (60%) and lymphocytes (21%). Histologically, the transbronchial lung biopsy specimen showed that the walls of pulmonary arteries and bronchioli were markedly infiltrated with eosinophils, and that alveolar septa were edematous with mononuclear and eosinophilic cells infiltration. There were no prominent changes in the alveolar lumen except few macrophage exudates. Our case was of importance for two reasons: first, eosinophilic pneumonia could take the form of interstitial pneumonia both roentgenologically and histologically; second, Crofton's classification of P.I.E. could not be applied to this case.     

Ultrastructure of the lung in Loeffler's pneumonia

A case is presented fulfilling the diagnostic criteria of “Loeffler's eosinophilic pneumonia.” No etiologic factors could be determined, and the chest roentgenogram returned to normal. Lung biopsy at the peak of the disease demonstrated an interstitial eosinophilic pneumonia without tissue necrosis or vasculitis. By electron microscopy, the alveolar capillary basement membranes were intact and exhibited no immune deposits. Normal appearing eosinophils were abundant in the alveolar capillaries, interstitium and alveolar spaces. Occasional eosinophils released their granules within the alveolar wall. Macrophages were increased in number in both the alveolar wall and alveolar spaces.     

Chemotherapy-induced eosinophilic pneumonia. Relation to bleomycin

Three cases of eosinophilic pneumonia are associated with bleomycin chemotherapy. As opposed to the more common picture of diffuse alveolar damage, these cases appear to represent a hypersensitivity reaction resembling eosinophilic pneumonia.     

Serrapeptase-induced lung injury manifesting as acute eosiniphilic pneumonia]

An 84-year-old man was referred to our hospital because of fever, cough, and hemoptysis. The patient had acute respiratory failure (PaO2 < 40 mmHg) on admission, with diffuse interstitial infiltration and bilateral pleural effusion. The bronchoalveolar lavage fluid was bloody, and contained a high percentage of eosinophils (32%). A diagnosis of acute eosinophilic pneumonia was established, and the patient made a rapid recovery after corticosteroids were administered. When the DLST (drug lymphocyte stimulation test) was performed after the corticosteroid therapy was stopped, it was positive for serrapeptase, which had been prescribed for chronic cystitis for 3 months before the onset of the pneumonia. This was a case of drug (serrapeptase)-induced pneumonitis manifesting as acute eosinophilic pneumonia.     

Drug-, toxin-, and radiation therapy-induced eosinophilic pneumonia

A significant number of drugs and toxins have been associated with eosinophilic pneumonia. Antibiotics and NSAID, are the most commonly reported drugs. Toxins suspected to cause eosinophilic pneumonia include cigarette smoke and illicit drugs. Drug- or toxin-induced eosinophilic pneumonia is indistinguishable from idiopathic acute or chronic eosinophilic pneumonia by clinical, radiographic, and histopathologic criteria. The diagnosis is supported by a temporal relationship to a drug or toxin. The condition usually resolves with removal from the agent and recurs with rechallenge. Treatment involves discontinuation of the offending drug or toxin and treatment with corticosteroids in severe respiratory failure. There are also mass outbreaks of eosinophilic pneumonia reported, such as the toxic-oil syndrome in 1981 and the eosinophilia-myalgia syndrome related to the ingestion of L-tryptophan in 1989. A recent report has described an outbreak of acute eosinophilic pneumonia found in soldiers in Iraq. Radiation therapy has also been associated with the development of eosinophilic pneumonia in patients receiving this treatment for breast cancer.     

Drug-induced lung disease: a pragmatic classification incorporating HRCT appearances

Drug-induced lung disease frequently poses a diagnostic challenge. Knowledge of common radiological patterns of lung involvement and corresponding histopathologic diagnoses can facilitate management of individual patients. We outline a framework for understanding radiological and histologic patterns of drug-induced lung disease. Diffuse forms of drug-induced lung disease include processes that mimic acute respiratory distress syndrome (ARDS) and diffuse alveolar hemorrhage. These patterns of drug-induced lung disease are especially common in patients receiving cytotoxic chemotherapeutic agents. Chronic forms of drug-induced lung disease include many of the interstitial pneumonias seen more commonly in patients with idiopathic disease. Bronchiolitis obliterans organizing pneumonia and eosinophilic pneumonia are nonspecific patterns of drug-induced lung disease that are radiologically and histologically indistinguishable from their idiopathic counterparts. In some patients organizing pneumonia and eosinophilic pneumonia mimic the radiological appearance of neoplastic disease.     

Idiopathic hypereosinophilic syndrome presenting acute abdomen

We describe a 27-year-old man with hypereosinophilc syndrome (HES) presenting acute abdomen due to acute thrombosis of the mesenteric artery, who had a past history of eosinophilic pneumonia followed by multiple arterial thromboses of the extremities. At the recurrence of eosinophilia, he was treated with high-dose corticosteroids. Immediately after the reduction of peripheral blood eosinophils, he suddenly developed perforation of the intestine due to acute thromboses of mesenteric arteries despite sustained anticoagulation therapy. Molecular analysis demonstrated that the FIP1L1-PDGFRA fusion gene was negative. Histopathology showed thrombi and eosinophilic inflammation of arteries. It is important to recognize that HES could be a cause of acute abdomen.     

Severe acute interstitial pneumonia and gefitinib

Gefitinib is an oral selective inhibitor of the epidermal growth factor receptor tyrosine kinase that is an effective treatment for patients with advanced non-small cell lung cancer who do not respond to platinum-based chemotherapy. We assessed four patients who had non-small cell lung cancer causing severe acute interstitial pneumonia in association with gefitinib. Although two patients recovered after treatment with steroids, the other two died from progressive respiratory dysfunction. On the basis of autopsies and bilateral distribution of diffuse ground-glass opacities in chest CTs, we diagnosed diffuse alveolar damage, which was consistent with acute interstitial pneumonia. Patients with interstitial pneumonia also had other pulmonary disorders such as previous thoracic irradiation and poor performance status. Physicians should be aware of the alveolar damage induced by gefitinib, especially for patients with these characteristic features.     

Acute eosinophilic pneumonia in twins

The pathogenesis of eosinophilic pneumonia is currently poorly understood, and this disease has not been reported in twins since 1983. Herein, we report a case of acute eosinophilic pneumonia in twins, which appeared to be triggered by initial smoking at different times by both patients. One patient resumed smoking after recovering from eosinophilic pneumonia, with no observed recurrence. This study discussed the possibility of an association between susceptibility to eosinophilic pneumonia and genetic factors in twins.     

Leflunomide-related lung injury in patients with rheumatoid arthritis: imaging features

Imaging findings of 26 cases of leflunomide (Arava)-related acute lung injury were analyzed. Thirteen cases had pre-existing interstitial pulmonary disease on chest X-ray or computed tomography. The main features of clinically determined leflunomide-induced acute lung injury were similar to those caused by other drugs: diffuse or widespread patchy ground-glass opacities and/or consolidation, frequently accompanied by septal thickening and intralobular reticular opacities. We categorized these findings into four patterns: diffuse alveolar damage (DAD), acute eosinophilic pneumonia, hyperreaction, and cryptogenic organizing pneumonia. The DAD group had a higher mortality rate, but statistically not a significant one. It is impossible to exclude infectious disease such as pneumocystis carinii pneumonia based on imaging findings, and detailed correlation of imaging findings with clinical and laboratory findings is essential in order to make a correct diagnosis.     

Idiopathic chronic eosinophilic pneumonia

Idiopathic chronic eosinophilic pneumonia is a rare disorder of unknown cause with nonspecific respiratory and systemic symptoms but rather characteristic peripheral alveolar infiltrates on imaging. The disorder is highly responsive to oral corticosteroid therapy. However, relapses are frequent when tapering or after stopping treatment. Moreover, some patients develop severe asthma at some time in the follow-up. The high incidence of relapses and prevalence of severe asthma is responsible for the great proportion of patients with idiopathic chronic eosinophilic pneumonia who require prolonged oral corticosteroid therapy. There are tight links between asthma and idiopathic chronic eosinophilic pneumonia. These links might help in the comprehension of the pathogenesis of both diseases. Interestingly, there might exist a continuum between hypereosinophilic asthma, idiopathic chronic eosinophilic pneumonia, and the Churg-Strauss syndrome.     

A case of acute eosinophilic pneumonia induced by inhalation of acetylene]

A 17-year-old high school student, while carrying out soldering one morning, inhaled 100% acetylene, and experienced nausea and bilateral lower limb numbness several hours later. In the evening his symptoms worsened, dyspnea followed, and the patient was referred to our hospital the next day. On admission chest radiography and CT scanning revealed peripheral ground-glass opacity, patchy infiltrate and Kerley's B line in the right lung fields, and bilateral pleural effusion. Since the laboratory findings revealed leukocytosis without eosinophilia, increased CRP, and hypoxemia, bronchoalveolar lavage (BAL) and transbronchial biopsy (TBLB) was subsequently performed. Fluid analysis revealed marked increases in the total cell and eosinophil counts, and the biopsy result showed eosinophilic and lymphocytic infiltration of the alveolar septa. As a result, the case was diagnosed as acute eosinophilic pneumonia (AEP). Although inhalation of acetylene is known to induce pulmonary edema, all the typical findings of AEP but pulmonary edema were seen. This case demonstrates that AEP may be induced by inhalation of acetylene.