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*第12期*  Chronic Eosinophilic Pneumonia 慢性嗜酸粒细胞性肺炎Chronic eosinophilic pneumonia was first described by Carrington et al in 1969. It is a rare eosinophilic lung disease that manifests insidiously with constitutional symptoms of cough, fever, dyspnea, weight loss, malaise, and night sweats and develops over 4–8 months. The diagnosis is suggested if there is (a) persistence of respiratory symptoms over several months, (b) peripheral eosinophilia of more than 1000/μL or BAL fluid eosinophil count greater than 25% (usually >40%), (c)peripheral pulmonary infiltrates, and (d) no underlying cause such as parasitic infections. Chronic eosinophilic pneumonia occurs mainly in middle-aged individuals, and a female predominance has been described. Elevated erythrocyte sedimentation rates and immunoglobulin E (IgE) levels are seen in up to 75% of patients, and approximately one-half of patients have a history of asthma or atopy. Pulmonary function tests may reveal airflow obstruction due to underlying asthma and a restrictive defect caused by reduced diffusing capacity. Histologic findings include interstitial and alveolar eosinophilic exudates, bronchiolitis obliterans (seen in up to 25% of cases), eosinophilic microabscesses, Charcot-Leyden crystals, and foci of organizing pneumonia. 慢性嗜酸粒细胞性肺炎于1969年由Carrington等人首次描述。这是一种罕见的嗜酸粒细胞性肺病，隐匿地表现为咳嗽、发热、呼吸困难、体重减轻、不适和盗汗等全身症状，并在4-8月内进展。如果有(a)持续数月的呼吸道症状，(b)外周血嗜酸粒细胞计数超过1000/μL或BAL液中嗜酸粒细胞计数超过25%(常常>40%)，(c)外周肺浸润，(d)没有寄生虫感染等潜在因素，则可作出诊断。慢性嗜酸粒细胞性肺炎主要发生在中年患者，女性为主。高达75%的患者血沉和免疫球蛋白E水平升高，约半数患者有哮喘或过敏性疾病史。肺功能检查可显示因潜在哮喘所致气流阻塞，及弥散容积下降导致的限制性通气功能障碍。组织学表现包括肺间质和肺泡嗜酸性粒细胞渗出、闭塞性细支气管炎(在多达25%的病例中可见)、嗜酸细胞性微脓肿、夏科-雷登晶体和机化性肺炎。 Chest radiography demonstrates multifocal patchy peripheral infiltrates that can be unilateral or, more often, bilateral, with a predilection for the upper lung zones. Most characteristic chest radiographic findings mimic the photographic negative of acute pulmonary edema (Fig 3a). However, this pattern is seen in only 25%–34% of cases of chronic eosinophilic pneumonia. Airspace opacities range from ground-glass attenuation to consolidation with air bronchograms. CT demonstrates patchy consolidation with peripheral and upper lobe predominance, ground-glass opacities with crazy paving, and bandlike subpleural opacities(Fig 3b). Other less common CT findings include the “reverse halo” sign, which mimics findings of cryptogenic organizing pneumonia, solitary pulmonary nodule, pleural effusions, and subpleural reticulations.胸部X线片显示外周多灶性斑片状浸润，可为单侧，但双侧、上肺更多见。大多数具有特征性的胸部X线表现，类似于急性肺水肿的反转征象(反肺水肿征)(图3a)。然而，只有25%-34%的慢性嗜酸粒细胞性肺炎出现了这种情况。气腔阴影的变化较大，可出现磨玻璃影或含支气管充气征的实变影。CT表现为外周和上叶多发的斑片状实变，伴铺路石征的磨玻璃影和胸膜下带状渗出影(图3b)。其它比较少见的CT征象包括类似隐源性机化性肺炎的反晕征，孤立性肺结节、胸腔积液和胸膜下网状影。
A variety of other conditions may mimic chronic eosinophilic pneumonia, such as Churg-Strauss syndrome, simple pulmonary eosinophilia, and cryptogenic organizing pneumonia. One important BALfinding in cases of chronic eosinophilic pneumonia is that the number of eosinophils is always greater than the number of lymphocytes, in contrast to findings of cryptogenic organizing pneumonia, which is the principal differential diagnosis. Chronic eosinophilic pneumonia is highly responsive to oral corticosteroid therapy. However, relapses are frequent after treatment cessation, with a large proportion of patients requiring prolonged oral corticosteroid therapy or a second line of therapy. 其它类似于慢性嗜酸粒细胞性肺炎的情况，如Churg-Strauss综合征、单纯性肺嗜酸粒细胞增多症和隐源性机化性肺炎。慢性嗜酸性粒细胞肺炎BAL液的一个重要发现是嗜酸粒细胞数总是大于淋巴细胞数，而隐源性机化性肺炎则相反，这是两者鉴别的主要依据。慢性嗜酸粒细胞性肺炎对口服糖皮质激素治疗反应较好。然而，在停止治疗后，复发率很高，很大一部分患者需要长期口服糖皮质激素治疗或二线治疗。 Churg-Strauss Syndrome Churg-Strauss综合征Churg-Strauss syndrome, also known as eosinophilic granulomatosis with polyangiitis, was first described in 1951 by Churg and Strauss as a rare multisystemic disorder with necrotizing vasculitis of the small vessels, associated with extravascular eosinophilic granulomas that occur exclusively in patients with asthma and peripheral eosinophilia. Churg-Strauss syndrome affects both sexes equally and can manifest at any age (average age, 50 years), with an incidence of one to seven cases per million per year. Although the exact cause of Churg-Strauss syndrome is not yet established, it likely is multifactorial, with increased levels of immunoglobulins (IgE,G4), rheumatoid factor, and antibodies to ANCAs. ANCA positivity is seen in as many as 40% of cases, but interestingly, these patients are more likely than ANCA-negative patients to present with a clinical-pathologic picture of small-vessel vasculitides and are less likely to experience cardiac and nonhemorrhagic lung involvement. Clinically, Churg-Strauss syndrome has three distinct phases: (a)prodromal phase, characterized by asthma and rhinosinusitis; (b) eosinophilic phase, marked by peripheral eosinophilia and organ involvement; and (c) vasculitic phase, with clinical manifestations due to small-vessel vasculitis; these phases are not necessarily seen in the same order. The lungs and skin are most commonly involved in Churg-Strauss syndrome; however, any organ can be involved, including the central nervous system, heart, gastrointestinal tract, and musculoskeletal system. Churg-Strauss综合征也称为嗜酸性肉芽肿性多血管炎，在1951年Churg和Strauss首次将其描述为一种罕见的多系统疾病，表现为坏死性小血管炎，伴有血管外嗜酸性肉芽肿（仅发生于哮喘和外周嗜酸粒细胞增多症）。Churg-Strauss综合征发病率无性别差异，可以在任何年龄(平均年龄50岁)出现，每年发病率为百万分之一至百万分之七。虽然Churg-Strauss综合征的确切病因尚未确定，可能是多因素的，包括免疫球蛋白(IgE、IgG4)、类风湿因子和ANCA抗体水平增加。ANCA阳性率高达40%，但有趣的是，这些患者比ANCA阴性的患者更有可能出现小血管病变，较少发生心脏和非出血性肺受累。临床上，Churg-Strauss综合征有三个不同的阶段：(A)前驱期，以哮喘和鼻窦炎为特征；(B)嗜酸粒细胞增多期，以外周嗜酸粒细胞增多和器官受累为特征；(C)血管炎期，其临床表现为小血管炎；这些期不一定以相同的顺序出现。肺和皮肤是Churg-Strauss综合征最常见的累及部位；然而，任何器官都可能受累，包括中枢神经系统、心脏、胃肠道和肌肉骨骼系统。 The American College of Rheumatology proposed six criteria for diagnosis of Churg-Strauss syndrome in 1990. The diagnosis can be made if at least four of the following six criteria are present: asthma, eosinophilia greater than 10% in peripheral blood, paranasal sinusitis, migratory or transient pulmonary infiltrates, polyneuropathy, and biopsy-proven extravascular eosinophils. 1990年，美国风湿病学会提出了诊断Churg- Strauss综合征的六项标准。以下六项标准中至少符合四项可作出诊断：哮喘、外周血嗜酸粒细胞占比大于10%、副鼻窦炎、游走性或一过性肺浸润、多神经病变和经活检证实的血管外嗜酸粒细胞聚集。 At radiography, patients with Churg-Strauss syndrome show bilateral nonsegmental areas of airspace consolidation and airspace opacities in a lobular distribution without zonal predilection. These opacities are predominantly peripheral, resembling those in chronic eosinophilic pneumonia, and can be transient, resembling findings of simple pulmonary eosinophilia. In as many as 75% of patients, CT shows lung parenchymal abnormalities (Fig 4). Imaging findings correspond histologically to areas of eosinophilic pneumonia, necrotizing granulomas, and granulomatous vasculitis. Other manifestations include diffuse interstitial reticular or reticulonodular opacities, centrilobular nodules, bilateral nodules, and bronchial wall thickening. Pleural effusion (unilateral or bilateral) is seen in about 30% of patients (Fig 5). Pulmonary hyperinflation, hilar or mediastinal lymphadenopathy, and pericardial effusion are less common findings (Table 2). Pulmonary opacities can be classified into airspace and airway patterns. Patients with airspace pattern responded more readily to steroid treatment than those with airway pattern. Although Churg-Strauss syndrome has specific radiographic findings, some radiographic features mimic those of chronic eosinophilic pneumonia, hypereosinophilic syndrome, and bronchocentric granulomatosis. 在影像学上，Churg-Strauss综合征患者表现为小叶分布的双侧非节段性气腔实变和气腔模糊影。外周为主，类似于慢性嗜酸粒细胞性肺炎，也可能是一过性的，类似于单纯性肺嗜酸粒细胞增多症。在多达75%的患者中，CT可见肺实质异常(图4)。影像学表现符合嗜酸粒细胞性肺炎、坏死性肉芽肿和肉芽肿性血管炎的组织学特点。其他表现包括弥漫性间质网格影或网状结节影、小叶中央结节、双侧结节和支气管壁增厚。胸腔积液(单侧或双侧)约占30%(图5)。肺过度含气、肺门或纵隔淋巴结肿大、心包积液是较少见的表现(表2)。肺部阴影可分为气腔和气道两种类型。气腔型患者对激素的治疗反应比气道型患者更快。虽然Churg-Strauss综合征有特殊的X线表现，但有些X线表现类似于慢性嗜酸粒细胞性肺炎、嗜酸粒细胞增多症和支气管中心性肉芽肿病。
图5. 45岁男性，Churg-Strauss综合征，有哮喘和鼻窦炎病史8月。(a)心脏水平的薄层CT图像显示双侧胸腔积液、支气管壁增厚、左下叶弥漫性磨玻璃影(箭头)和右中叶部分肺不张(短箭头)。(b)鼻窦CT平扫显示双侧上颌窦粘膜增厚和右侧气液平(箭头)，与鼻窦炎相符。(c)左下叶支气管镜活检标本可见嗜酸性粒细胞浸润(短箭头)。(HE染色，×400.)
Allergic Bronchopulmonary Aspergillosis 变应性支气管肺曲霉病ABPA is a complex pulmonary disorder caused by immune reactions to antigens released by colonization of the tracheobronchial tree by Aspergillus fumigatus in patients with asthma or cystic fibrosis. The prevalence of ABPA is reported to be 2%–32% in patients with asthma and 2%–15% in patients with cystic fibrosis. Aspergillus-specific IgE-mediated type I hypersensitivity reaction and specific IgG-mediated type III hypersensitivity reactions are proposed in the pathogenesis of ABPA . ABPA is defined by combined clinical, laboratory, and radiographic criteria that include active asthma, peripheral eosinophilia, elevated IgE levels, fleeting pulmonary parenchymal opacities, bronchiectasis, and positive skin test to A fumigatus (Table 3). The presence of six of the major criteria makes the diagnosis almost certain. Elevated serum IgE levels correlate well with disease activity, and an increased total serum IgE level of 1000 IU/mL is the hallmark of ABPA. ABPA has five stages according to clinical presentation: acute, remission, exacerbation, corticosteroid dependent, and fibrotic (end stage). ABPA是一种复杂的肺部疾病，机体对烟曲霉在气管支气管内定植后释放的抗原产生的免疫反应引起的，多见于哮喘或囊性纤维化患者。ABPA在哮喘患者中的患病率为2%-32%，在囊性纤维化患者中的患病率为2%-15%。ABPA发病机制主要是曲霉特异性IgE介导的Ⅰ型超敏反应和特异性IgG介导的Ⅲ型超敏反应。ABPA诊断应结合临床、实验室和X线检查标准，包括活动性哮喘、外周血嗜酸粒细胞增多、IgE升高、一过性的肺实质阴影、支气管扩张和曲霉皮肤试验阳性(表3)。具备六个主要标准，诊断几乎是确定的。血清IgE水平升高与疾病活动密切相关，血清总IgE水平＞1000 IU/mL是ABPA的标志。根据临床表现，ABPA分为五个阶段：急性期、缓解期、加重期、糖皮质激素依赖性和纤维化期(终末期)。 Imaging findings of ABPA are diverse and are classified as acute or chronic . In the acute phase, findings at initial chest radiography can be normal in as many as 50% of cases . In patients with an abnormal chest radiograph, the most common abnormality (up to 90%) is transient ill-defined homogeneous pulmonary parenchymal opacities or “fleeting shadows,” with involvement of the upper lobes . Thickened bronchial walls appear as “tramline,” parallel line, or ring shadows. Mucoid impaction can occur in large airways and can extend into the smaller bronchi, resulting in the classic “finger-in-glove” appearance characterized by branching and tapering tubular opacities arising centrally and extending peripherally (Fig 6). Perihilar opacities simulating hilar and/or mediastinal lymphadenopathy occur because of mucus-filled dilated central bronchi . Air-fluid levels can be seen in patients who develop an eosinophilic abscess (Fig 6) . High-attenuation mucus within dilated bronchi is a characteristic CT finding in ABPA (Fig 7) . The hyperattenuating mucus plugging seen at CT is currently attributed to the presence of calcium salts and metals (iron and manganese) or desiccated mucus . Impacted mucus may also appear calcified at CT . Other CT findings of ABPA are centrilobular nodules, which can have a “tree-in-bud” distribution, and patchy areas of mosaic attenuation pattern within the lung secondary to concomitant small-airway disease and areas of air trapping . Centrilobular nodules are more common in asthmatic patients with ABPA than in those without ABPA . Chronic changes manifest as bronchiectasis and fibrosis, commonly seen in the upper lobes because of repeated inflammation and mucoid impaction. If untreated, the disease progresses to extensive bronchiectasis and end-stage pulmonary fibrosis, leading to respiratory and right heart failure . ABPA的影像学表现多种多样，分为急性或慢性。在急性期，多达50%的病例最初的胸部X线是正常的。在胸部X线异常的患者中，最常见的(高达90%)表现是肺实质内边界不清的游走性阴影或“一过性阴影”，多累及上叶。支气管壁增厚表现为双轨征或印戒指征。黏液嵌顿可发生在大气道，并可延伸到较小的支气管，导致典型的“指套征”，外观特征是分支样、锥形管状阴影，由中心产生、延伸到外周(图6)。充满粘液的中心性支气管扩张可引起肺门周围阴影和/或纵隔淋巴结肿大。在发展成嗜酸性脓肿的患者中可以看到液平(图6)。支气管扩张内的高衰减粘液是ABPA的一个特征性CT表现(图7)。CT所见的高张力黏液堵塞目前归因于钙盐和金属(铁和锰)或干燥黏液的存在。致密粘液在CT上也可能出现钙化。ABPA的其他CT表现为小叶中心结节，可呈“树芽”分布，肺内有斑片状的马赛克衰减区，继发于小气道疾病和空气滞留区域。支气管中央结节在合并ABPA的哮喘患者中比未合并ABPA者多见。慢性变化表现为支气管扩张和纤维化，常见于上叶，因为反复炎症和粘液嵌塞。如果不治疗，这种疾病会导致广泛的支气管扩张和终末期肺纤维化，导致呼吸衰竭和右心衰。
Bronchocentric Granulomatosis 支气管中心性肉芽肿Bronchocentric granulomatosis is a rare disorder characterized by a destructive necrotizing granulomatous inflammation centered around bronchial and bronchiolar walls, with associated chronic inflammatory changes in the surrounding lung parenchyma . About one-third to one-half of cases are associated with eosinophilia, asthma, ABPA, and histopathologic manifestations of fungal hypersensitivity . Although bronchocentric granulomatosis can affect any age group, the peak is seen in the 4th–7th decades, with nonspecific symptoms such as fever, night sweats, cough, dyspnea, and pleuritic chest pain. 支气管中心性肉芽肿病是一种罕见的疾病，其特征是以支气管和细支气管壁为中心的破坏性坏死性肉芽肿性炎症，伴随着周围肺实质的慢性炎症改变。大约三分之一至一半的病例与嗜酸性粒细胞增多症、哮喘、ABPA和真菌过敏的组织病理学表现有关。虽然支气管中心性肉芽肿病可以发生于任何年龄组，但高峰出现在40至70岁，伴有非特异性症状，如发烧、盗汗、咳嗽、呼吸困难和胸痛。 Radiographic manifestations of bronchocentric granulomatosis are varied and nonspecific, with little correlation to the clinical presentation; thus histologic confirmation is required for diagnosis . Imaging findings include parenchymal consolidation, endobronchial soft tissue, lung nodules, and masses that are unilateral with upper lobe predominance (Fig 8). Solitary nodules are more common than multiple lesions. Reticulonodular pattern, hilar lymphadenopathy, and pleural involvement are rare. 支气管中心性肉芽肿病的影像学表现多种多样，非特异性，与临床表现几乎不相关，因此需要进行病理学证实。影像学表现包括肺实质实变、支气管内软组织、肺结节和单侧上叶为主的肿块（图8）。相比多发病灶，孤立结节更多见。网状结节、肺门淋巴结肿大、胸膜受累少见。
Pleuropulmonary Parasitic Infections 胸膜肺寄生虫感染Parasitic infections of the lung are seen worldwide and are a major cause of morbidity. The lungs are affected in various ways. Larvae can enter the lungs during the migration phase of their life cycle before reaching their target destinations, or there can be direct invasion. The disease can be a primary infestation, an allergic reaction, or a feature of more generalized disease . Lung parasites that can cause pulmonary eosinophilia as well as pulmonary opacities are Strongyloides stercoralis, Paragonimus westermani, Ascaris lumbricoides, Schistosoma haematobium, Wuchereria bancrofti, Brugia malayi, Ancylostoma duodenale, and Necator americanus, of which S stercoralis and P westermani are discussed here. 肺部寄生虫感染在世界范围内普遍存在，是发病率的主要原因。肺部受到不同类型的影响。幼虫在到达目的地之前，可以在生命周期的迁移阶段进入肺部，也可以直接入侵。这种疾病可能是一种初级侵袭，一种过敏反应，或更广泛性疾病的一个特征。可引起肺嗜酸性粒细胞增多和肺浸润的肺寄生虫有肠类圆线虫、卫氏并殖吸虫、蛔虫、嗜血血吸虫、班氏乌氏菌、马来丝虫、十二指肠钩虫和美洲钩虫。 S stercoralis infection occurs when larvae from soil penetrate the skin and travel to the lungs through the blood. At presentation, patients may have peripheral blood eosinophilia, rash, and transient pulmonary opacities or may remain clinically asymptomatic for decades unless hyperinfection or dissemination occurs. Strongyloides hyperinfection is a life-threatening condition with a high mortality rate and is associated with immunocompromised status, hematologic malignancies, and malnutrition . At chest radiography, rapidly developing bilateral airspace opacities are seen mimicking findings of multifocal pneumonia or acute respiratory distress syndrome pattern. Other pulmonary findings are reticulonodular opacities, cavitary or miliary nodules, lung abscesses, and pleural effusions (Fig 9). 当土壤中的幼虫穿透皮肤并通过血液进入肺部时，就会发生卫氏并殖吸虫感染。患者可能有外周血嗜酸性粒细胞增多症、皮疹和短暂的肺部阴影，除非发生过度感染或扩散，否则可能在临床上数十年无症状。类圆线虫感染是一种危及生命的病症，死亡率高，与免疫功能低下、血液系统恶性肿瘤和营养不良有关。在胸部X线中表现为快速进展的双侧气腔阴影，类似多灶性肺炎或急性呼吸窘迫综合征的表现。其他肺表现为网状结节性阴影、空洞性或粟粒性结节、肺脓肿和胸腔积液(图9)。 Paragonimiasis, caused by infection by P westermani, occurs when infected raw or undercooked crustaceans are consumed. A recent outbreak of paragonimiasis in the North American Midwest was due to consumption of raw crayfish infected with the species Paragonimus kellicotti . Two phases of disease are seen: the acute phase, when organisms are ingested and migrate to the lungs; and the chronic phase, when organisms reside and reproduce in the lung parenchyma. Radiologic findings usually correlate with disease stage and activity . The most common finding in the acute stage of paragonimiasis is unilateral or bilateral pleural effusion with or without pleural thickening or empyema and is seen in almost all cases because of migration of P westermani into the pleural space . Airspace consolidation and pulmonary nodules are also common with parenchymal involvement (Fig 10). A linear migration track can be seen in up to 50% of cases. Other findings associated with paragonimiasis include pneumothorax, empyema, and mediastinal lymphadenopathy . Bronchiectasis and cavity formation may be encountered in the chronic stage of infection. The diagnosis is usually confirmed by identifying the eggs of the parasite in the sputum or pleural or BAL fluid. 食用生甲壳动物或未充分煮熟的甲壳类动物，会导致卫氏并殖吸虫感染，引起的肺吸虫病。最近在北美中西部爆发卫氏并殖吸虫病，原因是食用了感染卡利科蒂并殖吸虫的生小龙虾。疾病可分为两个阶段：急性期，有机体被摄入并迁移到肺部；慢性期，生物体在肺实质中寄生和繁殖。放射学表现通常与疾病的分期和活动有关。肺吸虫病急性期最常见的表现为，单侧或双侧胸腔积液伴或不伴胸膜增厚或脓胸，由于卫氏并殖吸虫迁移到胸膜间隙，这些征象在几乎所有的病例中都可以见到。气腔型实变和肺结节也是常见的实质受累征象(图10)。在50%的情况下可以看到线性偏移轨迹。肺吸虫病的其他表现包括气胸、脓胸和纵隔淋巴结肿大。在慢性感染阶段，可能会出现支气管扩张和空洞形成。诊断通常是通过鉴别痰、胸膜或BAL液中的寄生虫卵来确认的。 图9. 35岁女性，肾移植术后类圆线虫感染综合征。(a)胸片显示双侧网状结节及气腔阴影。(b)隆突下方薄层CT图像为双侧弥漫性磨玻璃影及结节状阴影。(c)右上叶经支气管镜活检标本可见类圆线虫幼虫。(H-E染色；×400.)
Idiopathic Hypereosinophilic Syndrome 特发性高嗜酸性粒细胞综合征Idiopathic hypereosinophilic syndrome, as the name suggests, is a primary hypereosinophilia without an underlying cause that is characterized by persistent marked eosinophilia (>1500 eosinophils/μL) for several months and evidence of eosinophil-mediated end organ damage. Hypereosinophilic syndrome is a multisystem disorder that can involve nearly every organ system. Cardiovascular and central nervous system complications of hypereosinophilic syndrome are a major source of morbidity and mortality. As many as 60% of patients with hypereosinophilic syndrome can have cardiac and/or pulmonary involvement. At imaging, pulmonary abnormalities are nonspecific and consist of nodules, ground-glass opacities, interlobular septal thickening, and pleural effusion (Fig 11). CT features include ground-glass opacities and consolidation in a patchy and peripheral distribution similar to that associated with chronic eosinophilic pneumonia. Unlike Churg-Strauss syndrome, there is no vasculitis. Other organs involved include the skin (urticaria and angioedema), nervous system (peripheral neuropathy and encephalopathy), bone marrow, spleen, gastrointestinal tract, and renal and musculoskeletal systems. Hypereosinophilic syndrome is differentiated from eosinophilic leukemia by the absence of immature eosinophils. 特发性高嗜酸性粒细胞综合征，顾名思义，是一种原发性嗜酸性粒细胞增多症，没有潜在的病因，其特征是持续数个月的嗜酸性粒细胞(>1500嗜酸性粒细胞/μL)，以及嗜酸性粒细胞介导的终末器官损害的证据。嗜酸性粒细胞增多综合征是一种多系统疾病，可累及几乎每个器官系统。心血管和中枢神经系统并发症是高嗜酸性粒细胞综合征发病和死亡主要原因。多达60%的高嗜酸性粒细胞综合征患者可能有心脏和(或)肺受累。在影像学上，肺部异常是非特异性的，包括结节、磨玻璃影、小叶间隔增厚和胸腔积液(图11)。CT表现包括磨玻璃影和实变，并呈片状及外周分布，与慢性嗜酸粒细胞性肺炎相似。与Churg-Strauss综合征不同，没有血管炎。其他累及的器官包括皮肤(荨麻疹和血管神经性水肿)、神经系统(周围神经病变和脑病)、骨髓、脾脏、胃肠道、肾脏和肌肉骨骼系统。高嗜酸性粒细胞综合征与嗜酸性粒细胞白血病不同，没有未分化成熟的嗜酸性粒细胞。
图11. 12岁男童，高嗜酸性粒细胞综合征，持续性咳嗽、呼吸急促、外周血嗜酸性粒细胞增多(1700个/μL)。(a)胸片显示双侧片状气腔和结节状阴影。(b，c)胸部薄层CT平扫提示远端气管(b)和心脏(c)水平层面可见双侧弥漫性结节和磨玻璃影，主要位于肺底部。(该病例由哥伦比亚波哥大国立大学医学博士Jorge Carrillo提供。) 彩虹、麦子校对 未完待续 资料来源： |
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