Greenberger P A
Zentralbl Bakteriol Mikrobiol Hyg A. 1986 Jul;261(4):487-95. doi: 10.1016/s0176-6724(86)80081-5.
Allergic bronchopulmonary aspergillosis (ABPA) is much more common than originally suspected, can have its onset in childhood and remain undiagnosed for years or decades, at which time it presents in a patient with end-stage fibrotic lung disease. In other patients, ABPA may cause a finite number of roentgenographic lesions and not be associated with chronic sputum production or widespread bronchiectasis. Clinical symptoms range from the patient being asymptomatic with a new roentgenographic infiltrate being suspected only by a sharp elevation of total serum IgE to wheezing dyspnea or status asthmaticus. Serologic assays that are of major value in diagnosis of ABPA include elevation of total serum IgE--not all of which is directed against Aspergillus fumigatus, precipitating antibodies to A. fumigatus--unless the patient is in remission, and elevated serum IgE-A. fumigatus and IgG-A. fumigatus compared to serum from patients with asthma with immediate cutaneous reactivity to A. fumigatus but without evidence of ABPA. Five stages have been identified which reflect the time of recognition of ABPA and disease activity. They are Acute, Remission, Recurrent Exacerbation, Corticosteroid-Dependent Asthma, and Fibrotic. Stage I (Acute) patients have the classic clinical, serologic, and radiologic features of ABPA. Stage II (Remission) occurs after prednisone has resulted in resolution of the chest infiltrate and can be tapered and discontinued for 6 months without new infiltrates. Stage III (Exacerbation) occurs when a new roentgenographic infiltrate occurs associated with elevation of total serum IgE. Stage IV (Corticosteroid-Dependent Asthma) is present when repeated attempts to discontinue prednisone results in severe wheezing that cannot be prevented with other therapy. Some Stage IV patients continue to develop new ABPA infiltrates. Stage V (Fibrotic) patients have irreversible obstructive and restrictive pulmonary function abnormalities and may present or progress to respiratory failure and death.
变应性支气管肺曲霉病(ABPA)比最初怀疑的更为常见,可在儿童期起病,多年或数十年未被诊断,此时患者表现为终末期纤维化肺病。在其他患者中,ABPA可能导致有限数量的影像学病变,且与慢性咳痰或广泛支气管扩张无关。临床症状范围从患者无症状,仅因总血清IgE急剧升高怀疑有新的影像学浸润,到喘息性呼吸困难或哮喘持续状态。对ABPA诊断具有重要价值的血清学检测包括总血清IgE升高——并非所有升高均针对烟曲霉,烟曲霉沉淀抗体——除非患者处于缓解期,以及与对烟曲霉有即刻皮肤反应但无ABPA证据的哮喘患者血清相比,血清IgE-烟曲霉和IgG-烟曲霉升高。已确定五个阶段,反映了ABPA的识别时间和疾病活动情况。它们是急性期、缓解期、反复加重期、依赖糖皮质激素的哮喘期和纤维化期。I期(急性期)患者具有ABPA的典型临床、血清学和影像学特征。II期(缓解期)发生在泼尼松导致胸部浸润消退后,且可逐渐减量并停药6个月而无新的浸润。III期(加重期)发生在出现新的影像学浸润且总血清IgE升高时。IV期(依赖糖皮质激素的哮喘期)表现为反复尝试停用泼尼松导致严重喘息,且其他治疗无法预防。一些IV期患者继续出现新的ABPA浸润。V期(纤维化期)患者有不可逆的阻塞性和限制性肺功能异常,可能出现或进展为呼吸衰竭和死亡。