Allergic bronchopulmonary aspergillosis treated successfully with omalizumab.

Allergic bronchopulmonary aspergillosis (ABPA) is caused by a hypersensitivity response of type 2 T helper (Th2) lymphocytes to antigens, mostly Aspergillus fumigatus (A. fumigatus).1 This abnormal host response to A. fumigatus in a subset of patients with asthma or cystic fibrosis (CF) is likely due to genetic susceptibility that predisposes patients to the risk of developing ABPA. This is characterised by an increased total IgE and Aspergillus-specific IgE, IgG, and IgA in the serum and bronchoalveolar lavage.2 The International Society for Human and Animal Mycology (ISHAM) and the Rosenberg--Patterson criteria are most often used to diagnose ABPA.3,4 Omalizumab is a humanized monoclonal anti-IgE antibody with licensed indication in severe allergic asthma. There are clinical studies that have also shown benefit in the use of omalizumab in ABPA patients without and with cystic fibrosis.5,6 However, the safety and efficacy of omalizumab in ABPA needs further evidence. The authors described a 45-year-old caucasian man with long standing atopic asthma with frequent exacerbations, and ABPA diagnosed at the age of 42 years. CF was excluded. At the time of ABPA diagnosis, his predicted forced expiratory volume in 1 s (FEV1) was 58% and after bronchodilator was 62%. All Rosenberg--Patterson criteria were met, including central bronchiectasis with pulmonary infiltrates in all lobes evidenced in a thoracic CT scan. Peripheral blood eosinophils were 570/mm3 under systemic steroids, total IgE was 2674 IU/mL and AF-specific IgE was 30.50 kU/L. No precipitating antibody against AF antigen was found. The patient was treated with prednisolone 40 mg/day, inhaled salmeterol/fluticasone propionate combination 50/500 mcg twice a day and montelukast 10 mg/day. We could not taper the prednisolone dose because of frequent exacerbations. Oral itraconazole was not administered because the