Nevertheless, the role of eosinophils in mucus hypersecretion and airway hyperresponsiveness is still controversial on the basis of studies involving eosinophil\deficient mice in an asthma model [3]. Asthma is increasingly recognized as a heterogeneous disease involving multiple phenotypes and endotypes, such as eosinophilic or non\eosinophilic [4]. was removed by bronchofiberscopy and the atelectasis was completely resolved. No exacerbation has been observed for nine months after discontinuation of benralizumab and initiation of erythromycin. This is the first documented case that developed atelectasis by mucoid impaction during treatment with anti\IL\5 receptor antibody. strong class=”kwd-title” Keywords: Asthma, atelectasis, benralizumab, interleukin\5, mucus hypersecretion Abstract We herein report a case of a patient who developed massive atelectasis by mucoid impaction during treatment with anti\interleukin (IL)\5 receptor antibody. Introduction Asthma remains a significant cause of mucoid impaction of the airways and mortality. Mucoid impaction results from increased mucus production, which is often caused by eosinophilic inflammation in asthma, as is typically seen in allergic bronchopulmonary aspergillosis (ABPA). Benralizumab is an interleukin\5 (IL\5) receptor \directed cytolytic monoclonal antibody that reduces rapid and nearly complete depletion of eosinophils by enhancing antibody\dependent cell\mediated cytotoxicity, which is an apoptotic process of eosinophil elimination [1]. The depletion of eosinophilic inflammation is expected to reduce mucus hypersecretion and mucoid impaction; however, we herein report a case of a patient who developed massive atelectasis by mucoid impaction during treatment with anti\IL\5 receptor antibody. Case Report A 75\year\old non\smoking female patient was referred to our hospital for an asthma attack. She had LDK-378 been previously LDK-378 treated for uncontrolled bronchial asthma with multiple drugs, including inhaled corticosteroids, long\acting \agonists, and leukotriene receptor antagonists, for 28?years. She had LDK-378 allergic rhinitis and sinusitis, but not nasal polyps or atopic dermatitis. At initial visit, wheezes were heard on auscultation. The laboratory data showed an elevated C\reactive protein level (7.24?mg/dL) and neutrophil count (9510/L). The blood eosinophil count, serum immunoglobulin (Ig) E, and fractional exhaled nitric oxide (FeNO) were 210C692/L, 159?IU/mL, and 28?ppb, respectively. Specific IgE and IgG to Aspergillus and anti\neutrophil cytoplasmic antibodies were negative. The forced expiratory volume in 1 sec was 1.18?L (FEV1%: 65.6%). Chest X\ray (Fig. ?(Fig.1A)1A) and thoracic computed tomography (CT) (Fig. ?(Fig.2A)2A) demonstrated bronchial wall thickening and centrilobular nodules diffusely in both lungs, without central bronchiectasis. Following treatment with antibiotics and systemic corticosteroids, treatment with benralizumab was initiated. Open in a separate window Figure 1 (A) Chest X\ray at initial visit. (B) Chest X\ray on exacerbation of the atelectasis, leading to the tracheal deviation. (C) Chest X\ray showing a complete resolution of the atelectasis. Open in a separate window Figure 2 (A) Thoracic computed tomography (CT) at initial visit. Transverse (B) and coronal (C) view of thoracic CT on readmission, showing atelectasis by mucoid impaction in the left lung. (D) Thoracic CT on day 17 of readmission, showing a complete resolution of the atelectasis. Four months later, she was readmitted to our hospital for severe respiratory failure. Physical examination revealed decreased respiratory sounds in the left lung. LDK-378 Thoracic CT (Fig. 2B, C) demonstrated atelectasis by mucoid impaction in the left lung. The laboratory data showed elevated C\reactive protein level (9.25?g/dL) and neutrophil count (8310/L). Blood eosinophils were almost completely depleted, and the serum IgE level was not elevated. Pathogens, including bacteria and fungus, and CharcotCLeyden crystals were not detected in the sputum (0.75% of eosinophil counts). Systemic corticosteroids, antibiotics, and expectorants were administered; however, her respiratory condition exacerbated on the next day, due to the massive atelectasis leading to the tracheal deviation, to the extent that nasal high\flow therapy was required (Fig. ?(Fig.1B).1B). The thick mucus was removed from the left main bronchus and the lower lobe bronchi by bronchofiberscopy and a complete resolution of the atelectasis was confirmed by chest X\ray (Fig. ?(Fig.1C)1C) and thoracic CT (Fig. ?(Fig.2D)2D) on day 17 of readmission. No exacerbation has been observed for nine months after discontinuation of benralizumab and initiation of erythromycin. Discussion This is the first documented case of a patient who developed atelectasis by mucoid impaction during treatment with an anti\IL\5 receptor antibody. Benralizumab treatment nearly completely depleted the eosinophils in blood, which is consistent with the previous report [2]. In that report, benralizumab produced decrease from baseline of 95.8% in airway mucosal eosinophils, 89.9% in sputum, and 100% in blood, 12?weeks after treatment. These LDK-378 data raise the intriguing question: What Rabbit polyclonal to AGAP is the cause of mucus development during anti\IL\5 therapy? Eosinophilic inflammation has a pivotal role in mucus plug formation. Recent evidence highlighted the eosinophil\derived cytolytic extracellular.