Yoshiro Kai

Chronic rhinosinusitis with nasal polyp (CRSwNP) is a type 2 inflammatory disease frequently associated with asthma. Patients with CRSwNP are typically treated with endoscopic sinus surgery and oral corticosteroids. However, they often experience recurrence; in addition, oral corticosteroids have several adverse effects. CRSwNP is an important factor influencing asthma control, and total control of both CRSwNP and asthma is important for treatment. Dupilumab and mepolizumab, which are anti-interleukin (IL)-4R and anti-IL-5 monoclonal antibodies, respectively, have been approved for the treatment of severe asthma and CRSwNP. Here, we discuss the successful treatment of a patient with severe asthma comorbid with CRSwNP after switching from dupilumab and mepolizumab to tezepelumab. The patient was initially treated with high-dose inhaled corticosteroids/long-acting β2-agonist/long-acting muscarinic antagonist treatment, without success. Treatment with dupilumab improved asthma and CRSwNP; however, it later induced hypereosinophilia with exacerbated asthma. Although subsequent treatment with mepolizumab improved asthma, the nasal symptoms recurred. After attempting dupilumab treatment again, the nasal symptoms improved; however, the asthma symptoms worsened parallel with an increased eosinophil count. Finally, the antithymic stromal lymphopoietin monoclonal antibody tezepelumab, was selected for treatment; the worsening asthma symptoms then improved with the control of CRSwNP. This report illustrates the potential utility of tezepelumab for the treatment of asthma and CRSwNP. Tezepelumab therapy may enhance total control of comorbidities of both the upper and lower airways. Further studies are required to identify effective therapies for asthma and CRSwNP.

Sarcoidosis is a multisystemic granulomatous disease that is frequently localized in the lungs and lymph nodes. We herein report a case of pulmonary sarcoidosis secondary to shin'iseihaito administration. During remission with 5 mg prednisolone/day of maintenance treatment, chest computed tomography revealed a mass in the left lower lobe with re‐enlarged bilateral hilar/mediastinal lymph nodes. Transbronchial lung biopsy of the mass and endobronchial ultrasound‐guided transbronchial needle aspiration of mediastinal lymph nodes revealed adenocarcinoma and noncaseating granulomas, respectively. Based on these findings, the patient was diagnosed with sarcoidosis recurrence associated with lung cancer without cancer metastasis. We present the case of sarcoidosis recurrence associated with lung cancer after drug‐induced pulmonary sarcoidosis with lung injury. To our knowledge, this is the first report of sarcoidosis triggered by drug administration and lung cancer. Histological diagnosis of mediastinal lymphadenopathy with lung cancer is essential for differentiating metastasis from sarcoidosis.

Severe asthma affects approximately 5%–10% of patients with asthma. Herein, we describe a case of non‐type 2 asthma that progressively worsened over the years. An 80‐year‐old woman was diagnosed with asthma 11 years back. She experienced repeated exacerbations requiring treatment with systemic corticosteroid despite therapy with medications including high‐dose inhaled corticosteroids/long‐acting beta‐agonists plus long‐acting muscarinic antagonist. The patient presented with non‐eosinophilic asthma. Therefore, the patient was initially treated with bronchial thermoplasty, which was effective for 1 year only. Treatment with bronchial thermoplasty, benralizumab, dupilumab, and mepolizumab was ineffective. The fourth treatment, which included tezepelumab, was initiated. The patient's symptoms and quality of life improved significantly. This is the first case of a patient who did not respond to sequential bronchial thermoplasty, benralizumab, dupilumab, and mepolizumab but who presented with good clinical response to tezepelumab. Therefore, tezepelumab may be useful for patients with non‐type 2 asthma.

Chronic eosinophilic pneumonia (CEP) is an eosinophilic lung disease. Treatment for CEP includes corticosteroids; however, CEP often recurs. A 53‐year‐old woman was referred to our hospital because of poorly controlled asthma. She was treated with combination of moderate‐dose inhaled corticosteroid (ICS), a long‐acting β2‐agonist (LABA), and betamethasone/dexchlorpheniramine. She was switched to single‐inhaler triple therapy, after which her asthma control improved; thus, betamethasone/dexchlorpheniramine was discontinued. Ten weeks later, she was diagnosed with CEP due to marked eosinophilia and pulmonary eosinophilic infiltrates. Oral corticosteroid treatment was initiated, symptoms improved, and peripheral blood eosinophilia decreased with improved infiltrative shadows. Remission induction therapy was initiated with benralizumab combined with corticosteroid therapy. Eosinophilia and inflammatory responses decreased. After 7 months, corticosteroid was discontinued, and she was treated with benralizumab alone. She remained in remission for 4 months. This case suggests that benralizumab may be useful as a remission induction therapy in patients with CEP.