Recently, air pollution has become more and more severe globally and has decreased the quality of life significantly in subjects with or without allergic diseases. Air pollution more severely affects patients with allergic diseases, including allergic rhinitis (AR); therefore, it could devastate quality of life. Many epidemiological studies have shown that air pollutants increased outpatient clinic visits as well as the prevalence/severity of AR and decreased quality of life in patients with AR. Traffic-related air pollution also increases the severity and occurrence rate of AR, and heavy traffic is also associated with an increased prevalence of AR. Immunologically, air pollutants increase airway inflammation and mucin production by triggering the generation of reactive oxygen species and inducing the nucleotide-binding domain, leucine-rich repeat protein 3 inflammasome and apoptosis. Since air pollution affects both the upper and lower airways and is known to be a risk factor for AR, proper diagnosis and treatment should be applied. In this review article, we will address several epidemiological and clinical studies about the effects of air pollution on AR, mechanisms by which air pollutants aggravate AR, and treatment of AR triggered by air pollutant. (Allergy Asthma Respir Dis 2021;9:3-11)

Purpose: Respiratory virus infection is a common cause of hospitalization in children. Rapid testing for respiratory viruses, such as the FilmArray method, can be clinically useful. However, insufficient evidence exists to support its use in standard clinical care.
Methods: We retrospectively analyzed data from children under 18 years old who received the multiplex real-time polymerase chain reaction array (multiplex RT-PCR) method in 2017 and by FilmArray respiratory panel (FilmArray RP) in 2018.
Results: Between January, 2017 and December, 2018, we reviewed data from 1,480 hospitalized children. The number of children with virus detection in respiratory viral PCR was 523 in the multiplex RT-PCR method and 419 in the FilmArray method. Seasonal virus outbreak patterns were similar to those of Korea Centers for Disease Control and Prevention in both groups. There was no difference between the 2 groups in the mean length of hospital stay. The time from admission to isolation by influenza infection was significantly shorter in the FilmArray group than in the multiplex RT-PCR group among patients who were not diagnosed with influenza infection by rapid antigen test at the time of admission.
Conclusion: The use of FilmArray method for respiratory viruses did not diminish length of hospital stay. However, the FilmArray method may quickly detect the prevalence of respiratory infection and aid in clinical treatment. In addition, it was related with a reduced time from admission to isolation by influenza infection in hospitalized children who were not identified with influenza infection by rapid antigen test at the time of admission. (Allergy Asthma Respir Dis 2021;9:12-20)

Purpose: Congenital pulmonary airway malformation (CPAM) is a rare developmental abnormality of the lungs. We investigated clinical characteristics of CPAM based on patient age at diagnosis.
Methods: In this retrospective study, we analyzed the medical records of 51 patients diagnosed with CPAM at Pusan National University Hospital between January 2000 and December 2019.
Results: We investigated 39 children and 12 adults. The mean age at the diagnosis of the patients was 15.9±14.3 years. The mean ages of children and adults at the time of diagnosis of CPAM were 6.8±5.8 years and 31.2±10.2 years, respectively. Among the 51 patients investigated, 20 (39%) were asymptomatic and 31 (61%) showed clinical symptoms, such as dry cough, recurrent respiratory infections, and dyspnea at the time of diagnosis. Notably, clinical symptoms at diagnosis were observed in 28 children (72%) and in only 3 adults (25%) (P=0.006), and children were more symptomatic than adults. Children with large cysts tended to be more symptomatic than those with small cysts (P<0.001). Combined anomalies were detected in 12 patients (23%). Patients with cystic lesions in the right lower lobe of the lung showed a higher prevalence of combined anomalies (P=0.015). Surgical resection was performed in 40 patients (78%), and all patients showed good prognosis.
Conclusion: This study revealed that the presence of clinical symptoms of CPAM differed between children and adults, depending on the age at diagnosis and that patients with cysts in the right lower lobe of the lungs tended to show a higher prevalence of combined anomalies. (Allergy Asthma Respir Dis 2021;9:21-26)

Purpose: Asthma is a chronic airway inflammatory disorder and is associated with macrophages. Statin, a well-known lipid-lowering agent, has recently been noted for its anti-inflammatory effect on macrophage. This study was designed to evaluate the antiasthmatic effect of atorvastatin via modulation of macrophage activation by using an animal model of allergic asthma.
Methods: Atorvastatin 40 mg/kg was given by gavage once a day for 3 days before challenge of ovalbumin (OVA); airway hyperre-sponsiveness (AHR), airway inflammatory cells, and cytokines were evaluated in the murine asthma model. The direct effect of atorvastatin on the activation of macrophages in vitro was determined using the alveolar macrophage cell line CRL-2456.
Results: Administration of atorvastatin reduced the numbers of total inflammatory cells, macrophages, and eosinophils as well as lung histology enhanced in the murine asthma model. AHR measured by enhanced pause was significantly reduced after atorvastatin administration in the murine asthma model (P<0.05). Atorvastatin administration resulted in the reduction in serum OVA-specific IgE levels and the increase in serum OVA-specific IgG2a levels (P<0.05). The mRNA levels of Ccr3, Il-17, and Muc5ac enhanced by OVA challenge were decreased by treatment with atorvastatin (P<0.05). Along with these improvement in allergic inflammatory changes, the population of CD11c-CD206+ macrophages as well as the expression of Ym-1 and Relm-α in the lungs were reduced with atorvastatin (P<0.05). In vitro test with CRL-2456 showed that atorvastatin reduced the expression of Cd206, Arg-1, and Fgf-2 induced by IL-4 stimulation (P<0.05).
Conclusion: This study highlighted the antiasthmatic effect of atorvastatin on the suppression of M2 macrophage activation in allergic asthma. (Allergy Asthma Respir Dis 2021;9:27-35)

Mycoplasma pneumoniae pneumonia is one of the most common causes of community-acquired pneumonia in school-aged pediatric patients. Its severity varies ranging from mild respiratory symptoms to severe complications with atypical pneumonia. It can rarely produce nonpulmonary manifestations including thrombosis. We report a case of a 10-year-old girl with M. pneumoniae pneumonia accompanied by pulmonary embolism and splenic infarction. She was readmitted with fever and left lower chest pain when coughing and left upper abdominal pain. Chest radiography showed abnormalities in the lower lobe of the left lung and pleural effusion. Blood tests revealed an elevated C-reactive protein level. Chest computed tomography (CT) showed left pleural effusion, thromboembolism of the descending branch of the right pulmonary arterial as well as infarction at the upper portion of the spleen. Laboratory evaluations revealed positivity to antimycoplasma antibodies; IgM, sputum mycoplasma polymerase chain reaction, anticardiolipin IgM (18MPL: normal<11), and IgG (32GPL: normal<23). She was treated with intravenous clarithromycin and low-molecular heparin (LMWH, 1 mg/kg/day). Chest CT was performed on the 6th day of hospitalization, which showed improvement in thrombosis. We administered warfarin instead of LMWH to achieve an international normalized ratio 2.0-3.0. On the 11th day of hospitalization, the patient was uneventfully discharged. Following her discharge, we continued to administer warfarin to the patient. Three months later, we noticed that pulmonary embolism and splenic infarction had disappeared. (Allergy Asthma Respir Dis 2021;9:36-41)

Severe respiratory difficulty can be more prominent, when combined with severe pectus excavatum and cardiovascular manifestations in infants with Marfan syndrome. There have been few reports on severe laryngomalacia as a cause of severe respiratory difficulty in an infant with Marfan syndrome. A 1-month-old boy was admitted due to severe respiratory difficulty. Immediately after birth, he had dysmorphic features, such as micrognathia, wrinkles on the forehead, and down-slanting palpebral fissures. On echocardiography, aortic root dilation with a mitral valve prolapse was observed. Due to severe laryngomalacia accompanied by severe respiratory difficulty and feeding difficulty, a partial epiglottectomy was performed at 1 month of age. After the surgery, suprasternal retraction and inspiratory stridor disappeared, and he started gaining weight with improvement in respiratory difficulty. On whole exome sequencing, a missense mutation on the FBN1 gene (c.3560A>C on exon 29, p.His1187Pro, calcium-binding epidermal growth factor-like #21) was identified. Despite higher perioperative risk due to comorbidities in Marfan syndrome, early intervention of laryngomalacia can be helpful in improving quality of life even in infants with Marfan syndrome. (Allergy Asthma Respir Dis 2021;9:42-45)

Nonepisodic angioedema with eosinophilia (NEAE) is a rare disease characterized by nonrecurrent angioedema with eosinophilia and normal serum IgM levels occurring predominantly in an East Asian female population. A 49-year-old male patient visited our clinic due to swelling of both the scrotums and the lower extremities, and fever. He had history of nasal polyp, cephalosporin allergy, and asthma. He was diagnosed as having NEAE and was treated with systemic corticosteroid, then he was symptom-free for more than 8 months. He had been administered omalizumab for 3 months due to uncontrolled asthma prior to the onset of angioedema which had helped taper the oral corticosteroid, and this may be associated with presentation of NEAE. Here, we report a case of NEAE in a male patient which presented with constitutional symptoms such as fever and scrotal edema. (Allergy Asthma Respir Dis 2021;9:46-49)

Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare systemic disease and a potentially life-threatening systemic necrotizing vasculitis predominantly affecting small vessels. Herein, we describe a 47-year-old man with EGPA misdiagnosed as non-ST-segment elevation myocardial infarction. He presented to the Emergency Department with indigestion and diarrhea. He had been diagnosed with asthma and chronic rhinosinusitis 3 years earlier and was taking antibiotics due to worsening sinusitis. In laboratory tests, peripheral blood eosinophils, serum creatinine, and serum troponin were elevated to 4,641 cells/μL, 13.40 ng/mL, and 1.26 ng/mL, respectively. Electrocardiography showed ST-segment depression on the inferior wall, and echocardiography indicated an ischemic insult in the right coronary artery territory. A non-ST-segment elevation myocardial infarction as well as antibiotic-associated diarrhea, eosinophilia and acute kidney injury was initially suspected. However, fever persisted and eosinophilia worsened despite cessation of antibiotics after admission. There was no significant stenosis of the coronary arteries on coronary angiography. Meanwhile, abdominal computed tomography suggested medical renal disease, and magnetic resonance imaging showed late gadolinium enhancement at the mid wall and the subepicardial area in the left ventricle of the heart. As a workup for eosinophilia, serum anti-MPO was measured and turned out to be positive. A kidney biopsy was performed, which yielded membranous nephropathy superimposed on antineutrophil cytoplasmic antibodies-mediated crescent formation. He was diagnosed as EGPA with cardiac and renal involvement, and received systemic steroid, cyclophosphamide, and plasmapheresis. Then, peripheral eosinophil counts and renal function were normalized. He is now in clinical remission even after stopping the use of steroids and immunosuppressive agents. (Allergy Asthma Respir Dis 2021;9:50-55)