The most frequent affected IgG subclass was IgG3 (58.27%), accompanied by IgG4 (11.02%) and IgG2 in addition IgG3 (7.09%) (Fig. those without PID was categorized as the non-PID group. IgG subclass insufficiency (58%) can be most common, among which IgG3 subclass insufficiency was most common (58%). The comparative threat of asthma exacerbation was 1.70 times higher in the Digoxigenin PID group set alongside the non-PID group (1.696; 95% self-confidence period, 1.284 to 2.239; < 0.001); the prevalence of serious asthma was considerably higher in the PID group than in the non-PID group (32.48% vs. 13.00%, < 0.001). Thirty-five among 157 individuals in the PID group d taken care of IVIG to avoid asthma exacerbation. Conclusions It's advocated that PID, Digoxigenin igG3 subclass deficiency especially, is a substantial risk element for asthma exacerbation. Testing of IgG subclass IVIG and amounts replacement unit is highly recommended in the administration in adult asthmatics. Keywords: Asthma, Immunologic insufficiency syndromes, Prevalence, Asthma exacerbation, Immunoglobulins Intro Major immunodeficiency (PID) can be caused by problems of innate and/or adaptive immune system systems. PID includes a large clinical spectral range of acquired and congenital forms in the pediatric human population [1]; nevertheless, the prevalence of adult-onset PID isn't common [2]. Even though the prevalence of PID in the overall human population continues to be reported as 1:10,000 to at least one 1:1,200 in Traditional western countries, it varies with regards to the types of PID and cultural groups. A earlier report demonstrated how the prevalence of PID was 11.25/1,000,000 inside a Korean pediatric human population [1], as the prevalence Digoxigenin of PID within an adult human population isn’t reported in Korea. Main medical top features of PID in adults are repeated infections in various organs, in which recurrent top and lower respiratory infections, such as pneumonia and sinusitis, are characteristic. Furthermore, these repiratoty infections are known as major triggering factors for asthma exacerbation in adult asthmatics [3]. Recently, we shown that immunoglobulin G3 (IgG3 ) subclass deficiency (IgG3 SCD) is the most common type of PID associated with asthma exacerbation in adult asthmatics [4], in which regular monthly intravenous immunoglobulin (IVIG) therapy was beneficial Digoxigenin for avoiding asthma exacerbation [5]. We hypothesized that PID is definitely associated with frequent asthma exacerbations and severe asthma in adult asthmatics. The present study aimed to evaluate the prevalence/characteristics of PID individuals and to analyze its association with asthma exacerbation inside a cohort of adult asthmatics. METHODS Study subjects This is a retrospective study to enroll 2,866 adult asthmatics that experienced went to the Division of Allergy and Clinical Immunology of Ajou University or college Hospital, Suwon, South Korea, from April 1994 to March 2016 and was authorized by the Institutional Review Table of the Ajou University or college Hospital (IRB No. AJIRB-MED-MDB-17-432). Written educated consent from the individuals was waived due to a retrospective nature of our study. A analysis of asthma was founded by typical medical symptoms (such as wheezing, dyspnea, and cough), evidence of airway reversibility (defined as pressured expiratory volume of 1 second [FEV1 ] > 12% or 200 mL from pre-bronchodilator use) and/or airway hyperresponsiveness to methacholine (defined as a methacholine concentration causing FEV1 fall of 20% or a methacholine concentration of < 16 mg/mL) according to the Global Initiative for Asthma guideline. Severe asthma was defined according to the Western Respiratory Society/American Thoracic Society guideline [6]. Asthma exacerbation was defined when subjects who had managed anti-asthmatic medications and had episodes of sign worsening requiring systemic corticosteroids (prednisolone equal dose of 15 mg per day for 3 consecutive days). Demographic data on the study subjects, including age, sex, previous medications, associated allergic diseases as well as laboratory findings, were collected. Any individuals having comorbid conditions and malignancies to impact PID and asthma exacerbation were excluded. Results of pores and skin prick screening and spirometry performed at the initial check out Digoxigenin were collected. Atopy was defined as (1) at least one positive result in serum specific IgE or (2) more than 1 positive skin-prick test response to aeroallergens (pet cats, dogs, house dust mites, trees, TRADD grasses, weeds, or fungi). Using the skin prick test, a imply wheal diameter of 3 mm or a imply erythema diameter of 10 mm in the absence of any reaction to the bad control was considered to indicate a positive reaction. Total IgE and specific IgE levels in sera were measured from the Immuno CAP system (ThermoFisher Scientific, Waltham, MA, USA). Sputum eosinophil/neutrophil counts were assessed; eosinophilic asthma was defined as study subjects having sputum eosinophilia of 3%, while neutrophilic asthma was defined as those having sputum neutrophilia of 65%. The PID group was defined as a group of asthmatics with.