On page 289 of this paper, the x-axis title in Fig. 3A has been incorrectly spelled.

Some parts of Tables 1 and 2 in this paper was described incorrectly.

PURPOSE: Long-term treatment with inhaled steroids (ICS), especially fluticasone that developed lately, may suppress the hypothalamic-pituitary-adrenal (HPA) axis. This study investigated the relationship between ICS use and HPA axis suppression in asthmatics under ICS treatment for average 4.5 years. METHODS: The medical records of 129 adult asthmatics who received ICS treatment for 6 months or more and underwent a corticotropin stimulation test from January 2005 to August 2013 were retrospectively reviewed. RESULTS: The patients received ICS only (n=87) were found to have an abnormal response to the corticotropin test in as high as 32.2%, and those received ICS in combination with oral steroids (n=42) had a significantly higher prevalence of the response (71.4%, P<0.001). Abnormal responses to corticotropin occurred depending on ICS daily doses (low, n=8, 12.5%; medium, n=19, 36.8%; high, n=102, 49.0%; chi2=4.384, P=0.036). Among the subjects received ICS only, nasal steroid doses (P=0.016) but not ICS doses (P=0.159) were significantly higher in those with abnormal responses than the others. Among all the subjects, oral steroid use (odds ratio [OR], 4.27; 95% confidence interval [CI], 2.35-11.80; P<0.001) and nasal steroid dose (OR, 1.02; 95% CI, 1.00-1.04; P=0.015) were significant risk factors for HPA axis suppression. CONCLUSION: One-third of asthmatics under long-term treatment with ICS showed a suppression of the HPA axis in a dose-dependent manner. Oral or nasal steroid use may be a risk factor for the suppression. However, since our results may have been overestimated due to subject selection bias, further prospective case-control studies are warranted.
Adrenal Glands ; Adrenocorticotropic Hormone ; Adult ; Asthma* ; Axis, Cervical Vertebra* ; Case-Control Studies ; Humans ; Medical Records ; Prevalence ; Retrospective Studies ; Risk Factors ; Selection Bias ; Steroids* ; Fluticasone

The concept of personalized medicine for disease diagnosis, treatment, and management, considering individual variability, including susceptibility, clinical manifestations, and drug responsiveness, is a global emerging trend in medicine, which is also inevitable. However, clinical applications of personalized medicine in the real-world practice have been limited to certain cancers so far. Furthermore, this new concept to the diagnosis and treatment of adult asthma has not been applied to clinical use. Asthma is a multifactorial and heterogeneous disease. It seems to encompass a broad spectrum of clinical manifestations with different underlying pathophysiological mechanisms. Thus, it is not easy to categorize by their clinical features alone. Endotypical categorization that considering specific pathophysiological mechanisms will be more helpful in applying the concept of personalized medicine. The success of personalized medicine depends on patient selection for precise prescription of asthma medications. In the recent years, many investigators and physicians have devoted a lot of effort to the discovery of reliable biomarkers in asthmatic patients, which will be able to actualize the personalized medicine in near future. Despite such great efforts toward investigation of good biomarkers, few things have turned out to be practical in the clinic. Easily interpretable biomarkers of asthma are necessary to assess early detection, determination of treatment, prognosis prediction, and monitoring of exacerbation. Herein, we review recent studies regarding disease classifications and biomarkers of asthma.
Adult* ; Asthma* ; Biomarkers* ; Classification ; Diagnosis ; Humans ; Precision Medicine* ; Patient Selection ; Phenotype ; Prescriptions ; Prognosis ; Research Personnel

Hereditary angioedema is a disease of congenital deficiency or functional defect in the C1 esterase inhibitor (C1-INH) consequent to mutation in the SERPING1 gene, which encodes C1-INH. This disease manifests as recurrent, non-pitting, non-pruritic subcutaneous, or submucosal edema as well as an erythematous rash in some cases. These symptoms result from the uncontrolled localized production of bradykinin. The most commonly affected sites are the extremities, face, gastrointestinal tract, and respiratory system. When the respiratory system is affected by hereditary angioedema, swelling of the airway can restrict breathing and lead to life-threatening obstruction. Herein, we report a case of a 24-year-old woman with type 2 hereditary angioedema who presented with recurrent episodic abdominal pain and swelling of the extremities. She had no family history of angioedema. Although her C4 level was markedly decreased (3.40 mg/dL; normal range: 10-40 mg/dL), she presented with a very high C1-INH level (81.0 mg/dL; normal range: 21.0-39.0 mg/dL) and abnormally low C1-INH activity (less than 25%; normal range: 70%-130%). The SERPING1 gene mutation was confirmed in this patient. She was treated with prophylactic tranexamic acid, as needed, and subsequently reported fewer and less severe episodes. To our knowledge, this is the first reported case of type 2 hereditary angioedema in Korea that was consequent to SERPING1 mutation and involved a significantly elevated level of C1-INH as well as a low level of C1-INH activity.
Abdominal Pain ; Angioedema ; Angioedemas, Hereditary* ; Bradykinin ; Complement C1 Inhibitor Protein ; Edema ; Exanthema ; Extremities ; Female ; Gastrointestinal Tract ; Humans ; Korea ; Reference Values ; Respiration ; Respiratory System ; Tranexamic Acid ; Young Adult

Chronic urticaria may often be associated with interleukin (IL)-1-mediated autoinflammatory disease, which should be suspected if systemic inflammation signs are present. Here, we report a case of Schnitzler's syndrome without monoclonal gammopathy treated successfully with the IL-1 receptor antagonist anakinra. A 69-year-old man suffered from a pruritic urticarial rash for 12 years. It became aggravated episodically and was accompanied by high fever, arthralgia, leukocytosis, and an elevated C-reactive protein and erythrocyte sedimentation rate. The episodes each lasted for over one week. Neutrophilic and eosinophilic inflammation was found on skin biopsy. However, serum and urine electrophoresis showed no evidence of monoclonal gammopathy. The cutaneous lesions were unresponsive to various kinds of anti-histamines, systemic glucocorticoids, colchicine, cyclosporine, dapsone, and methotrexate, which were administered over a span of 3 years immediately preceding successful treatment. A dramatic response, however, was observed after a daily administration of anakinra. This observation suggests that the correct diagnosis of this case is Schnitzler's syndrome without monoclonal gammopathy. For an adult patient with refractory chronic urticaria and systemic inflammation, Schnitzler's syndrome could be considered as a possible differential diagnosis. Although the typical form of Schnitzler's syndrome exhibits the presence of monoclonal gammopathy as a diagnostic criterion, monoclonal gammopathy may be absent in an atypical form. In such a situation, an IL-1 antagonist should be effective for the management of chronic urticaria.
Aged ; Blood Sedimentation ; C-Reactive Protein/metabolism ; Chronic Disease ; Humans ; Interleukin 1 Receptor Antagonist Protein/therapeutic use ; Leukocytes/metabolism ; Male ; Paraproteinemias/complications ; Schnitzler Syndrome/blood ; Schnitzler Syndrome/drug therapy ; Urticaria/complications

PURPOSE: We aimed to analyze the frequency of eosinophilia-associated diseases and to search for possible markers that may be useful for their differential diagnosis. METHODS: We retrospectively reviewed the medical records of 148 patients with peripheral blood eosinophil count of more than 500/µL who visited the Allergy Department of Chonnam National University Hospital for the first time from January to December 2016. Blood eosinophilia was categorized as mild (<1,500/µL), moderate (1,500–5,000/µL), and severe (>5,000/µL). RESULTS: Blood eosinophilia was mostly caused by allergic diseases (41.9%), parasitic infestation (23.6%), and drug allergy (19.6%). Eosinophil count was higher in patients with parasitic infestation (P<0.01), drug allergy (P<0.01), hypereosinophilic syndrome (HES, P<0.001), or eosinophilic granulomatosis with polyangiitis (EGPA, P<0.001) than in those with allergic diseases. The eosinophilic cationic protein level was higher in patients with HES than in those with allergic diseases (P<0.05) and parasitic infestation (P<0.05). The total IgE level was lower in patients with HES than in those with parasitic infestation (P<0.05) and EGPA (P<0.05). The vitamin B12 level was higher in patients with HES than in those with parasitic infestation (P<0.05). There was no statistically significant difference in tryptase levels between the groups. The most common cause of mild eosinophilia was allergic diseases (59.8%), followed by parasitic infestation (22.7%) and drug allergy (13.4%). The common causes of moderate eosinophilia were drug allergy (37.8%), parasitic infestation (29.7%), and allergic diseases (10.8%). The common causes of severe eosinophilia were EGPA (28.6%), HES (21.4%), parasitic infestation (14.3%), and drug allergy (14.3%). CONCLUSION: Common causes of blood eosinophilia in patients who visit the allergy department are allergic diseases, parasitic infestation, and drug allergy. Several markers, including eosinophil count, total IgE, and vitamin B12, may be useful for the differential diagnosis of eosinophilia-associated diseases.
Diagnosis, Differential ; Drug Hypersensitivity ; Eosinophilia ; Eosinophils ; Granulomatosis with Polyangiitis ; Humans ; Hypereosinophilic Syndrome ; Hypersensitivity ; Immunoglobulin E ; Jeollanam-do ; Medical Records ; Parasitic Diseases ; Retrospective Studies ; Tryptases ; Vitamin B 12

Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome and toxic epidermal necrolysis (TEN) are severe cutaneous adverse reactions. Although viral reactivation is associated with DRESS syndrome, its role in TEN remains unclear. An 80-year-old woman visited our hospital because of fever and skin eruption. DRESS syndrome was diagnosed and was thought to caused by the use of the drug allopurinol. She was treated by discontinuation of the drug and administration of systemic steroids. She recovered from DRESS syndrome and was discharged from the hospital with tapering doses of steroids prescribed. One week after discharge, she visited our hospital again as the skin rash recurred and oral pain as well as oral and ocular mucosal lesions developed. In addition to the skin rash, blisters and Nikolsky's sign that were different from the skin lesions present in the previous DRESS syndrome were observed. Unlike those in DRESS syndrome, the viral serological test results were positive for anti-cytomegalovirus (CMV) IgM and CMV polymerase chain reaction. Therefore, it was thought that TEN was due to reactivation of CMV and she was treated this with ganciclovir and intravenous immunoglobulin. Here, we report a case of TEN caused by viral reactivation after DRESS syndrome developed after use of allopurinol which recovered after steroid treatment.
Aged, 80 and over ; Allopurinol ; Blister ; Cytomegalovirus Infections ; Cytomegalovirus ; Drug Hypersensitivity Syndrome ; Eosinophilia ; Exanthema ; Female ; Fever ; Ganciclovir ; Humans ; Immunoglobulin M ; Immunoglobulins ; Polymerase Chain Reaction ; Serologic Tests ; Skin ; Steroids ; Stevens-Johnson Syndrome

Purpose: Asthma phenotypes are often defined by relative cell counts of airway granulocytes. Induced sputum test results enable clinicians to determine the inflammatory phenotype of asthma based on the eosinophil and neutrophil counts. This study aimed to investigate clinical characteristics of patients with asthma according to the inflammatory phenotype of their condition. Methods: Data from 107 patients with asthma reported at a single tertiary allergy center in Korea during October 2016 to January 2019 were obtained. Patients were categorized into 4 asthma phenotypes based on the cell counts on the induced sputum test: eosinophilic, neutrophilic, mixed, and paucigranulocytic types. Blood eosinophil count, total IgE level, eosinophil cationic protein, spirometric measurements, fractional exhaled nitric oxide, atopy based on the skin prick test, PC20 (provocative concentration of methacholine causing a 20% fall in forced expiratory volume in 1 second) in methacholine provocation test, type of asthma controller used, frequency of exacerbation, and use of systemic corticosteroids were examined. Results: The frequency of phenotype is as follows: eosinophilic (21.4%), neutrophilic (34.8%), mixed (13.4%), and paucigranulocytic types (30.4%). During the observation period, the proportion of patients who experienced an exacerbation and received systemic glucocorticosteroids were significantly lower in patients with the paucigranulocytic type of asthma than in those with the mixed type of asthma (6.3% vs. 40.0%; P = 0.007 and 5.9% vs. 40.0%; P = 0.004, respectively). Conclusion Paucigranulocytic asthma may be associated with lower incidence rates of asthma exacerbation and systemic corticosteroid use than the other phenotypes, classified according to induced sputum test results.

PURPOSE: Clinical features of peanut allergy can range from localized to systemic reactions. Because peanut and birch pollen have cross-reactivity, peanut can lead to localized allergic reaction in Fagales pollen-sensitized oral allergy syndrome (OAS) patients without peanut sensitization per se. The purpose of this study was to discriminate true peanut food allergy from cross-reactive hypersensitivity in birch-sensitized peanut allergy. METHODS: Birch-sensitized (n=81) and peanut anaphylaxis patients (n=12) were enrolled. Peanut-related allergic reactions and sensitization profiles were examined. Specific IgE to Fagales tree pollens (birch, oak), peanut, and their component allergens (Bet v 1, Bet v 2, Ara h 1, Ara h 2, Ara h 3, Ara h 8, and Ara h 9) were evaluated. Based on these specific IgEs and clinical features, the patients were classified into 4 groups: group 1 (Fagales pollen allergy without OAS), group 2 (Fagales pollen allergy with OAS), group 3 (OAS with peanut anaphylaxis), and group 4 (peanut anaphylaxis). RESULTS: After peanut consumption, one-third of OAS patients experienced oral symptoms not associated with peanut sensitization. Ara h 1 or Ara h 2 was positive in peanut anaphylaxis patients, whereas Ara h 8 was positive in OAS patients. There were 4 patients with both peanut anaphylaxis and OAS (group 3). Both Ara h 2 and Ara h 8 were positive in these patients. Foods associated with OAS in Korea showed unique patterns compared to Westernized countries. CONCLUSIONS: Ara h 2 and Ara h 8 may be important component allergens for discriminating peanut allergy.
Allergens* ; Anaphylaxis ; Arachis* ; Betula ; Food Hypersensitivity ; Humans ; Hypersensitivity ; Immunoglobulin E ; Korea* ; Peanut Hypersensitivity* ; Pollen ; Rhinitis, Allergic, Seasonal ; Trees