Although it is difficult to find a cause of chronic urticaria in children, previous studies have been identified some triggers, such as autoimmunity, physical stimuli, food and its additives, and infection. History taking and physical examination remain the best tool for identifying an underlying cause of urticaria. First investigations include a complete blood count with differential, erythrocyte sedimentation rate, and C-reactive protein in children with chronic urticaria. If physical stimuli are suspected as triggers of chronic urticaria, appropriate provocation tests can be performed. Although the frequency of autoimmune urticaria was relatively high compared to the other causes in children with chronic urticaria, it is not easy to apply routine use of autologous serum skin tests to clinical practice. Additional extensive laboratory investigations are not required in the majority of cases. Second-generation H1-antihistamines are the mainstay of treatment from current guidelines in children with chronic urticaria, and dosage can be increased if the standard dose is not effective. Data on chronic urticaria in children are scarce, and causes have been considered to be similar to those in adults. Therefore, diagnostic approaches and treatment principles of chronic urticaria in children have been derived from extrapolating data in adults. In the future, comparative studies for the causes of chronic urticaria between children and adults, and therapeutic modalities for refractory cases will be needed.
Adult ; Autoimmunity ; Blood Cell Count ; Blood Sedimentation ; C-Reactive Protein ; Child* ; Humans ; Physical Examination ; Skin Tests ; Urticaria*

No abstract available.
Glass*

No abstract available.
Asthma* ; Folic Acid* ; Gene-Environment Interaction*

No abstract available.
Bronchiolitis ; Inflammation

No abstract available.
Child* ; Humans ; Mycoplasma pneumoniae* ; Mycoplasma* ; Pneumonia, Mycoplasma*

Postinfectious bronchiolitis obliterans (PIBO) is an irreversible obstructive lung disease characterized by subepithelial inflammation and fibrotic narrowing of the bronchioles after lower respiratory tract infection during childhood, especially early childhood. Although diagnosis of PIBO should be confirmed by histopathology, it is generally based on history and clinical findings. Irreversible airway obstruction is demonstrated by decreased forced expiratory volume in 1 second with an absent bronchodilator response, and by mosaic perfusion, air trapping, and/or bronchiectasis on computed tomography images. However, lung function tests using spirometry are not feasible in young children, and most cases of PIBO develop during early childhood. Further studies focused on obtaining serial measurements of lung function in infants and toddlers with a risk of bronchiolitis obliterans (BO) after lower respiratory tract infection are therefore needed. Although an optimal treatment for PIBO has not been established, corticosteroids have been used to target the inflammatory component. Other treatment modalities for BO after lung transplantation or hematopoietic stem cell transplantation have been studied in clinical trials, and the results can be extrapolated for the treatment of PIBO. Lung transplantation remains the final option for children with PIBO who have progressed to end-stage lung disease.
Adrenal Cortex Hormones ; Airway Obstruction ; Bronchiectasis ; Bronchioles ; Bronchiolitis Obliterans* ; Bronchiolitis* ; Child* ; Diagnosis ; Fibrosis ; Forced Expiratory Volume ; Hematopoietic Stem Cell Transplantation* ; Hematopoietic Stem Cells* ; Humans ; Infant ; Inflammation ; Lung Diseases ; Lung Diseases, Obstructive ; Lung Transplantation* ; Lung* ; Perfusion ; Respiratory Function Tests ; Respiratory Tract Infections ; Spirometry

PURPOSE: Atopic dermatitis (AD) is the most common chronic and relapsing inflammatory skin disease with skin barrier defects and altered immune responses. Chronic inflammation leads to irreversible fibrosis in the skin and there is no treatment to completely abolish the inflammation and fibrosis. To prevent or treat the chronic process of AD, it is necessary to develop a murine model of AD that reflects the chronic process to identify the mechanism. The aims of this study were to develop a chronic AD model with a crude extract Aspergillus fumigatus (Af) antigen. METHODS: We applied Af extract (40 µg) epicutaneously to the dorsal skin of BALB/c mice for 5 consecutive days per week during a period of 5 weeks for a chronic AD model, and 5 consecutive days repeatedly with 2 weeks interval for an acute AD model. RESULTS: The clinical score and transepidermal water loss were more increased in the chronic AD model than in the acute AD model. Histologic findings showed that more increased epidermal thickness, neutrophil infiltration and hyperkeratosis in the chronic model than in the acute model. Skin fibrosis was more prominent in the chronic model than in the acute model. The mRNA expression levels of transforming growth factor (TGF)-β, thymic stromal lymphopoietin, and interleukin-33 were increased in the skin of the chronic model compared to the acute model. The levels of total IgE, Af-specific IgE, IgG1, and IgG2a were significantly increased in the chronic model compared to controls. CONCLUSION: The Af-induced chronic AD model showed prominent fibrosis and increased TGF-β expression in the skin, which suggests that these models may be useful in the research for the mechanism of the chronic process in AD.
Animals ; Aspergillus fumigatus ; Aspergillus ; Dermatitis, Atopic ; Fibrosis ; Immunoglobulin E ; Immunoglobulin G ; Inflammation ; Interleukin-33 ; Mice ; Neutrophil Infiltration ; RNA, Messenger ; Skin ; Skin Diseases ; Transforming Growth Factors ; Water

In this article, the funding resource was misprinted unintentionally.

PURPOSE: It is becoming generally recognized that wheezing in early childhood is a heterogeneous condition and does not always develop into asthma. This study aimed to determine characteristics of wheezing phenotypes in early childhood and investigate their relation to asthma. METHODS: Two hundreds and sixty 6-8 year old children with past or present wheezeing were enrolled, and their history of wheezing was examined through medical records. Forty-three age- matched children who had never suffered from wheezing served as controls. Each subject underwent methacholine bronchial challenge and skin prick tests with airbone allergens. RESULTS: Forced expiratory volume in 1 second(FEV1) % predicted value was significantly lower in early-onset persistent wheezers(EP group) and late-onset wheezers(LW group) than in non-wheezers (NW group)(P<0.01, P<0.05, respectively). EP and LW groups demonstrated enhanced bronchial hyperresponsiveness(BHR), compared with early-onset transient wheezers(ET group) and NW group(all P<0.001). But there was no significant difference between the ET and NW groups. Atopy was significantly more prevalent in EP and LW groups than ET and NW groups, and serum IgE levels also showed similar figures(all P<0.001). CONCLUSION: Persistent wheezing with early childhood onset and late-onset wheezing are associated with high levels of atopy and BHR. It suggests that these two wheezing phenotypes are more closely related to asthma than transient wheezing phenotype.
Allergens ; Asthma ; Child* ; Forced Expiratory Volume ; Humans ; Immunoglobulin E ; Medical Records ; Methacholine Chloride ; Phenotype ; Respiratory Sounds* ; Skin

PURPOSE: This study was undertaken to compare blood eosinophilic inflammatory markers between the acute period and clinical remission in children with upper respiratory infection (URI) -induced wheezing, and to assess the effects of atopy and age on these changes. METHODS: In 77 children with URI-induced wheezing, blood eosinophil count and serum eosinophil cationic protein (ECP) were measured during the acute wheezing phase and clinical remission period. The data were analyzed in the subgroups divided by atopy and age, respectively. RESULTS: Blood eosinophil count was significantly lower during acute period (181.6/microliter, 67.3-490.0) than that during clinical remission period (261.8/microliter, 120.7-567.7, P=0.001), and this significant eosinopenic response was found in non-atopic children (n=36) [92.2 (41.3-206.0) /microliter vs 204.5 (106.6-392.2) /microliter, P< 0.001], but not in atopic children (n=41). A significantly higher level of serum ECP was observed during acute period (15.1 microgram/L, 7.2-31.6) than during clinical remission (13.0 microgram/L, 6.6-25.7, P=0.05), and this difference was significant only in atopic children[24.2 (15.3-38.1) microgram/L vs 16.2 (8.3-31.6) microgram/L, P< 0.001]. A significant fall in blood eosinophil count during acute period was found only in children < or=4 years (n=37), while a significant rise in serum ECP was detected only in children > 4 years (n=40). However, these differences a due to dissimilar distribution of atopy in the two age groups. CONCLUSION: Our results showed different eosinophil responses to infection in non-atopic and atopic children with URI-induced wheezing. It appears that the blunted eosinopenic response in atopic children may be associated with the predominant Th2-like response to infection.
Child* ; Eosinophil Cationic Protein ; Eosinophils* ; Humans ; Respiratory Sounds*