The incidence of allergic diseases is increasing, and research on their epidemiology, pathophysiology, and the prevention of onset is urgently needed. The onset of allergic disease begins in infancy with atopic dermatitis and food allergy and develops into allergic asthma and allergic rhinitis in childhood; the process is defined as “atopic march”. Atopic march is caused by multiple immunological pathways, including allergen exposure, environmental pollutants, skin barrier dysfunction, type 2 inflammation, and oxidative stress, which promote the progression of atopic march. Using recent evidence, herein, we explain the involvement of allergic inflammatory conditions and oxidative stress in the process of atopic march, its epidemiology, and methods for prevention of onset.
Although breastfeeding has been well-established as the preferred method for infant nutrition, its prophylactic effects on food allergy remain controversial. Infantile eczema has been linked to food allergy via percutaneous sensitization; however, this relationship has not been considered in previous studies. We aimed to uncover the prophylactic effects of breastfeeding on food allergy, focusing on eczema-mediated percutaneous sensitization. This retrospective cohort study was based on 46,616 children from the Longitudinal Survey of Newborns in the 21st Century in Japan, begun in 2001. We classified participants into three groups based on infant feeding practices (exclusive breastfeeding, partial breastfeeding including only colostrum, and formula feeding only) and used information from at least one outpatient visit for food allergy during two observation periods (age 6-18 months and age 6-66 months) as health outcomes. We performed log-binomial regression analysis adjusted for potential confounders and stratified analysis according to infantile eczema status. Compared with formula feeding, partial breastfeeding including only colostrum reduced the risk of food allergy only in children with infantile eczema, (RR = 0.66, 95% CI: 0.46, 0.96 for age 6-66 months), whereas exclusive breastfeeding increased this risk in those without infantile eczema (RR = 2.41, 95% CI: 1.40, 4.15, age 6-66 months). The prophylactic effects of breastfeeding on food allergy in the infantile eczema group increased with shorter breastfeeding duration. Our results showed that breastfeeding, especially colostrum, had prophylactic effects on food allergy only among high-risk children with infantile eczema whereas prolonged breastfeeding increased the risk of food allergy.
Background: School closures and social distancing may have affected mental health among preadolescent and adolescent children, who are in a social developmental stage. Rates of anxiety, depression, and stress have been reported to have increased during the COVID-19 pandemic among teenagers worldwide. However, most studies have measured children's mental health in cross-sectional studies or short-term comparisons before and after lockdowns and school closures, and few studies have tracked the long-term effects on mental health among children and adolescents, despite the pandemic lasting more than 2 years. Methods: An interrupted time-series analysis was performed for longitudinal changes in the monthly number of new mental disorders (eating disorders, schizophrenia, mood disorders, and somatoform disorders). Using a nationwide multicenter electronic health records database in Japan, we analyzed data of patients aged 9 to 18 years from 45 facilities that provided complete data throughout the study period. The study period covered January 2017 to May 2021, defining a national school closure as an intervention event. We modeled the monthly new diagnoses of each mental disorder using a segmented Poisson regression model. Results: The number of new diagnoses throughout the study period was 362 for eating disorders, 1104 for schizophrenia, 926 for mood disorders, and 1836 for somatoform disorders. The slope of the regression line in monthly number of new diagnoses increased in the post-pandemic period for all targeted mental disorders (change in slope for eating disorders 1.05, 95% confidence interval [CI] 1.00–1.11; schizophrenia 1.04, 95% CI 1.01–1.07; mood disorders 1.04, 95% CI 1.01–1.07; and somatoform disorders 1.04 95% CI 1.02–1.07). The number of new diagnoses for schizophrenia and mood disorders increased early after school closure; while eating disorders showed an increasing trend several months later. Somatoform disorders showed a decreasing trend followed by an increasing trend. Time trends by sex and age also differed for each mental disorder. Conclusions: In the post-pandemic period, the number of new cases increased over time for eating disorders, schizophrenia, mood disorders, and somatoform disorders. The timing of increase and trends by sex and age differed for each mental disorder.
Global concern over COVID-19 vaccine distribution disparities highlights the need for strategic booster shots. We explored longitudinal antibody responses post-booster during the Omicron wave in a Japanese cohort, emphasizing prior infection and booster doses. This prospective cohort study included 1763 participants aged 18 years and older with at least three vaccine doses (7376 datapoints). Antibody levels were measured every 2 months. We modeled temporal declines in antibody levels after COVID-19 vaccine boosters according to prior infection status and booster doses using a Bayesian linear mixed-effects interval-censored model, considering age, sex, underlying conditions, and lifestyle. Prior infection enhanced post-booster immunity (posterior median 0.346, 95% credible interval [CrI] 0.335–0.355), maintaining antibody levels (posterior median 0.021; 95% CrI 0.019–0.023) over 1 year, in contrast to uninfected individuals whose levels had waned by 8 months post-vaccination. Each additional booster was correlated with higher baseline antibody levels and slower declines, comparing after the third dose. Female sex, older age, immunosuppressive status, and smoking history were associated with lower baseline post-vaccination antibodies, but not associated with decline rates except for older age in the main model. Prior infection status and tailored, efficient, personalized booster strategies are crucial, considering sex, age, health conditions, and lifestyle.
Kawasaki disease (KD) is an acute febrile vasculitis that occurs mostly in children younger than five years. KD involves multiple intricately connected inflammatory reactions activated by a cytokine cascade. Despite therapeutic advances, coronary artery damage may develop in some patients, who will be at risk of clinical cardiovascular events and even sudden death. The etiology of KD remains unclear; however, it may involve both genetic and environmental factors leading to aberrant inflammatory responses. Given the young age of onset, prenatal or perinatal exposure may be etiologically relevant. Multisystem inflammatory syndrome in children, a post-infectious hyper-inflammatory disorder associated with severe acute respiratory syndrome coronavirus 2, has features that overlap with those of KD. Available evidence indicates that vascular endothelial dysfunction is a critical step in the sequence of events leading to the development of cardiovascular lesions in KD. Oxidative stress and the dysregulation of the nitric oxide (NO) system contribute to the pathogenesis of inflammatory responses related to this disease. This review provides current evidence and concepts highlighting the adverse effects of oxidative injury and NO system derangements on the initiation and progression of KD and potential therapeutic strategies for cardiovascular pathologies in affected children.