Characterization and Incidence of Sunflower Seed Allergy in a Pediatric Allergy Clinic.

BACKGROUND: Sunflower seeds are a popular allergen-free peanut alternative. OBJECTIVE: To describe sunflower seed allergy incidence and characteristics. METHODS: We conducted a retrospective cohort study of patients with sunflower seed allergy from 1995 to 2021 in a pediatric allergy clinic. We described demographic characteristics, testing results, atopic comorbidities, and reaction histories of patients with sunflower seed allergy and calculated the annual cumulative incidence of the allergy. Logistic regression was used to estimate the increase in odds of sunflower seed allergy diagnosis for each year from 1995 to 2021. RESULTS: From 1995 to 2021, we identified 235 patients with sunflower seed allergy. Among patients with sunflower seed allergy, the median age at diagnosis was 3.9 years. More than three-quarters of patients had another atopic condition. Half of the reactions consisted of mild urticaria or rash, and a quarter met criteria for anaphylaxis. The cumulative incidence ranged from 0% (1995-1999, 2001-2004, and 2006) to 0.38% (2021). From 1995 to 2021, the odds of sunflower seed allergy diagnosis increased annually by 21% (odds ratio, 1.21; 95% CI, 1.17-1.25). CONCLUSIONS: In our single-center cohort of children with sunflower seed allergy, most children were diagnosed in early childhood, had high rates of comorbid atopic conditions, and had high rates of cutaneous reactions to sunflower seed products. Moreover, in our cohort, incidence of sunflower seed allergy increased.

The association between child food allergy and family food insecurity in a nationally representative US sample.

OBJECTIVE: To assess whether child food allergy is associated with family food insecurity, overall, and across different income levels. METHODS: We used the 2011-2018 National Health Interview Survey, a nationally representative cross-sectional survey. The exposure was child food allergy, and our main outcome was odds of family food insecurity, which was calculated using multivariable logistic regression models adjusted for child demographics, family characteristics and survey year. We examined for effect modification by the ratio of family income to the poverty threshold using stratification and tests for statistical interaction. RESULTS: Among 83,287 children 6% had food allergy and 22% experienced family food insecurity. Child food allergy was associated with a 1.39-fold (95% confidence interval [CI]: 1.26, 1.53) increased odds of family food insecurity overall. Child food allergy was associated with a 1.46-fold (95% CI: 1.29, 1.66) increased odds of family food insecurity among children whose families lived below 200% of the federal poverty level, and a 1.26-fold (95% CI: 1.05, 1.51) increased odds of family food insecurity among children whose families lived at 200 to 399% of the federal poverty level, with no association among children whose families lived at or above 400% of the federal poverty level (P =.04 for interaction). CONCLUSION: There is an association between child food allergy and family food insecurity, and this association is modified by the ratio of family income to the poverty threshold. Improved availability and subsidy of allergen-free foods in nutrition assistance programs and food pantries are urgently needed.

Global warming and implications for epithelial barrier disruption and respiratory and dermatologic allergic diseases.

Global warming has direct and indirect effects, as well as short- and long-term impacts on the respiratory and skin barriers. Extreme temperature directly affects the airway epithelial barrier by disrupting the structural proteins and by triggering airway inflammation and hyperreactivity. It enhances tidal volume and respiratory rate by affecting the thermoregulatory system, causing specific airway resistance and reflex bronchoconstriction via activation of bronchopulmonary vagal C fibers and upregulation of transient receptor potential vanilloid (TRPV) 1 and TRPV4. Heat shock proteins are activated under heat stress and contribute to both epithelial barrier dysfunction and airway inflammation. Accordingly, the frequency and severity of allergic rhinitis and asthma have been increasing. Heat activates TRPV3 in keratinocytes, causing the secretion of inflammatory mediators and eventually pruritus. Exposure to air pollutants alters the expression of genes that control skin barrier integrity and triggers an immune response, increasing the incidence and prevalence of atopic dermatitis. There is evidence that extreme temperature, heavy rains and floods, air pollution, and wildfires increase atopic dermatitis flares. In this narrative review, focused on the last 3 years of literature, we explore the effects of global warming on respiratory and skin barrier and their clinical consequences.

Human inherited complete STAT2 deficiency underlies inflammatory viral diseases.

STAT2 is a transcription factor activated by type I and III IFNs. We report 23 patients with loss-of-function variants causing autosomal recessive (AR) complete STAT2 deficiency. Both cells transfected with mutant STAT2 alleles and the patients' cells displayed impaired expression of IFN-stimulated genes and impaired control of in vitro viral infections. Clinical manifestations from early childhood onward included severe adverse reaction to live attenuated viral vaccines (LAV) and severe viral infections, particularly critical influenza pneumonia, critical COVID-19 pneumonia, and herpes simplex virus type 1 (HSV-1) encephalitis. The patients displayed various types of hyperinflammation, often triggered by viral infection or after LAV administration, which probably attested to unresolved viral infection in the absence of STAT2-dependent types I and III IFN immunity. Transcriptomic analysis revealed that circulating monocytes, neutrophils, and CD8+ memory T cells contributed to this inflammation. Several patients died from viral infection or heart failure during a febrile illness with no identified etiology. Notably, the highest mortality occurred during early childhood. These findings show that AR complete STAT2 deficiency underlay severe viral diseases and substantially impacts survival.