RESUMO
Food insecurity is a rising concern for US households and leads to adverse child health outcomes. Pediatric gastroenterology providers are uniquely equipped to help guide families experiencing this challenge given their specialized training in nutritional support and dietary therapy for disease management. Hence, this study aimed to evaluate food insecurity screening practices from the perspectives of patient caregivers and healthcare providers in a tertiary pediatric gastroenterology practice. A survey was administered to 1279 caregivers and 121 providers. Of the 248 completed caregiver responses, 10%-15% reported being asked about food insecurity. Among the 36 healthcare provider responses, 53% expressed comfort in conducting food insecurity screening but only 14% routinely screened. The most cited barrier to screening was the lack of readily available patient resources. Further research is imperative to address these screening barriers and assess the impact of food insecurity screening and interventions on pediatric gastrointestinal health outcomes.
RESUMO
Type 1 diabetes (T1D) and celiac disease (CeD) cluster in families and can occur in the same individual. Genetic loci have been associated with susceptibility to both diseases. Our aim was to explore the genetic differences between individuals developing both these diseases (double autoimmunity) versus those with only one. We hypothesized that double autoimmunity individuals carry more of the genetic risk markers that are shared between the two diseases independently. SNPs were genotyped in loci associated with T1D (n=42) and CeD (n=28) in 543 subjects who developed double autoimmunity, 2,472 subjects with T1D only, and 2,223 CeD-only subjects. For identification of loci that were specifically associated with individuals developing double autoimmunity, two association analyses were conducted: double autoimmunity versus T1D and double autoimmunity versus CeD. HLA risk haplotypes were compared between the two groups. The CTLA4 and IL2RA loci were more strongly associated with double autoimmunity than with either T1D or CeD alone. HLA analyses indicated that the T1D high-risk genotype, DQ2.5/DQ8, provided the highest risk for developing double autoimmunity (odds ratio 5.22, P=2.25×10(-29)). We identified a strong HLA risk genotype (DQ2.5/DQ8) predisposing to double autoimmunity, suggesting a dominant role for HLA. Non-HLA loci, CTLA4 and IL2RA, may also confer risk to double autoimmunity. Thus, CeD patients who carry the DQ2.5/DQ8 genotype may benefit from periodic screening of autoantibodies related to T1D.