Impact of Vitamin A Status on Environmental Enteric Dysfunction in Children with Schistosomiasis
BACKGROUND: There is limited evidence describing associations between vitamin A deficiency, environmental enteric dysfunction (EED), and schistosomiasis, which all contribute to undernutrition and linear growth faltering in children. The parent trial underway in Uganda is investigating EED as a schistosomiasis-related morbidity and is measuring EED biomarkers at baseline, 6 months, and 12 months following praziquantel (PZQ) treatment in children with Schistosoma mansoni infection. GAP: While vitamin A deficiency and EED are both associated with similar features of gut dysfunction, few studies have directly addressed whether vitamin A deficiency is a risk factor for EED in children, and none of these have applied inflammation adjustment for vitamin A assessment. HYPOTHESIS: We hypothesize that participants with vitamin A deficiency will have higher measures of EED biomarkers at baseline due to the role of vitamin A in maintaining intestinal epithelial integrity, compared to those with replete vitamin A status. We also anticipate that vitamin A deficiency will modify (diminish) the impact of PZQ treatment on EED biomarkers longitudinally compared to replete vitamin A status. METHODS: This research pertains to the de-identified serum samples and clinical data provided by the parent trial: a randomized, controlled phase II trial of PZQ in children age 12-48 months with S. mansoni infection recruited from the Lake Albert region of Uganda. The current proposal seeks to measure vitamin A in parent trial samples, apply inflammation adjustment to assess vitamin A status, and examine cross-sectional and longitudinal relationships between adjusted vitamin A status and EED biomarkers. RESULTS: Pending. IMPACT: Determining the role that vitamin A status plays in the pathogenesis of intestinal schistosomiasis will offer a modifiable risk factor for improving the long-term health of children living areas with overlapping burdens of vitamin A deficiency, EED, and S. mansoni infection.