Associação entre concentrações séricas de retinol e de hepcidina em crianças de 6 a 59 meses de idade

Abstract

Anemia is one of the main deficiency diseases in the world and the lack of vitamin A (VAD), usually determined by serum retinol concentrations, is one of the most important nutritional deficiencies in developing countries. Iron deficiency is believed to be one of the main causes of anemia, however, it can be determined by several factors. It is possible for a functional iron deficiency to develop due to changes in your homeostasis even when the iron stores are suitable. Systemically, iron homeostasis is controlled by the hormone hepcidin, which acts by reducing tissue mobilization and intestinal absorption of this mineral. Hepcidin synthesis is activated by the inflammation, but this activation mechanism has been poorly investigated in children. Additionally, it is known that VAD has been linked to inflammation. We aimed to evaluate the influence of serum retinol on hepcidin levels and anemia in children. This cross-sectional study included 312 children, aged 6–59 months, from Rio de Janeiro, Brazil. Multiple logistic regression was performed using anemia as the outcome and retinol and C-reactive protein (CRP) levels as predictive variables. The association between hepcidin and retinol levels, hematological parameters and body mass index (BMI) was analyzed using a generalized linear model with and without adjustment for CRP level. Logistic regression analysis was used to test anemia as an outcome and serum retinol level as a predictive variable using the odds ratio (OR) function. A total of 312 children were included in the study. Of them, about 67% were older than 24 months and 52% were male. Anemia was present in 14.6% of the children, 5.8% presented iron deficiency anemia and 9.6% had vitamin A deficiency. The increase in serum retinol levels reduced the chances of anemia (OR = 0.13; confidence interval = 0.29–0.59). When CRP level was not adjusted for in the multiple regression analyses, retinol level was a predictor of serum hepcidin levels, ferritin levels, and BMI/age (β = -3.36, 0.14, 1.02, respectively; p = 0.032). Accordingly, serum retinol levels were inversely associated with CRP levels (β = -0.025 and p = 0.000). Socioeconomic indicators were included and did not influence hepcidin levels in the studied population, suggesting a connection determined by biological factors. The association observed between retinol and hepcidin levels may explain why strategies to control anemia based on iron supplementation alone have limited impact on the overall prevalence of anemia. In the sample studied, anemia without iron deficiency was present in approximately two-thirds of the children with anemia, which could be explained by inflammation anemia and the need to improve the understanding of the relationship between vitamin A, hepcidin levels, and anemia in children. To our knowledge, this is the first study to assess the connection between serum retinol and hepcidin in children aged 6 to 59 months. Conclusions: The association between serum retinol and hepcidin levels in children aged 6–59 months seems to be dependent on inflammation. Taken together, these results reinforce the need for nutritional care and public policies to include vitamin A supplementation in anemia prevention and treatment regimens.