Alterações no Metabolismo de Ferro em Pessoas com Doença Falciforme

• Ano de defesa: 2016
• Autor(a) principal: Mendonça, Juliana Omena Braga de
• Orientador(a): Reis, Marta Citelli dos
• Banca de defesa: Figueiredo, Maria Stella , Bezerra, Flávia Fioruci
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade do Estado do Rio de Janeiro
• Programa de Pós-Graduação: Programa de Pós-Graduação em Alimentação, Nutrição e Saúde
• Departamento: Centro Biomédico::Instituto de Nutrição
• País: BR
• Palavras-chave em Português: Doença falciforme; Hepcidina; Sobrecarga de ferro; Nutrição
• Palavras-chave em Inglês: Sickle cell disease; Hepcidin; Iron overload
• Área do conhecimento CNPq: CNPQ::CIENCIAS DA SAUDE::NUTRICAO::BIOQUIMICA DA NUTRICAO
• Link de acesso: http://www.bdtd.uerj.br/handle/1/7341

Introduction: Sickle cell disease (SCD) is a type of hemoglobinopathy characterized by inflammation and chronic hemolysis. Intense erythropoiesis and inherent anemia may suggest that hepcidin reduction, which is the key regulator of iron metabolism, may result in increased iron absorption. In contrast, inflammatory condition and the iron overload due to chronic blood transfusions experienced by sickle cell patients would be able to induce the transcription of this hormone, leading to reduced absorption of this micronutrient. The lack of knowledge about hepcidin behavior on SCD impairs the development of a specific nutritional protocol for these people. The aim of this study was to evaluate the hepcidin behavior in people with SCD. Methods: Cross-sectional study with 115 adults divided into groups with SCD and iron overload (n=13; 41.0±11.6 years); SCD without iron burden (n=59; 30.9±10.7); and adults without SCD (n=43; 29.4±8.9). Blood samples were collected for evaluation of the following parameters: hematocrit, hemoglobin, hemoglobin S and fetal, serum hepcidin, ferritin, serum iron, total iron-binding capacity (TIBC) and lactate dehydrogenase (LDH). Results: Hepcidin was significantly higher in subjects with SCD with iron overload than SCD without iron burden group (12.0 ng/mL versus 4.2 ng/mL, respectively) and adults without SCD (12.0 ng/mL versus 7.2 ng/mL, respectively). In contrast, patients with SCD without iron burden has presented lower hepcidin concentration than other groups. Except in the SCD with iron overload group, ferritin was strong and positively correlated with serum hepcidin, appearing also as the main variable able to influence the variation of hepcidin levels; hemoglobin S, LDH, female gender and age also appear as variables able to influence the variability of this hormone, but with less intensity. Conclusion: Serum hepcidin is increased in individuals with SCD and iron overload, suggesting that high hepcidin concentration could decrease the iron absorption and, therefore, it would not be necessary to restrict iron rich foods from the diets of SCD individuals