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BACKGROUND: Hyperbilirubinaemia (bilirubin >51.3 µmol/L) alone is not indicative of severe malaria, and the immune response underlying hyperbilirubinaemia remains largely unexplored. Liver damage associated with hyperbilirubinaemia may alter the expression of hepcidin, which regulates systemic iron by degrading ferroportin. For this study, the association between hepcidin and the levels of cytokines and chemokines in the serum of individuals with mild and severe vivax malaria and subjects with malaria with isolated hyperbilirubinaemia was evaluated. METHODS: Cytokines/chemokines and hepcidin were measured in individuals with mild (n = 72) and severe (n = 17) vivax malaria, as well as in the serum of subjects with vivax malaria with isolated hyperbilirubinaemia (n = 14) from the Brazilian Amazon between 2009 and 2013 by multiplex assay and ELISA, respectively. The polymorphism 744 G > T in the ferroportin gene was identified by restriction fragment-length polymorphism analysis and the restriction enzyme PvuII. RESULTS: The polymorphism at position 744 G > T in the ferroportin gene was typed and no differences in the distributions of genotypes or alleles were observed between the study groups. Subjects with severe malaria had higher levels of interleukin (IL)-2 and IL-13 than subjects with hyperbilirubinaemia. No differences in the expression of immune markers were observed between subjects with mild malaria and those with hyperbilirubinaemia. However, hepcidin levels were higher in individuals with severe malaria and hyperbilirubinaemia than those with mild malaria (p = 0.0002 and p = 0.0004, respectively) and cut-off values of hepcidin differentiated these groups from subjects with mild malaria. Hepcidin was positively associated with IL-6 and IL-10 levels and with parasitaemia in subjects with mild malaria and with IFN-γ in subjects with severe malaria. CONCLUSIONS: Malaria in the presence of hyperbilirubinaemia produces a less robust inflammatory response compared to severe cases of malaria. Hepcidin levels are positively associated with immune markers in vivax malaria outcomes.

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Se estudiaron 251 recién nacidos a término y sus respectivas madres en la Maternidad Concepción Palacios, Caracas-Venezuela, con el fin de establecer la frecuencia de enfermedad hemolítica (EH) y tratar de determinar parámetros útiles para la predicción de la severidad de la EH-ABO. Hubo 23 casos de incompatibilidad ABO con los siguientes hallazgos serológicos: 9 (39) por ciento presentaron la prueba de autoaglutinación positiva, 5(21 por ciento) el Coombs directo positivo, 20 (36 por ciento) el eluido positivo. De cuatro (2 por ciento) casos con EH-ABO, dos (50 por ciento) tuvieron Coombs directo positivo y tres (75 por ciento) la prueba de autoaglutinación y el eluido positivo. El título de anticuerpos maternos varió entre 1:12 y 1:4096. La determinación semicuantitativa de las subclases IgG en 3 casos de EH-ABO demostró en forma constante la presencia de IgG3 e IgG4 y en 2 casos se asoció la IgG2. Se determinó la presencia de sustancia A en el suero de 14 niños con incompatibilidad ABO, no observándose aparentemente el efecto protector del carácter secretor. Se presentaron 2 casos de EH-Rh, los cuales tuvieron un comportamiento diferente, lo cual podría atribuirse a las subclases de IgG presentes en el suero materno

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PIP: The inhibiting agent of UDP-glucuronyl transferase (UDPGT), inhibition of which is associated with breast milk jaundice syndrome in infants, was thought to be 3(alpha),20(beta)-pregnandiol. European researchers have begun in vitro investigations to discover the inhibiting substance, and all studies have confirmed it is a nonesterified fatty acid. The strong association between breast milk jaundice, elevated values of nonesterified fatty acids, and unstimulated lipase in UDPGT-inhibitory milk was confirmed by electrophoretic technique. The mechanisms responsible for production of prolonged unconjugated hyperbilirubeinemia in infants, however, is not understood. 2 theories have been offered: 1) that milk triglyceride digestion before the milk reaches the duodenum leads to early absorption of most of the liberated glycerol that might otherwise be used by intestinal epithelium to resynthesize triglycerides; or 2) inhibitory human milk may facilitate the enterohepatic recirculation of bilirubin (reabsorption of bilirubin from intestinal lumen). Breast-feeding per se does not result in an increased incidence of neonatal hyperbilirubinemia; it is rather those infants who receive insufficient amounts of breast milk who develop the condition.^ieng

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