ABSTRACT OBJECTIVE To describe feeding practices and the risk factors for the mixed breastfeeding and early weaning in the neonatal period. METHODS Cohort study, which we collected socioeconomic, demographic, health care and feeding data from 415 mother/child binomials born in four public maternity hospitals in Natal/Brazil. They were followed-up at 48 hours, 7 and 28 days after birth. The association was established using Pearson’s Chi-square test and Poisson’s regression, after adjusting it to other variables. RESULTS The prevalence of mixed breastfeeding in the first 2 days was 47,2% and early weaning in 7 and 28 days was 8,4% and 16,2% in that order. The main reasons for mixed breastfeeding and early weaning were: colostrum deficiency (33.8%), difficulty in latching/sucking (23.5%) and “little milk” (70.0%). The use of formula/milk/porridge remained associated with maternal age ≤ 20 years (RR = 0.64; 95%CI: 0.47–0.86), age 20–29 years (RR = 0,70; 95%CI: 0,57–0,87), primiparity (RR = 1.37; 95%CI: 1.11–1.60) and cesarean delivery (RR = 1.20; 95%CI: 1.00–1.45) at 2 days; absence of paternal support (RR = 4.98; 95%CI: 2.54–9.79) and pacifier use (RR = 3.21; 95%CI: 1.63–6.32) at 7 days; and only pacifier use (RR = 2.48; 95%CI: 1.53–4.02) at 28 days. CONCLUSIONS Early weaning was associated with maternal and health care factors, thus suggesting the need to readjust good practices and educational actions to achieve the exclusive offer to the maternal breast in the neonatal period.

ABSTRACT OBJECTIVE To describe feeding practices and the risk factors for the mixed breastfeeding and early weaning in the neonatal period. METHODS Cohort study, which we collected socioeconomic, demographic, health care and feeding data from 415 mother/child binomials born in four public maternity hospitals in Natal/Brazil. They were followed-up at 48 hours, 7 and 28 days after birth. The association was established using Pearson’s Chi-square test and Poisson’s regression, after adjusting it to other variables. RESULTS The prevalence of mixed breastfeeding in the first 2 days was 47,2% and early weaning in 7 and 28 days was 8,4% and 16,2% in that order. The main reasons for mixed breastfeeding and early weaning were: colostrum deficiency (33.8%), difficulty in latching/sucking (23.5%) and “little milk” (70.0%). The use of formula/milk/porridge remained associated with maternal age ≤ 20 years (RR = 0.64; 95%CI: 0.47–0.86), age 20–29 years (RR = 0,70; 95%CI: 0,57–0,87), primiparity (RR = 1.37; 95%CI: 1.11–1.60) and cesarean delivery (RR = 1.20; 95%CI: 1.00–1.45) at 2 days; absence of paternal support (RR = 4.98; 95%CI: 2.54–9.79) and pacifier use (RR = 3.21; 95%CI: 1.63–6.32) at 7 days; and only pacifier use (RR = 2.48; 95%CI: 1.53–4.02) at 28 days. CONCLUSIONS Early weaning was associated with maternal and health care factors, thus suggesting the need to readjust good practices and educational actions to achieve the exclusive offer to the maternal breast in the neonatal period.

We aimed to investigate the association of CD14 -260C/T (rs2569190) polymorphism and Chagas cardiomyopathy and the functional characteristics of CD14+ and CD14- monocytes upon infection with Trypanosoma cruzi. We observed an association between the T- genotype (absence of allele -260T) related to low CD14 expression and the dilated cardiomyopathy type of Chagas disease. Furthermore, we observed that CD14- monocytes showed a more activated profile upon in vitro infection with T. cruzi than CD14+ monocytes. Our findings suggest that T- genotype is associated with susceptibility to develop Chagas dilated cardiomyopathy, likely linked to the T. cruzi-induced inflammatory profile of CD14- monocytes.

Perhaps one of the most intriguing aspects of human Chagas disease is the complex network of events that underlie the generation of protective versus pathogenic immune responses during the chronic phase of the disease. While most individuals do not develop patent disease, a large percentage may develop severe forms that eventually lead to death. Although many efforts have been devoted to deciphering these mechanisms, there is still much to be learned before we can fully understand the pathogenesis of Chagas disease. It is clear that the host's immune response is decisive in this process. While characteristics of the parasite influence the immune response, it is becoming evident that the host genetic background plays a fundamental role in the establishment of pathogenic versus protective responses. The involvement of three complex organisms, host, parasite and vector, is certainly one of the key aspects that calls for multidisciplinary approaches towards the understanding of Chagas disease. We believe that now, one hundred years after the discovery of Chagas disease, it is imperative to continue with highly interactive research in order to elucidate the immune response associated with disease evolution, which will be essential in designing prophylactic or therapeutic interventions.