ContextTo assess the global burden of late and/or poor management of severe neonatal jaundice (SNJ), a common problem worldwide, which may result in death or irreversible brain damage with disabilities in survivors. Population-based data establishing the global burden of SNJ has not been previously reported.ObjectiveDetermine the burden of SNJ in all WHO regions, as defined by clinical jaundice associated with clinical outcomes including acute bilirubin encephalopathy/kernicterus and/or exchange transfusion (ET) and/or jaundice-related death.Data sourcesPubMed, Scopus and other health databases were searched, without language restrictions, from 1990 to 2017 for studies reporting the incidence of SNJ.Study selection/data extractionStratification was performed for WHO regions and results were pooled using random effects model and meta-regression.ResultsOf 416 articles including at least one marker of SNJ, only 21 reported estimates from population-based studies, with 76% (16/21) of them conducted in high-income countries. The African region has the highest incidence of SNJ per 10 000 live births at 667.8 (95% CI 603.4 to 738.5), followed by Southeast Asian, Eastern Mediterranean, Western Pacific, Americas and European regions at 251.3 (132.0 to 473.2), 165.7 (114.6 to 238.9), 9.4 (0.1 to 755.9), 4.4 (1.8 to 10.5) and 3.7 (1.7 to 8.0), respectively. The incidence of ET per 10 000 live births was significantly higher for Africa and Southeast Asian regions at 186.5 (153.2 to 226.8) and 107.1 (102.0 to 112.5) and lower in Eastern Mediterranean (17.8 (5.7 to 54.9)), Americas (0.38 (0.21 to 0.67)), European (0.35 (0.20 to 0.60)) and Western Pacific regions (0.19 (0.12 to 0.31). Only 2 studies provided estimates of clear jaundice-related deaths in infants with significant jaundice [UK (2.8%) and India (30.8%).ConclusionsLimited but compelling evidence demonstrates that SNJ is associated with a significant health burden especially in low-income and middle-income countries.
Background Critically ill preterm and term neonates are at high risk for negative iron balance due to phlebotomy that occurs with frequent laboratory monitoring and the high iron demand of rapid growth. Understanding the prioritization of iron between red blood cells (RBCs) and brain is important given iron’s role in neurodevelopment. Methods Ten neonatal twin lamb pairs (n = 20) underwent regular phlebotomy for 11 days. Lambs were randomized to receive no iron or intravenous daily iron supplementation from 1–5 mg/kg. Serum hemoglobin concentration and reticulocyte count were assayed, iron balance calculated, and iron content of RBCs, liver, brain, muscle, and heart measured at autopsy. Results Among phlebotomized lambs: 1) liver iron concentration was directly related to net iron balance (r=0.87; p<0.001); and 2) brain iron concentration was reduced as a function of net iron balance (r=0.63) only after liver iron was depleted. In animals with negative iron balance, total RBC iron was maintained while brain iron concentration decreased as a percentage of the iron present in RBCs (r=−0.70; p<0.01) and as a function of reticulocyte count (r=−0.63; p<0.05). Conclusion Phlebotomy induced negative iron balance limits iron availability to the developing brain.
Low- and middle-income countries need to pay urgent attention to G6PD deficiency to curtail the preventable burden of jaundice-related morbidity, mortality and disability.
Background Phlebotomy-induced anemia (PIA) is common in premature infants and affects neurodevelopment. PIA alters hippocampal metabolism in neonatal mice through tissue hypoxia and iron deficiency. The mammalian target of rapamycin (mTOR) pathway senses the status of critical metabolites (e.g., oxygen, iron), thereby regulating hippocampal growth and function. We determined the effect of PIA and recombinant human erythropoietin (rHuEpo) treatment on mTOR signaling and expression of genes related to mTOR pathway functions. Methods Mice receiving an iron-supplemented diet were phlebotomized from postnatal day (P)3 to a target hematocrit of <25% by P7. Half were maintained at <25% until P14; half received rHuEpo from P7 to increase the hematocrit to 25–28%. Hippocampal phosphorylated to total protein ratios of 4 key mTOR pathway proteins were measured by Western blot at P14 and compared to nonphlebotomized, non-anemic control mice. mRNA levels of genes regulated by mTOR were measured by qPCR. Results PIA suppressed phosphorylation of all mTOR proteins. rHuEpo restored AMPK and AKT status, and partially rescued the mTOR output protein, S6K. PIA and rHuEpo treatment also altered expression of genes regulated by S6K. Conclusions PIA compromises and rHuEpo treatment partially rescues a pathway regulating neuronal DNA transcription, protein translation and structural complexity.
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