12 Thus, the knowledge of pediatricians for the prevention of these forms of maltreatment may indirectly contribute to the prevention of AHT, and vice versa. Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq). The authors Carfilzomib solubility dmso declare no conflicts of interest. “
“Hyperbilirubinemia is the most common clinical condition in newborns. Between 8% and 11% of neonates develop significant hyperbilirubinemia, defined as total serum bilirubin (TSB) above the 95th percentile for age (high-risk zone) during the first week of life.1 The levels of TSB

rise to the high-risk zone, leading to long-term consequences, including bilirubin-induced encephalopathy and kernicterus.2 Despite the advent of phototherapy and exchange transfusion, kernicterus continues to be reported worldwide, especially in developing countries.3 Therefore, the identification of infants at risk of developing neonatal hyperbilirubinemia has become particularly important.4 There are many factors that could account for the development of neonatal hyperbilirubinemia, including ABO or Rh incompatibilities, deficiency of glucose-6-phosphate dehydrogenase (G6PD) and pyruvate kinase, hereditary spherocytosis, defective hemoglobin synthesis, hypothyroidism, breast milk jaundice, and cephalohematoma, among others.5 Several clinical genetic disorders influence

bilirubin physiology. The UDP-glycosyltransferase 1 family, polypeptide A1 (UGT1A1), and solute carrier organic anion transporter family enzymes organic anion transporter polypeptide 2 (OATP2) are responsible for glucuronidation and cellular uptake of bilirubin, respectively, and DAPT in vivo play an important role in regulating the bilirubin levels.6 OATP2 is located on the basolateral (sinusoidal) membrane of human hepatocytes, and is encoded by the gene of the

solute carrier organic anion transporter family member 1B1 (SLCO1B1). Recent studies have suggested that the variations 388 G>A, 521 T>C, and 463 C>A of the SLCO1B1 gene may predispose subjects to neonatal hyperbilirubinemia by limiting hepatic bilirubin uptake.7 They vary in different populations, with a high prevalence of the 388 G>A (73.4%) and 521 T>C (14.0%) variants occurring in Chinese Ribonucleotide reductase subjects.8 A 16% prevalence of the 463 C>A variant has been reported in Europeans and Americans.9 Neonatal hyperbilirubinemia is known to occur more frequently and to be more severe in Asians than in whites.10 The authors hypothesized that SLCO1B1 mutation may be one of the risk factors for neonatal hyperbilirubinemia, which possibly accounts for the variability in prevalence rates among different ethnic groups. The role of SLCO1B1 gene in neonatal hyperbilirubinemia is still controversial. Thus, the objective of this systematic review with meta-analysis was to assess the impact of the three variants (388 G>A, 521 T>C, 463 C>A) of SLCO1B1 on hyperbilirubinemia in neonates of different ethnicities.