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Objective: To assess the oxidant and antioxidant status in neonates with and without hyperbilirubinemia and their association with early manifestations of acute bilirubin encephalopathy (ABE), in addition to eliciting the possible oxidative effects of phototherapy. Methods: This prospective observational study was conducted with 104 full-term newborns at Menoufia University Hospitals from January 2020 to January 2021 to help resolve the debate regarding whether bilirubin is an antioxidant. The cases group (Group I) included 52 full-term newborns (37−40 weeks) with hyperbilirubinemia during the neonatal period, while the control group (Group II) included 52 healthy, full-term age and sex-matched newborns who did not have hyperbilirubinemia. The cases group was further subdivided into Group Ia (n = 12), which included newborns who presented with neurological manifestations suggesting early ABE, and Group Ib (n = 40), which included newborns with no signs suggestive of ABE. All newborns were subjected to clinical and neurological examinations, as well as laboratory investigations. Results: Comparing the specific biological markers between the Group 1 subgroups before phototherapy, the mean plasma levels of prostaglandin-Em, prostaglandin E2, and TSB were significantly higher in Subgroup I(a) (all p < 0.05). After phototherapy, Subgroup I(a) patients had significantly higher levels of prostaglandin-Em, DSB, and TSB (p < 0.05). The biological marker levels improved after phototherapy in terms of TAC (0.811 vs. 0.903), MDA (8.18 vs. 5.13), prostaglandin-Em (37.47 vs. 27.23), prostaglandin E2 (81.09 vs. 31.49), DSB (1.21 vs. 0.55), and TSB (16.63 vs. 8.26; p-value < 0.05). Conclusion: Our study showed that an elevated level of serum bilirubin increases oxidative stress and decreases antioxidant capacity. The reduction in bilirubin levels by phototherapy is associated with a decrease in oxidative stress markers (MDA, PGEm, and PGE2) and an upsurge in TAC, highlighting the absence of oxidative stress effects arising from phototherapy. Neonates with neurological manifestations suggesting ABE had higher levels of oxidative stress markers and lower levels of total antioxidant capacity than those without.
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INTRODUCTION: Idiopathic nephrotic syndrome (INS) is a glomerular disease with completely unclear pathogenesis and different responses to steroid therapy. This study aimed to investigate the role of cytokine genes promoter polymorphisms in steroid therapy responses. MATERIALS AND METHODS: One hundred children with INS and 30 healthy controls were studied. Genotyping of TNF-α-G308A single nucleotide polymorphism was done using polymerase chain reaction-restriction fragment length polymorphism method, while of IL-6-G174C single nucleotide polymorphism was done using real-time polymerase chain reaction. RESULTS: The IL-6-G174C exhibited a significantly different genotype distribution among the children with INS compared with the controls (GG versus CC, P = .02; GG versus GC, P = .003; odds ratio [OR], 5.83; 95% confidence interval [CI], 1.64 to 20.70; as well as alleles distribution of G versus C, P ? .001; OR, 7.57; 95% CI, 2.28 to 25.17). With regard to TNF-α-G308A genotype, there was no significant difference in genotype distribution of the children with INS compared with the controls, but a significant difference was observed at the alleles level. Comparing the steroid-resistant group with the steroid-sensitive group, significant association was found at genotypic level in case of IL-6-G174C (GG versus CC, P = .03; OR, 5.52; 95% CI, 1.39 to 21.89), but no association was found regarding GG versus GC. At the allelic level of IL-6-G174C, there was no significant association either. CONCLUSIONS: IL-6-G174C and TNFα-G308A polymorphisms may affect susceptibility to idiopathic nephrotic syndrome and might affect steroid response in INS patients.
