Background: Hyperbilirubinemia is a common neonatal problem. Studies conducted on the effectiveness of zinc salts on serum indirect bilirubin levels in newborns have yielded different results, all calling for further research. This study aimed to determine the effect of oral zinc sulfate on indirect hyperbilirubinemia in preterm infants admitted to the neonatal intensive care unit. Methods: A randomized double-blind clinical trial was performed in the neonatal intensive care unit of Vali-e-Asr Hospital in Birjand, Iran. The study population comprised neonates aged between 31 and 36 gestational weeks, who required phototherapy in the neonatal intensive care unit. A total of 60 neonates were selected by census and allocated into an experimental group and a control group. In addition to phototherapy, the experimental group received 1 cc/Kg zinc sulfate syrup (containing 5 mg/5 cc zinc sulfate; Merck Company, Germany), and the control group received a placebo syrup (containing 1 cc/kg sucrose). Data were analyzed in SPSS-21 software using the independent t-test, repeated-measures ANOVA, Bonferroni post-hoc test, and Mann-Whitney test. P-values smaller than 0.05 were considered significant. Results: Bilirubin level changes in the experimental and control groups six hours after intervention were − 1.45 ± 3.23 and − 0.49 ± 0.37 (p = 0.024), respectively. The changes 24 and 48 h after intervention were-3.26 ± 2.78 and − 1.89 ± 1.20 (p = 0.017) in the experimental group and − 4.89 ± 2.76 and − 3.98 ± 2.32 (p = 0.23) in the control group, respectively. There was no significant difference in the phototherapy duration between the two groups (p = 0.24). Conclusions: The results of this study showed that the use of zinc sulfate syrup in preterm infants with indirect hyperbilirubinemia significantly reduced bilirubin levels within 48 h of treatment.

DiGeorge syndrome was described for the first time in 1968 as a defect affecting structures derived from the third and fourth embryonic pharyngeal arches along with absent parathyroid glands. According to the low incidence of this disease as well as a wide spectrum of symptoms, it is essential to report cases with less prevalent features. In this case report, a child was introduced with a diagnosis of DiGeorge syndrome presenting with seizures. The patient was a 27-day-old baby girl due to seizures admitted to Hospital Imam Reza (AS), Mashhad, Iran. Hypocalcemia was observed in early clinical trials requested. The patient underwent echocardiography according to holosystolic murmur grade 3/6 auscultation, which showed a patent ductus arteriosus (PDA), tetralogy of Fallot (TOF), ventricular septal defect (VSD), atrial septal defect (ASD), and pulmonary atresia (PA). No thymus was found on chest X-ray, and evidence of previous conflicts was observed in the heart. Finally, fluorescent in situ hybridization (FISH) was performed to check out Tuple gene deletion on chromosome 22q11.2, and the diagnosis was confirmed for DiGeorge syndrome. Although the incidences of neurological symptoms associated with hypocalcemia suggest a wide range of diseases as a differential diagnosis, pediatrics should consider the heart disorders for DiGeorge syndrome through clinical examinations and imaging, if necessary.