Objective According to the most recent metanalysis, the best way to establish safe enteral feeding in preterm babies using nasogastric or orogastric tubes is still not well understood. This study aimed to determine the effects of bolus nasal tubes versus bolus orogastric tubes on the time required to reach full enteral feeding in preterm infants, as well as to compare the incidence rates of adverse events including nonintentional removal or displacement of the feeding tube, aspiration pneumonia/pneumonitis, apnea, necrotizing enterocolitis, gastric residual, and growth parameters between the studied cohort of preterm infants. Study Design We conducted an unblinded pilot randomized clinical trial on hemodynamically stable preterm infants (>28 weeks) recruited from level 2 neonatal intensive care unit at Mansoura University Children's Hospital from June 2015 to May 2017. Results Our study included 98 stable preterm infants with mean gestational age (orogastric group: 33.27 ± 1.08, nasogastric group: 33.32 ± 1.57) and mean birthweight (orogastric group: 1,753.3 ± 414.51, nasogastric group: 1,859.6 ± 307.05). Preterm infants who were fed via bolus nasogastric tube achieved full enteral feeding in a significantly shorter duration compared with the infants fed via bolus orogastric tube. The incidence rates of aspiration and feeding tube displacement were significantly higher in the bolus orogastric tube group compared with the bolus nasogastric tube group. There was no difference in the incidence rates of apnea, necrotizing enterocolitis, bradycardia, oxygen desaturation, and gastric residual in both groups. Conclusion Preterm infants without any respiratory support receiving bolus nasogastric tube feeding achieved full enteral feeding significantly sooner than those receiving bolus orogastric tube feeding. Additionally, bolus nasogastric tube feeding had a lower incidence of aspiration, tube displacement, and the infants regained birthweight more quickly than those receiving orogastric tube feeding. Key Points

Following reports of increased new-onset diabetes and worse severity of DKA for children with diabetes following SARS-CoV-2 infection, we studied hospitalization rates for children with type 1 diabetes (T1DM) and type 2 diabetes (T2DM) in our center during the citywide shutdown. Methods. We conducted a retrospective chart review of children admitted to our two hospitals from January 1, 2018, to December 31, 2020. We included ICD-10 codes for diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar syndrome (HHS), and hyperglycemia only. Results. We included 132 patients with 214 hospitalizations: 157 T1DM, 41 T2DM, and 16 others (14 steroid induced, 2 MODY). Overall admissions rates for patients with all types of diabetes were 3.08% in 2018 to 3.54% in 2019 ( p = 0.0120 ) and 4.73% in 2020 ( p = 0.0772 ). Although there was no increase of T1DM admissions across all 3 years, T2DM admission rates increased from 0.29% to 1.47% ( p = 0.0056 ). Newly diagnosed T1DM rates increased from 0.34% in 2018 to 1.28% ( p = 0.002 ) in 2020, and new-onset T2DM rates also increased from 0.14% in 2018 to 0.9% in 2020 ( p = 0.0012 ). Rates of new-onset diabetes presenting with DKA increased from 0.24% in 2018 to 0.96% in 2020 ( p = 0.0014 ). HHS increased from 0.1% in 2018 to 0.45% in 2020 ( p = 0.044 ). The severity of DKA in newly diagnosed was unaffected ( p = 0.1582 ). Only 3 patients tested positive for SARS-CoV-2 infection by PCR. Conclusion. Our urban medical center is located in Central Brooklyn and serves a majority who are Black. This is the first study investigating pediatric diabetes cases admitted to Brooklyn during the first wave of the pandemic. Despite the overall pediatric admissions declining in 2020 due to the citywide shutdown, overall hospitalization rates in children with T2DM and in new-onset T1DM and T2DM increased, which is not directly associated with active SARS-CoV-2 infection. More studies are needed to elucidate the reason for this observed increase in hospitalization rates.

Introduction Rickets is a condition that can affect bones of infants and children. It is characterized by growth plate demineralization and can occur secondary to, most commonly, vitamin D deficiency or various problems with vitamin D, Calcium or Phosphate metabolism. Hypophosphatemic rickets (HR) is a type of rickets that is inherited by X linked dominant pattern mainly however it can be also inherited by autosomal dominant and recessive patterns in rare cases. X linked dominant type (XLH) affects about 1 in 20,000 newborns. Each of the other hereditary forms of HR has been identified in only a few families. Clinical features of XLH is similar to other types of rickets including metaphyseal widening, palpable rachitic rosaries, frontal prominence, malformation of the horizontal depression along the lower border of the chest, insufficient weight gain and leg bowing. Case presentation: A 10-month-old infant presented to endocrinology with vitamin D deficiency, low serum phosphorus and hyperparathyroidism. Physical examination showed macrocephaly with frontal bossing, widening of the wrists and rachitic rosaries. His lab results showed low 25 OH vitamin D (11 ng/ml) (N:20-50 ng/ml), low phosphorus (PO4) (3.3 mg/dl) (N:4-6.5 mg/dl), high PTH (113 pg/ml) (N: 20-65pg/ml), high alkaline phosphatase (ALP) (836 IU/L) (N: 135-518 IU/L) and normal calcium (Ca2+) (9.6 mg/dl) (N:9-11 mg/dl). Vitamin D treatment was started however his follow up lab results showed persistent hypophosphatemia for age (2.8mg/dl) and elevated ALP (600IU/l) despite normalization of vitamin D (38 ng/ml). Additional lab tests were done showing high PO4 excretion (19.5 mg/dl)(N:1:3.5 mg/dl), Ca/Cr ratio 0.005 (N <0.14), inappropriately normal FGF23 level (129 RU/ml) (N: >124 RU/mL). Genetic testing showed de novo mutation in PHEX gene (871C>T) which is consistent with XLH. PHEX gene mutation is the most common mutation associated with XLH. Normally this gene can directly or indirectly regulate a protein called fibroblast growth factor 23 (produced from FGF23 gene). This protein normally inhibits renal reabsorption of phosphate into the bloodstream. Gene mutations increase the production or reduce the breakdown of fibroblast growth factor 23 leading to an overactivation of this protein and reduction of phosphate reabsorption by the kidneys, resulting in hypophosphatemia. The patient was maintained on Burosomab (0.4 mg/kg biweekly); a recombinant human monoclonal antibody (IgG1) that binds to and inhibits the activity of fibroblast growth factor 23 (FGF23) and increases the phosphate reabsorption in the renal tubules. Conclusion: XLH due to PHEX gene mutation should be considered in rachitic children who have persistently low phosphate levels despite treating vitamin D deficiency.

No abstract