A Randomized Trial of an Exclusive Human Milk Diet in Neonates with Single Ventricle Physiology.

OBJECTIVE: To determine whether weight gain velocity (g/kg/day) 30 days after the initiation of feeds after cardiac surgery and other clinical outcomes improve in infants with single ventricle physiology fed an exclusive human milk diet compared with a mixed human and bovine diet. STUDY DESIGN: In this multicenter, randomized, single blinded, controlled trial, term neonates 7 days of age or younger with single ventricle physiology and anticipated cardiac surgical palliation within 30 days of birth were enrolled at 10 US centers. Both groups received human milk if fed preoperatively. During the 30 days after feeds were started postoperatively, infants in the intervention group received human milk fortified once enteral intake reached 60 mL/kg/day with a human milk-based fortifier designed for term neonates. The control group received standard fortification with formula once enteral intake reached 100 mL/kg/day. Perioperative feeding and parenteral nutrition study algorithms were followed. RESULTS: We enrolled 107 neonates (exclusive human milk = 55, control = 52). Baseline demographics and characteristics were similar between the groups. The median weight gain velocity at study completion was higher in exclusive human milk vs control group (12 g/day [IQR, 5-18 g/day] vs 8 g/day [IQR, 0.4-14 g/day], respectively; P = .03). Other growth measures were similar between groups. Necrotizing enterocolitis of all Bell stages was higher in the control group (15.4 % vs 3.6%, respectively; P = .04). The incidence of other major morbidities, surgical complications, length of hospital stay, and hospital mortality were similar between the groups. CONCLUSIONS: Neonates with single ventricle physiology have improved short-term growth and decreased risk of NEC when receiving an exclusive human milk diet after stage 1 surgical palliation. TRIAL REGISTRATION: This trial is registered with ClinicalTrials.gov (www. CLINICALTRIALS: gov, Trial ID: NCT02860702).

Delayed Management of Insulin-Dependent Diabetes Mellitus in Children.

INTRODUCTION: Diabetic ketoacidosis (DKA) is a common presentation for pediatric new-onset insulin-dependent diabetes mellitus (IDDM). Delayed diagnosis is the major risk factor for DKA at disease onset. METHOD: Two pediatric endocrinologists independently reviewed the admission records to assess the appropriateness of preadmission management in various health care settings. RESULTS: Eighteen percent (n = 45) of patients with new-onset IDDM had a delayed diagnosis. Twenty-eight were misdiagnosed (respiratory [n = 9], nonspecific [n = 7], genitourinary [n = 4], gastrointestinal [n = 8] issues) and 17 were mismanaged. One child died within 4 hr of hospitalization, presumably because of a hyperosmolar coma. Forty-six percent (n = 21) of patients with delayed diagnosis presented with DKA, comprising 18% of all DKA cases. DISCUSSION: A significant number of patients with new-onset IDDM were either misdiagnosed or mismanaged. All providers must be appropriately trained in diagnosing new-onset IDDM and follow the standard of clinical care practices.

Diabetes Control and Adherence in Adolescence.

Type 1 diabetes is a chronic disease that can lead to severe complications if poorly controlled. Adolescents are particularly vulnerable to worsening diabetes control due to changes in physiology, family dynamics, and social interactions. Good diabetes control requires following a regimen of frequent blood glucose checks, accurate carbohydrate counts, and compliance with insulin administration. Patients who are challenged in controlling their diabetes do tend to respond to behavioral interventions; however, the effect of the intervention wanes over time. Using technology to provide interventions has shown promise in terms of improving compliance. Positive family support and adequate knowledge of the developmental stages is important to ensure a successful transition from childhood to adolescence. Providers should also incorporate a structured transition from adolescent to adult diabetes care. [Pediatr Ann. 2016;45(9):e327-e331.].

Prolonged hypoxia increases ROS signaling and RhoA activation in pulmonary artery smooth muscle and endothelial cells.

Phase I of the hypoxic pulmonary vasoconstriction (HPV) response begins upon transition to hypoxia and involves an increase in cytosolic calcium ([Ca(2+)](i)). Phase II develops during prolonged hypoxia and involves increases in constriction without further increases in [Ca(2+)](i), suggesting an increase in Ca(2+) sensitivity. Prolonged hypoxia activates RhoA and RhoA kinase, which may increase Ca(2+) sensitivity, but the mechanism is unknown. We previously found that reactive oxygen species (ROS) trigger Phase I. We therefore asked whether ROS generation during prolonged hypoxia activates RhoA in PA smooth muscle cells (PASMCs) and endothelial cells (PAECs) during Phase II. By using a cytosolic redox sensor, RoGFP, we detected increased oxidant signaling in prolonged hypoxia in PASMCs (29.8 +/- 1.3% to 39.8 +/- 1.4%) and PAECs (25.9 +/- 2.1% to 43.7.9 +/- 3.5%), which was reversed on the return to normoxia and was attenuated with EUK-134 in both cell types. RhoA activity increased in PASMCs and PAECs during prolonged hypoxia (6.4 +/- 1.2-fold and 5.8 +/- 1.6-fold) and with exogenous H(2)O(2) (4.1- and 2.3-fold, respectively). However, abrogation of the ROS signal in PASMCs or PAECs with EUK-134 or anoxia failed to attenuate the increased RhoA activity. Thus, the ROS signal is sustained during prolonged hypoxia in PASMCs and PAECs, and this is sufficient but not required for RhoA activation.