Key PointsQuestionUnlike candidate biomarkers inclusive for all forms of systemic inflammation, can dysfunction in host management of microbiota have a high positive predictive value as a biomarker for necrotizing enterocolitis?FindingsIn this diagnostic study of 136 premature infants, high amounts of intestinal alkaline phosphatase protein in stool and low intestinal alkaline phosphatase enzyme activity were associated with diagnosis of necrotizing enterocolitis. There was no association of intestinal alkaline phosphatase measures with non–gastrointestinal tract infections.MeaningMeasuring the inability of intestinal alkaline phosphatase to maintain host-microbiota homeostasis can potentially guide decisions for personalized care and treatment when an infant is most susceptible to developing necrotizing enterocolitis.

Perinatal Depression Screening (EPDS), Personal Health Questionnaire (PHQ) 2 and 9, demographics, and psychiatric history. Screening rates and incidence of mood disorders were compared between preand intra-COVID-19 cohorts. RESULTS:Of the 850 women included, 43.5% (n5370) were screened during perinatal visits and 49.8% (n5424) postpartum. Screenings were completed more frequently during postpartum checks pre-COVID-19 compared to during the pandemic with PHQ-2 (27.4% vs. 16.1%, P5.0001) and PHQ-9 (10.3% vs. 5.4%, P5.011). More women screened positive for depression at perinatal checks during the pandemic compared to pre-pandemic (13.2% vs. 4.7%, P5.0377). CONCLUSION:The COVID-19 pandemic has affected rates of maternal depression screening and has significant mental health impacts on this population. This study reveals baseline rates of screening in perinatal and postpartum visits at our institution, which is critical to delivery of quality care. This information will help inform strategies to increase rates of screening and ensure that mental health needs are being addressed, especially in times of emergency.

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Necrotizing enterocolitis (NEC) in preterm infants is an often fatal, gastrointestinal emergency. There is a need for a robust NEC biomarker that can be adopted in pathology labs and that is not confounded by sepsis. Use of such a NC biomarker could improve bedside management, lower morbidity and mortality, and permit patient selection in clinical trials for therapeutic candidates. We evaluated if aberrant intestinal alkaline phosphatase (iAP) biochemistry in infant stool is a molecular biomarker for necrotizing enterocolitis and not correlated to sepsis in the absence of NEC. There were 136 premature infants enrolled in three hospitals in this observational and prospective study. Median birthweight (IQR) was 1050 g (790‐350 g) and median gestational age was 28.4 weeks (26‐0.9 wks). Twenty‐five infants were diagnosed with severe NEC, 19 were suspected of having NEC, and 91 were non‐NEC infants. Twenty‐six patients were diagnosed with late‐onset sepsis and 14 had other non‐GI infections. Infant stool samples were collected between 24–40+ weeks postconceptual age (PCA). Enrolled infants were subject to abdominal radiography at physician and hospital site discretion. Enzyme activity and relative abundance of iAP were measured using fluorometric detection and immunoassays, respectively. Post‐measurement, biochemical data were evaluated against clinical entries from infants’ hospital stay. Fecal iAP content was 99±19, 123±41, and 5±3 (median±SE) for severe, suspected, and non‐NEC samples, respectively. Enzyme activity was 183±108, 355±180, and 613±218 kU/g (median±SE) for severe, suspected, and non‐NEC samples, respectively. ROC area under the curve (AUC) values were 0.96, 0.97, 0.54, and 0.58 for relative iAP content measurements at time of severe NEC, suspected NEC, sepsis, and other non‐GI infections; AUC values for iAP activity were 0.60, 0.76, 0.52 and 0.57, respectively. High amounts of iAP protein in stool and low iAP enzyme activity are reliable and specific biomarkers for NEC: iAP biochemistry uniquely has clinical utility in distinguishing NEC from sepsis. Support or Funding Information This work was supported by the National Institutes of Health (R41HD095779 to RB and SK; R01GM097350 to SK; K08DK101608, R03DK111473 and R01DK118568 to MG), National Science Foundation (IIP‐1713220 and IIP‐1547932 to RB and SK); March of Dimes (5‐FY17‐79 to MG), Louisiana Board of Regents (LEQSF‐RD‐D‐07 to SK), LSU LIFT2 (HSCNO‐2017‐LIFT‐006 to SK), Children’s Discovery Institute of Washington University and St. Louis Children’s Hospital (MG), Department of Pediatrics at Washington University School of Medicine, St. Louis (MG), LSU School of Medicine (BB, SK, and MH), and LSU Health Foundation (MH, ZG, and SK).