No abstract

BACKGROUND Neonates with necrotizing enterocolitis (NEC) have higher calprotectin levels in stool than do healthy neonates. However, it is not known whether high stool calprotectin at the onset of bowel symptoms identifies neonates who truly have NEC vs. other bowel disorders. STUDY DESIGN Neonates were eligible for this study when an x-ray was ordered to “rule-out NEC”. Stool calprotectin was quantified at that time and in a follow-up stool. Each episode was later categorized as NEC or not NEC. The location of calprotectin in the bowel was determined by immunohistochemistry. RESULTS Neonates with NEC had higher initial and follow-up stool calprotectin levels than did neonates without NEC. Calprotectin in bowel from neonates with NEC was within neutrophil extracellular traps (NETs). CONCLUSION At the onset of signs concerning for NEC, fecal calprotectin is likely to be higher in neonates with NEC. Calprotectin in their stools is exported from neutrophils via NETs.

OBJECTIVE Small-for-gestational-age (SGA) neonates, infants of diabetic mothers (IDM) and very-low-birth weight premature neonates (VLBW) are reported to have increased risk for developing iron deficiency and possibly associated neurocognitive delays. STUDY DESIGN We conducted a pilot study to assess iron status at birth in at-risk neonates by measuring iron parameters in umbilical cord blood from SGA, IDM, VLBW and comparison neonates. RESULTS Six of the 50 infants studied had biochemical evidence of iron deficiency at birth. Laboratory findings consistent with iron deficiency were found in one SGA, one IDM, three VLBW, and one comparison infant. None of the infants had evidence of iron deficiency anemia. CONCLUSIONS Evidence of biochemical iron deficiency at birth was found in 17% of screened neonates. Studies are needed to determine whether these infants are at risk for developing iron-limited erythropoiesis, iron deficiency anemia or iron-deficient neurocognitive delay.

In our health system, severe hemolytic disease in neonates born to group O (+) woman is not more likely in group A or B neonates than in controls (group O). We recognize that in other practices, particularly those who do not have a universal bilirubin screening/management program, ABO hemolytic disease severity might be different than in our system.

OBJECTIVE: The immature platelet fraction (IPF) is a laboratory measurement analogous to the reticulocyte count, but reflecting the thrombopoietic state. Similar to a reticulocyte count, it can be expressed as a percent (IPF% = percent of platelets that are immature) or as an absolute number per μl blood;the immature platelet count (IPC = IPF% × platelets per μl of blood). STUDY DESIGN: Using a retrospective analysis of de-identified data from non-thrombocytopenic neonates, we created reference intervals for IPF% and IPC. We then tested the value of these measurements for categorizing thrombocytopenic neonates. RESULTS: New charts display reference intervals for IPF% and IPC on the day of birth according to gestational age, and during the first 90 days after birth. Neonates with hyporegenerative varieties of thrombocytopenias (syndromes, small for gestational age, birth asphyxia) had lower IPF% and IPC than did neonates with consumptive thrombocytopenias (immune-mediated, infection, disseminated intravascular coagulation, necrotizing enterocolitis;both P < 0.0001). CONCLUSION: The new reference interval charts can be used to recognize abnormal IPFs. The IPF parameters can help clarify the kinetic mechanism responsible for thrombocytopenias in neonates.