Search

BACKGROUND/OBJECTIVES: Preterm infants have low vitamin A stores at birth, and parenteral administration of high-dose vitamin A reduces pulmonary morbidity. The aim was to characterize vitamin A transport and status. SUBJECTS/METHODS: Prospective study of 69 preterm infants (median birth weight 995 g, gestational age 28 weeks), in which 51 received 5000 IU vitamin A three times per week intramuscular (i.m.) for 4 weeks and 18 infants without i.m. vitamin A served as controls. Serum retinol, retinyl palmitate, total retinol-binding protein 4 (RBP4), retinol-unbound RBP4 (apo-RBP4) and transthyretin concentrations were determined at days 3 (D3) and 28 (D28) of life. RESULTS: D3 retinol concentrations were low for the entire group (382 (285/531) nmol/l; median/interquartile range) and unrelated to gestational age. D28 retinol was unchanged in controls (382 (280/471) nmol/l), but increased in the vitamin A group (596 (480/825) nmol/l; P < 0.001). A similar pattern was observed for RBP4. The calculated retinol-to-RBP4 ratio rose in vitamin A infants (D3: 0.81 (0.57/0.94), D28: 0.98 (0.77/1.26); P < 0.01) but not in controls. In the vitamin A group, the retinol-to- RBP4 ratio was > 1 in 15% of all infants on D3 and in 45% of infants on D28, but was ≤ 1 in all, but one, controls on D28. CONCLUSIONS: In preterm infants receiving a 4-week course of high-dose i.m. vitamin A, serum retinol concentrations increased by 55%, with molar concentrations of retinol exceeding those of RBP4 in 45% of the infants suggesting transport mechanisms other than RBP4. European Journal of Clinical Nutrition (2014) 68, 1300-1304; doi: 10.1038/ejcn.2014.202; published online 15 October 2014, INTRODUCTION An adequate vitamin A supply is essential for normal fetal and postnatal development. During pregnancy, retinol reaches the fetus via the placenta, whereas after birth it is ingested as [...]

OBJECTIVE: Periventricular leukomalacia is the predominant type of brain injury in preterm infants underlying the development of cerebral palsy. Periventricular leukomalacia has its peak incidence at 23 to 32 weeks postconceptional age characterized by extensive oligodendrocyte migration and maturation. Oxygen toxicity has been identified as a possible contributing factor to the pathogenesis of cerebral palsy in survivors of preterm birth. 17beta-estradiol (E2) is important for the development and function of the central nervous system. Furthermore, neuroprotective properties have been attributed to estrogens. We examined the effect of E2 on hyperoxia-induced cell death in the developing white matter in the rat brain. METHODS: Six-day-old (P6) rat pups, the immature oligodendroglial cell line (OLN-93), and primary oligodendrocyte cultures were subjected to 80% O(2) in the presence or absence of E2 (600 microg/kg intraperitoneally in vivo, 10(-6)-10(-10)M in vitro). Cell counts and lactate dehydrogenase assay were used to assess cell survival. Immunoblot analysis was used for detection of estrogen receptor expression and investigation of apoptotic signaling pathways. White matter injury was assessed by myelin basic protein immunocytochemistry at P11. RESULTS: E2 produced significant dose-dependent protection against oxygen-induced apoptotic cell death in primary oligodendrocytes. Treatment with E2 prevented hyperoxia-induced proapoptotic Fas-upregulation and caspase-3 activation. Finally, E2 antagonized hyperoxia-induced inactivation of extracellular signal-regulated kinase 1 and 2 and Akt, key kinases of the mitogen-activated protein kinase and phosphatidylinositol 3-kinase cell survival promoting pathways, respectively. Loss of myelin basic protein labeling was seen in P11 pups after oxygen exposure, and E2 attenuated this injury. INTERPRETATION: These results suggest a possible role for estrogens in the prevention of neonatal oxygen-induced white matter injury. [ABSTRACT FROM AUTHOR]

BACKGROUND: Outbreaks of health care-associated infections in neonatal intensive care units (NICUs) are frequent and have received more attention in medical literature than outbreaks from other types of intensive care units (ICUs). The objective of this systematic review was to identify differences between outbreaks of health care-associated infections in NICUs and other ICUs as reported to date in the medical literature. METHODS: Screening the outbreak database (http://www.outbreak-database.com), a systematic comparison of outbreaks was performed with the following categories: causing pathogen, type of infection, sources identified, and measures taken to stop the outbreak. RESULTS: Two hundred and seventy-six outbreaks were reported from NICUs and 453 from other ICU types. Enterobacteriaceae were significantly more often responsible for NICU outbreaks, whereas nonfermenting bacteria are more frequently identified in other ICU types. On average, 23.9 patients and 1.8 health care workers were involved in NICU outbreaks. Average mortality in NICU outbreak was 6.4% (1.5 newborns on average). In 48.6% of NICU outbreaks the authors were unable to identify the sources compared with 38.0% in other ICU outbreaks. The most important infection control measures were significantly more often implemented in NICUs than in other ICUs. CONCLUSIONS: Systematic outbreak analysis is essential for gaining insights into the control of NICU outbreaks. [ABSTRACT FROM AUTHOR]