Neonatal alloimmune thrombocytopenia (NAIT) is a fetomaternal incompatibility most commonly induced by maternal anti-HPA-1a, IgG alloantibodies against a polymorphic epitope of the glycoprotein IIb/ IIIa complex in approximately 97.5% of white patients. Current guidelines recommend transfusion of immunologically compatible platelets to prevent cerebral hemorrhage, the most severe complication in affected newborns. Such platelet concentrates, however, are often not readily available. In a retrospective analysis in German and Canadian centers, 27 newborns with NAIT were identified who received platelets from random donors. Unexpectedly, 24 of 27 newborns showed an increase above a threshold of 40 ؋ 10 9 platelets per liter, with moderate (n ؍ 8) or significant (n ؍ 16) platelet count increments (more than 80 ؋ 10 9 /L). We conclude that transfusion of platelet concentrates from random donors is an appropriate strategy in the management of unexpected, severe NAIT predominantly in first pregnancies, pending the availability of compatible platelets. IntroductionNeonatal alloimmune thrombocytopenia (NAIT) is an immunemediated fetomaternal incompatibility. It occurs after maternal alloimmunization against polymorphic epitopes on fetal platelet glycoproteins (GPs) and diaplacental transfer of maternal IgG alloantibodies to the fetus. Alloantibodies implicated in NAIT are directed against antigens on GP IIb/IIIa, Ib/IX, Ia/IIa, and CD109. The most common antibody is anti-HPA-1a (originally referred to as anti-Zw(a) 1 ), which accounts for about 75% of cases. 2 A leucine-proline polymorphism of GP IIIa of amino acid 33 is the molecular basis of the HPA-1a/1b polymorphism. 3 NAIT has an incidence of 1:1000 to 1:2000 births in white populations and may occur if a pregnant, HPA-1b/1b homozygous woman is immunized with HPA-1a-positive platelets by her fetus. 4,5 NAIT is a self-limiting and transient disorder with an excellent prognosis in the absence of cerebral bleeding. Approximately 42% of newborns with NAIT are born to primiparous women. 6 Prenatal screening for maternal platelet-specific alloantibodies has not been established, 5 and the birth of a first affected child therefore occurs unexpectedly. Because a significant proportion of untreated newborns with NAIT (approximately 7% to 14% 6,7 ) are affected by cerebral hemorrhage in the first days of life, a liberal attitude toward platelet transfusion of the severely thrombocytopenic newborn is considered appropriate. 8 While intravenous ␥-globulin (IVIG) has been shown to be of some benefit in the antenatal management of alloimmune thrombocytopenia, 9 high-dose IVIG can only be recommended as a complementary treatment modality in the management of NAIT because of the delayed rise in platelet counts and limited evidence from a small series of cases. 10,11 Currently, antigen-negative platelets are considered optimal for the prevention of hemorrhage in newborns with suspected NAIT. 8,12 To meet this need, transfusion services have attempted to stock HPA-1a-negative an...
In the immature human brain, periventricular leukomalacia (PVL) is the predominant white matter injury underlying the development of cerebral palsy. PVL has its peak incidence during a well-defined period in human brain development (23-32 weeks postconceptional age) characterized by extensive oligodendrocyte migration and maturation. We hypothesized that the dramatic rise of oxygen tissue tension associated with mammalian birth and additional oxygen exposure of the preterm infant during intensive care may be harmful to immature oligodendrocytes (OLs). We therefore investigated the effects of hyperoxia on rat oligodendroglia cells in vitro and in vivo. Immature OLs (OLN-93), their progenitors [preoligodendrocytes (pre-OL)], and mature OLs were subjected to 80% hyperoxia (24-96 hr). Flow cytometry was used to assess cell death. Cell viability was measured by metabolism of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium (MTT). In addition, 6-day-old rat pups were subjected to 80% oxygen (24 hr) and then sacrificed, and their brains were processed for immunfluorescence staining. Apoptosis was detected at various stages (annexin-V, activated caspase-3) after 24-48 hr of incubation in 80% oxygen in pre- and immature OLs. Mature OLs were resistant to oxygen exposure. These results were confirmed by MTT assay. This cell death was blocked by administration of the pan-caspase inhibitor zVAD-fmk. Degeneration of OLs was confirmed in 7-day-old rat brains by positive staining for activated caspase-3. Hyperoxia triggers maturation-dependent apoptosis in immature and pre-OLs and involves caspase activation. This mechanism may be relevant to the white matter injury observed in infants born preterm.
Natural processes do not always function perfectly. In breastfeeding, problems are encountered in up to 80% of mother-infant dyads. Altogether, in Western societies, the difficulties reduce the breastfeeding rate within the first months drastically. To deal with the problems of breastfeeding efficiently requires a profound understanding of its physiology, as well as of its psychological and social determinants. This review focuses on the current knowledge of breastfeeding physiology, only touching the psychosocial factors, which are included in the promotion strategies. Subsequently, it scrutinizes definitions, incidences, prevention, and treatment of breastfeeding problems faced most frequently by nursing mothers and their consultants. Not all measures used in counseling mothers and not all treatments for the most common medical problems withstand a careful evaluation on the basis of current scientific data. However, applying proven prevention strategies will significantly improve the well being of mothers and their infants, and may contribute to an affective attitude that increases the success, frequency, and duration of breastfeeding.
Background: Milk curd obstruction as a cause of intestinal obstruction has been known since 1959, but has nearly disappeared. However, in recent years it has experienced a revival in small premature infants. Objective: The aim of this study was to evaluate the clinical characteristics of milk curd obstruction (lactobezoar) in preterm infants. Methods: Data of preterm infants with milk curd obstruction cared for at a large tertiary neonatal intensive care unit between 2012 and 2016 were retrieved from the electronic registry and paper records. Results: A total of 10 infants (2 girls, 8 boys) were identified: the median birth weight was 595 g (range 270–922), gestational age was 24.4 weeks (23.4–27.0), weight-for-gestational age percentile was 16 (0–62), and age at diagnosis was 28 days (16–64). Five infants (50%) were small for gestational age. All neonates had received fortified human milk (added protein 2.0 g/100 mL, range 0–2.8; added calcium 2,400 µmol/100 mL, range 0–6 844; added phosphate 2,400 µmol/100 mL, range 0–5,178). Seven neonates underwent surgery, and 2 infants died. Hyperechoic masses in extended bowel loops, visualised by abdominal ultrasound, and pale/acholic faeces were hallmarks of milk curd obstruction. Conclusions: In this study, milk curd obstruction occurred exclusively in infants with a birth weight < 1,000 g (2.2%) and < 28 weeks’ gestational age (2.4%). Male and small for gestational age infants appeared to be at increased risk. Paying attention to the colour of the faeces of infants at risk might help to diagnose milk curd obstruction at an early stage.
WHAT'S KNOWN ON THIS SUBJECT: Phototherapy decreases bilirubin concentration in skin more rapidly than in blood. During and after phototherapy, transcutaneous bilirubin measurements are considered unreliable and therefore discouraged. WHAT THIS STUDY ADDS:Transcutaneous bilirubin underestimates total serum bilirubin by 2.4 mg/dL (SD, 2.1 mg/dL) during the first 8 hours after phototherapy. This gives a safety margin of ∼7 mg/dL below the treatment threshold to omit confirmatory blood sampling. abstract OBJECTIVES: To compare transcutaneous bilirubin (TcB) readings with total serum bilirubin (TSB) after phototherapy, estimating the range of TcB where confirmation through blood sampling can be avoided. METHODS:Preterm and term neonates receiving in-hospital phototherapy underwent TcB measurements (device JM-103, TcB) alongside routine TSB before and after treatment. We calculated time-dependent safety margins for transcutaneous readings to correctly assign 99% of infants not to receive phototherapy. RESULTS:Between August 2011 and December 2012, 86 newborn infants (47 preterm, 39 term) underwent a total of 189 parallel measurements. Mean difference (TcB 2 TSB) before treatment was 20.6 mg/dL (SD, 1.9 mg/dL). Within the first 8 hours after phototherapy, TcB levels were 22.4 mg/dL (SD, 2.1 mg/dL) below TSB. Thereafter the difference gradually returned to pretreatment values (21.8 mg/dL in 8-16 hours, 21.1 mg/dL in 16-24 hours, and 20.8 mg/dL after 24 hours), while variations remained stable over time (SD, 1.4-1.8 mg/dL). In the first 8 hours after treatment, TcB levels of 27.3 mg/dL below the individual phototherapy threshold allowed safe rejection of confirmatory blood sampling. After 8 hours, that safety margin was reduced to approximately 25.0 mg/dL. CONCLUSIONS: TcB measurements remain a valuable tool after phototherapy when time-dependent underestimation of TcB is being accounted for.
In VLBW infants with PDA, ibuprofen treatment was associated with higher bilirubin levels than indomethacin.
In premature infants, oxygen free radicals generated following neonatal resuscitation are associated with subsequent diseases such as retinopathy of prematurity and bronchopulmonary dysplasia. Recent studies in brain tissue samples have shown that nonphysiologic oxygen levels play a key role in induction of apoptosis in the developing brain. Estrogen is a well-established agent in neuroprotection and, therefore, is thought to be neuroprotective even in the premature brain. Astrocytes appear to have a critical role in protection and survival of neurons in the brain. As one of the glial cell types, they have a great potential for possible involvement in the mediation of estrogen neuroprotective effects. The aim of our study was to analyze whether astrocytes in cell cultures are damaged by hyperoxia and whether 17beta-estradiol (E2) can protect them against apoptosis. Additionally, we investigated the mechanism of the protection by E2, hypothesizing that it is mediated through extracellular signal-regulated kinase (ERK1/2). Cells underwent eightfold more apoptosis when cultivated in hyperoxia compared with normoxia. Addition of E2 reduced apoptosis in hyperoxia by more than 50%. Levels of ERK1/2 and phosphorylated ERK1/2 were increased after hyperoxia compared with normoxia. Preincubation with E2 prior to exposure to hyperoxia resulted in decreased levels of ERK1/2 and pERK1/2. Hyperoxia induces apoptosis in C8-D1A cells, and E2 seems to be a protecting factor for astrocytes in hyperoxia. This effect is not mediated through up-regulation of pERK1/2.
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