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Erythroblastosis Fetalis [keywords]
- Bilirubin-induced neurologic damage. [Comment, Letter]
- N Engl J Med 2014 Mar 6; 370(10):978-9.
- Bilirubin-induced neurologic damage. [Comment, Letter]
- N Engl J Med 2014 Mar 6; 370(10):979.
- Mirror syndrome after fetoscopic laser therapy for twin-twin transfusion syndrome due to transient donor hydrops that resolved before delivery. A case report. [Case Reports, Journal Article]
- J Reprod Med 2014 Jan-Feb; 59(1-2):90-2.
Mirror syndrome is a rare complication of twin-twin transfusion syndrome (TTTS). Its clinical picture includes massive edema, oliguria, and hemodilution in the context of fetal hydrops. The occurrence of mirror syndrome after fetoscopic laser therapy for TTTS has been well documented, but resolution of mirror syndrome before delivery has not been reported in the literature.A 33-year-old woman was referred to our institution at 23(6)/7 weeks' gestation for TTTS, which had been treated with amnioreduction twice: at 21 and 22 gestational weeks, respectively. Mirror syndrome was diagnosed after fetoscopic laser therapy for TTTS at 24 weeks' gestation due to maternal manifestations of pulmonary edema, skin edema, anemia, low blood protein concentration and proteinuria accompanied by donor hydrops. The maternal respiratory symptoms then gradually abated in <2 weeks along with improved fetal condition, resulting in a delivery with favorable outcomes at 36 weeks' gestation.Manifestation of mirror syndrome after fetoscopic laser therapy in twin-twin transfusion due to donor hydrops doesn't necessarily predict a poor perinatal outcome.
- In response. [Comment, Letter]
- J Obstet Gynaecol Can 2014 Feb; 36(2):115.
- Investigation and management of non-immune fetal hydrops. [Comment, Letter]
- J Obstet Gynaecol Can 2014 Feb; 36(2):114.
- Developmental onset of bilirubin-induced neurotoxicity involves Toll-like receptor 2-dependent signaling in humanized UDP-glucuronosyltransferase1 mice. [Journal Article, Research Support, N.I.H., Extramural]
- J Biol Chem 2014 Feb 21; 289(8):4699-709.
Biological and signaling events that connect developmentally induced hyperbilirubinemia to bilirubin-induced neurological dysfunction (BIND) and CNS toxicity in humans are poorly understood. In mammals, UDP-glucuronosyltransferase 1A1 (UGT1A1) is the sole enzyme responsible for bilirubin glucuronidation, a rate-limiting step necessary for bilirubin metabolism and clearance. Humanized mice that express the entire UGT1 locus (hUGT1) and the UGT1A1 gene, develop neonatal hyperbilirubinemia, with 8-10% of hUGT1 mice succumbing to CNS damage, a phenotype that is presented by uncontrollable seizures. We demonstrate that neuroinflammation and reactive gliosis are prominent features of bilirubin brain toxicity, and a disturbed redox status resulting from activation of NADPH oxidase is an important contributing mechanism found in BIND. Using knock-out mice and primary brain cells, we connect a key pattern recognition receptor, Toll-like receptor 2 (TLR2), to hyperbilirubinemia-induced signaling. We illustrate a requirement for TLR2 signaling in regulating gliosis, proinflammatory mediators, and oxidative stress when neonatal mice encounter severe hyperbilirubinemia. TLR2-mediated gliosis strongly correlates with pronounced neuroinflammation in the CNS with up-regulation of TNFα, IL-1β, and IL-6, creating a pro-inflammatory CNS environment. Gene expression and immunohistochemistry staining show that hUGT1/Tlr2(-/-) mice fail to activate glial cells, proinflammatory cytokines, and stress response genes. In addition, bilirubin-induced apoptosis was significantly enhanced by blocking TLR2 signaling indicating its anti-apoptotic property. Consequently, a higher neonatal death rate (57.1%) in hUGT1/Tlr2(-/-) mice was observed when compared with hUGT1 mice (8.7%). These results suggest that TLR2 signaling and microglia neuroinflammation are linked to a repair and/or protection mode against BIND.
- Non-immune hydrops fetalis. [Journal Article, Review]
- Niger J Med 2013 Oct-Dec; 22(4):266-73.
Non-immune hydrops fetalis (NIHF) is a rare fetal condition with a very high mortality in spite of advances in prenatal diagnostic techniques, early detection, and individualized management. Despite advancement in fetal therapy and rapidly developing new knowledge about the aetiology and prenatal diagnosis, its management has remained controversial.This is a descriptive review ofNIHF.NIHF is a rare fetal condition that presents in an extremely acute manner with almost 90% mortality. Fetal cardiac anomalies are the most common cause and chromosome anomalies are the second-most-common cause. The worst prognosis was related to prematurity, severe hydrops, anaemia, cardiac malformations, chromosomal disorders and congenital infections. Fetal interventions includeboth medical and surgical modalities.NIHF is a rare condition with high prenatal mortality. The exact pathophysiology is still poorly understood. It is important to detect NIHF early, diagnose the underlying cause and institute appropriate treatment. There is need for autopsy of all fetuses or neonates who die from NIHF.
- Relation of placental diagnosis in stillbirth to fetal maceration and gestational age at delivery1). [JOURNAL ARTICLE]
- J Perinat Med 2013 Nov 21.:1-15.
Abstract Aim: To study the relation of retention of dead fetus resulting in its maceration and gestational age at delivery to placental diagnosis. Methods: Some 75 clinicoplacental phenotypes have been retrospectively analyzed in 520 consecutive stillbirths, 329 macerated and 191 nonmacerated, and at three gestational age interval cohorts (330 second trimester, 102 preterm third trimester, and 88 term). Chi-square and clustering methods (Ward dendrograms and multidimensional scaling) were used for statistical analysis. Results: Maternal diabetes mellitus, induction of labor, fetal growth restriction, various umbilical cord abnormalities, and placental clusters of sclerotic/hemosiderotic chorionic villi were more common in macerated stillbirths, while clinicoplacental signs and symptoms of ascending infection and placental abruption, i.e., retroplacental hematoma, premature rupture of membranes, and acute chorioamnionitis in nonmacerated stillbirths. Placental abnormalities were less common in the second trimester, other than the acute chorioamnionitis. Patterns of chronic hypoxic placental injury were common in preterm third trimester, while signs of in-utero hypoxia (abnormal cardiotocography, meconium, and histological erythroblastosis of fetal blood) in term pregnancy. In addition to classical statistics, the clustering analyses added new information to placental investigation of cause of stillbirth. Conclusions: Macerated third trimester stillbirths have multifactorial etiology more likely than the second trimester stillbirths and the likely stasis-induced fetal thrombotic vasculopathy secondary to occult umbilical cord compromise should be sought in placental investigation in such cases. Nonmacerated stillbirths are associated with ascending infection and placental abruption.
- Bilirubin-induced neurologic damage--mechanisms and management approaches. [Journal Article, Review]
- N Engl J Med 2013 Nov 21; 369(21):2021-30.
- [Diagnostic value of amplitude-integrated electroencephalography in predicting outcome of newborn patients in neonatal intensive care unit]. [English Abstract, Journal Article, Research Support, Non-U.S. Gov't]
- Zhonghua Er Ke Za Zhi 2013 Aug; 51(8):614-20.
To assess the diagnostic value of amplitude-integrated electroencephalography (aEEG) in predicting outcome of newborns who were at high risk for central nervous system without severe hypoxic-ischemic encephalopathy.Forty-two consecutive patients at risks for neurological disorders referred to our level-III NICU were prospectively enrolled in the study over a period of 3 years. They were classified on the basis of their primary diagnoses including hypoglycemic brain damage, meningoencephalitis, bilirubin encephalopathy, and metabolic disease. Clinical data were collected. Amplitude-integrated and raw EEG tracings were assessed for background pattern, sleep-wake cycling, and epileptiform activity. The neuromotor development of survivors was assessed by using the Infant Neurological International Battery (INFANIB).The characteristic of aEEG tracings in 42 infants showed continuous normal voltage (CNV)(n = 15), discontinuous voltage (DC)(n = 9), burst-suppression (BS) BS(+) (n = 6), BS(-)(n = 7), flat (FT, n = 5); mature sleep-wake cycling (SWC, n = 4), immature SWC (n = 14), no SWC (n = 24); 30 infants (71.4%) had electrical seizures: single seizure (n = 6); repetitive seizures (n = 7), and status epilepticus (SE) (n = 17).aEEG of 20 infants who had poor outcome showed FT (n = 5), BS(-)/SE (n = 6), BS(-)/ repetitive seizures (n = 1) , BS(+)/SE (n = 1), BS(+)/repetitive seizures (n = 1), DC/SE(n = 6). Chi-square analysis and Spearman rank correlation analysis showed the classification of aEEG background pattern, SWC and comprehensive score (score system was developed by evaluation of the above 3 variables) were correlated with the outcome of these infants at high neurological risks.Amplitude-integrated electroencephalography can provide important information of the status of cerebral function in neonates at high neurological risk and help to predict their outcome.