Database : MEDLINE
Search on : hydrops and fetalis [Words]
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[PMID]: 29476731
[Au] Autor:Sudrié-Arnaud B; Marguet F; Patrier S; Martinovic J; Louillet F; Broux F; Charbonnier F; Dranguet H; Coutant S; Vezain M; Lanos R; Tebani A; Fuller M; Lamari F; Chambon P; Brehin AC; Trestard L; Tournier I; Marret S; Verspyck E; Laquerrière A; Bekri S
[Ad] Address:Department of Metabolic Biochemistry, Rouen University Hospital, Rouen 76000, France.
[Ti] Title:Metabolic causes of nonimmune hydrops fetalis: A next-generation sequencing panel as a first-line investigation.
[So] Source:Clin Chim Acta;481:1-8, 2018 Feb 22.
[Is] ISSN:1873-3492
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:PURPOSES: Hydrops fetalis is a life-threatening fetal condition, and 85% of all cases are classified as nonimmune hydrops fetalis (NIHF). Up to 15% of NIHF cases may be due to inborn errors of metabolism (IEM), but a large proportion of cases linked to metabolic disorders remains undiagnosed. This lack of diagnosis may be related to the limitations of conventional biological procedures, which involve sequential investigations and require multiple samples and steps. In addition, this approach is time consuming. We have developed a next-generation sequencing (NGS) panel to investigate metabolic causes of NIHF, ascites, and polyhydramnios associated to another fetal abnormality. METHODS: The hydrops fetalis (HydFet) panel was designed to cover the coding regions and flanking intronic sequences of 41 genes. A retrospective study of amniotic fluid samples from 40 subjects was conducted. A prospective study was subsequently initiated, and six samples were analyzed using the NGS panel. RESULTS: Five IEM diagnoses were made using the HydFet panel (Niemann-Pick type C (NPC), Barth syndrome, HNF1Β deficiency, GM1 gangliosidosis, and Gaucher disease). This analysis also allowed the identification of 8p sequence triplication in an additional case. CONCLUSION: NGS combined with robust bioinformatics analyses is a useful tool for identifying the causative variants of NIHF. Subsequent functional characterization of the protein encoded by the altered gene and morphological studies may confirm the diagnosis. This paradigm shift allows a significant improvement of IEM diagnosis in NIHF.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 3297 MEDLINE  
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[PMID]: 29500832
[Au] Autor:Laterre M; Bernard P; Vikkula M; Sznajer Y
[Ad] Address:Centre for human Genetics, Cliniques Universitaires St. Luc, U.C.L., Brussels.
[Ti] Title:Improved diagnosis in non-immune hydrops fetalis using a standardized algorithm.
[So] Source:Prenat Diagn;, 2018 Mar 02.
[Is] ISSN:1097-0223
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: The aim of this study was to outline the disease etiology in a cohort of fetuses prenatally diagnosed with non-immune hydrops fetalis (NIHF). METHODS: Based on a literature review we defined precise criteria to select the NIHF cases. Those were further classified into 14 categories. To complete this first step, a literature review was performed using homogeneous criteria to compare our results. RESULTS: Over the 10-year period, 102 fetuses were diagnosed with NIHF and included in the analysis. The etiology was identified in 86.3% (88/102) of them, with diagnostic distribution from the most prevalent to the least frequent (number of fetuses; %) being: chromosomal (33/102; 32.4%), lymphatic dysplasia (14; 13.7%), cardiovascular (10; 9.8%), 'syndromic' (10; 9.8%), infection (8; 7.8%), and hematologic (8; 7.8%). CONCLUSION: This literature review enabled us to emphasize the absence of homogeneous criteria used to define NIHF. When compared to literature our data analysis highlighted the relevance of applying our full diagnostic approach to decrease the rate of idiopathic NIHF cases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180303
[Lr] Last revision date:180303
[St] Status:Publisher
[do] DOI:10.1002/pd.5243

  3 / 3297 MEDLINE  
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[PMID]: 29498944
[Au] Autor:Jnah A; Newberry DM; Eisenbeisz E
[Ad] Address:WakeMed Hospitals, Raleigh, North Carolina (Drs Jnah and Newberry); and Omega Statistics, Murrieta, California (Ms Eisenbeisz).
[Ti] Title:Comparison of Transcutaneous and Serum Bilirubin Measurements in Neonates 30 to 34 6/7 Weeks' Gestation Before, During, and After Phototherapy.
[So] Source:Adv Neonatal Care;, 2018 Mar 01.
[Is] ISSN:1536-0911
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: The use of noninvasive, transcutaneous bilirubin monitoring (TcB) as a jaundice screen in full-term infants is well established; however, there is a paucity of research evaluating the use of TcB in premature infants. PURPOSE: To compare agreement and consistency of transcutaneous and serum bilirubin measurements in a multiracial premature infant population ranging from 30 to 34 6/7 weeks' gestation before, during, and after phototherapy. METHODS: Forty-five neonates, 30 to 34 6/7 weeks' gestation, were enrolled in this prospective, correlational study over a 12-month period. One set of paired transcutaneous and serum bilirubin measurements, per neonate, was obtained before phototherapy, during therapy, and after phototherapy. Exclusion criteria included neonates with positive direct coombs test or evidence of hemolytic disease, major congenital anomalies, hydrops fetalis, and those not expected to survive. RESULTS: There was a strong, positive correlation between TcB and total serum monitoring (TSB) measurements obtained pretherapy (r = 0.797, P < .001). A moderate correlation was noted between TcB and TSB measurements obtained during therapy (r = 0.588, P < .001). A strong correlation was noted between TcB and TSB measurements obtained posttherapy (r = 0.869, P < .001). There were no significant differences between paired samples across time (F = 0.891, P = .41, partial η = 0.01). The TSB measurements were consistently lower than TcB pretherapy, during, and posttherapy. IMPLICATIONS FOR PRACTICE: The TcB measurements provide a reliable estimation, generally within 2 to 3 mg/dL of TSB levels, in premature infants 30 to 34 6/7 weeks' gestation. IMPLICATIONS FOR RESEARCH: Investigation of consumption of time and nursing personnel required to perform TcB testing, compared with TSB testing, is indicated. Cost analyses comparing TcB-driven screening protocols and interval TSB measurements, among premature infants, are indicated. As newer generations of TcB devices are approved for use, additional studies using mixed-race populations of premature infants will be necessary to continue to evaluate the reliability and validity of this screening tool within the everyday neonatal intensive care unit.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:Publisher
[do] DOI:10.1097/ANC.0000000000000469

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[PMID]: 29493331
[Au] Autor:He S; Li J; Huang P; Zhang S; Lin L; Zuo Y; Tian X; Zheng C; Qiu X; Chen B
[Ad] Address:a Prenatal Diagnostic Center, Institute of Birth Defect Prevention and Control , Guangxi Zhuang Autonomous Region Women and Children Care Hospital , Nanning , Guangxi Zhuang Autonomous Region , People's Republic of China.
[Ti] Title:Characterization of Hb Bart's Hydrops Fetalis Caused by - - and a Large Novel α -Thalassemia Deletion.
[So] Source:Hemoglobin;:1-4, 2018 Mar 01.
[Is] ISSN:1532-432X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Hb Bart's hydrops fetalis is the most severe and generally fatal clinical phenotype of α-thalassemia (α-thal), which is due to the deletion of all four functional α-globin genes of hemoglobin (Hb), resulting in no α-globin chain production (- -/- -). Homozygosity for the - - (Southeast Asian) α-globin gene deletion is the main cause of the Hb Bart's hydrops fetalis in Asia, especially South China. Occasionally, other α -thal deletions can also be found. In this study, we report a case with an atypical form of Hb Bart's hydrops fetalis that was caused by - - and a large novel α -thal deletion (- - ) (Guangxi). The fetus with Hb Bart's in our study presented fetal hydrops features in early gestation which was different from that of traditional Hb Bart's hydrops fetalis with a homozygous - - deletion. The early onset of fetal hydrops is attributed to the decreased formation of embryonic Hb Portland (ζ2γ2), which is proposed as a candidate for reactivation in cases of severe α-thal. Our findings indicated that it was important to characterize new or rare mutations, and highlighted the significance of using ultrasonography to identify signs of Hb Bart's hydrops fetalis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:Publisher
[do] DOI:10.1080/03630269.2018.1434198

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[PMID]: 29390381
[Au] Autor:Ek S; Rosenborg S
[Ad] Address:Department of Obstetrics and Gynecology, Center of Fetal Medicine, Karolinska University Hospital.
[Ti] Title:Mesalazine as a cause of fetal anemia and hydrops fetalis: A case report.
[So] Source:Medicine (Baltimore);96(50):e9277, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: Mesalazine and its prodrug sulfasalazine are both used for inflammatory bowel disease. Sulfasalazine has been associated with hematological side-effects such as aplastic and hemolytic anemia in patients, but also in fetuses after intrauterine exposure. To our knowledge, we describe the first case of a fetus with severe anemia, and subsequent hydrops, where this drug was found at concentrations in the fetus corresponding to those in the mother and most likely responsible for the fetal condition. PATIENT CONCERNS: A uniparous woman was referred at 31 weeks of gestation due to a hydropic fetus with massive ascites and cardiomegaly. DIAGNOSES: The patient had Crohn's disease and was thus treated with 4 g mesalazine daily. The fetus had severe anemia with an initial hemoglobin level of 51 g/L. INTERVENTIONS: The maternal medication was discontinued and four intrauterine erythrocyte transfusions were given during three weeks. Plasma samples were drawn from mother and fetus during cordocentesis for later analysis of mesalazine. OUTCOMES: A healthy baby was born after 37 full weeks of gestation. Plasma levels of mesalazine were non-conspicuous in neither mother nor fetus. The mesalazine half-life in the fetus (37 h) was half that of the mother (80 h), both considerably longer than previously reported (about 19 h). LESSONS: A causal relationship must be suspected between the fetal anemia and the maternal use of mesalazine. This fetal side-effect should be considered in pregnant women on mesalazine (and its prodrug sulfasalazine).
[Mh] MeSH terms primary: Anemia/chemically induced
Anti-Inflammatory Agents, Non-Steroidal/adverse effects
Fetal Diseases/chemically induced
Hydrops Fetalis/chemically induced
Mesalamine/adverse effects
[Mh] MeSH terms secundary: Anemia/therapy
Erythrocyte Transfusion
Female
Fetal Diseases/therapy
Humans
Hydrops Fetalis/therapy
Pregnancy
Pregnancy Outcome
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (Anti-Inflammatory Agents, Non-Steroidal); 4Q81I59GXC (Mesalamine)
[Em] Entry month:1802
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009277

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[PMID]: 29485829
[Au] Autor:Saldir M; Polat A; Babacan O; Keskin U; Gursel O; Gulgun M; Zeybek C; Tunc T
[Ti] Title:A Newborn with Down Syndrome, Developing Hydrops Fetalis Due to Transient Myeloproliferative Disorder and Liver Hamartoma.
[So] Source:Genet Couns;27(2):243-6, 2016.
[Is] ISSN:1015-8146
[Cp] Country of publication:Switzerland
[La] Language:eng
[Pt] Publication type:LETTER
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:In-Process

  7 / 3297 MEDLINE  
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[PMID]: 29480868
[Ti] Title:Mesalazine as a cause of fetal anemia and hydrops fetalis: A case report: Erratum.
[So] Source:Medicine (Baltimore);97(2):e9623, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180226
[Lr] Last revision date:180226
[St] Status:In-Data-Review
[do] DOI:10.1097/MD.0000000000009623

  8 / 3297 MEDLINE  
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[PMID]: 29476829
[Au] Autor:Ghesquière L; Garabedian C; Coulon C; Verpillat P; Rakza T; Wibaut B; Delsalle A; Subtil D; Vaast P; Debarge V
[Ad] Address:CHU Lille, Department of obstetrics, F-59000, Lille, France. Electronic address: louise.ghesquiere@etu.univ-lille2.fr.
[Ti] Title:Management of red blood cell alloimmunization in pregnancy.
[So] Source:J Gynecol Obstet Hum Reprod;, 2018 Feb 21.
[Is] ISSN:2468-7847
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:The main cause of fetal anemia is maternal red blood cell alloimmunization (AI). The search of maternal antibodies by indirect antiglobulin test allows screening for AI during pregnancy. In case of AI, fetal genotyping (for Rh-D, Rh-c, Rh-E and Kell), quantification (for anti-rhesus antibodies) and antibody titration, as well as ultrasound monitoring, are performed. This surveillance aims at screening for severe anemia before hydrops fetalis occurs. Management of severe anemia is based on intrauterine transfusion (IUT) or labor induction depending on gestational age. After intrauterine transfusion, follow-up will focus on detecting recurrence of anemia and detecting fetal brain injury. With IUT, survival of fetuses with alloimmunization is greater than 90% but 4.8% of children with at least one IUT have neurodevelopmental impairment.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180224
[Lr] Last revision date:180224
[St] Status:Publisher

  9 / 3297 MEDLINE  
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[PMID]: 29237843
[Au] Autor:Zou W; Wang Z; Xiong M; Chen AY; Xu P; Ganaie SS; Badawi Y; Kleiboeker S; Nishimune H; Ye SQ; Qiu J
[Ad] Address:Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas, USA.
[Ti] Title:Human Parvovirus B19 Utilizes Cellular DNA Replication Machinery for Viral DNA Replication.
[So] Source:J Virol;92(5), 2018 Mar 01.
[Is] ISSN:1098-5514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Human parvovirus B19 (B19V) infection of human erythroid progenitor cells (EPCs) induces a DNA damage response and cell cycle arrest at late S phase, which facilitates viral DNA replication. However, it is not clear exactly which cellular factors are employed by this single-stranded DNA virus. Here, we used microarrays to systematically analyze the dynamic transcriptome of EPCs infected with B19V. We found that DNA metabolism, DNA replication, DNA repair, DNA damage response, cell cycle, and cell cycle arrest pathways were significantly regulated after B19V infection. Confocal microscopy analyses revealed that most cellular DNA replication proteins were recruited to the centers of viral DNA replication, but not the DNA repair DNA polymerases. Our results suggest that DNA replication polymerase δ and polymerase α are responsible for B19V DNA replication by knocking down its expression in EPCs. We further showed that although RPA32 is essential for B19V DNA replication and the phosphorylated forms of RPA32 colocalized with the replicating viral genomes, RPA32 phosphorylation was not necessary for B19V DNA replication. Thus, this report provides evidence that B19V uses the cellular DNA replication machinery for viral DNA replication. Human parvovirus B19 (B19V) infection can cause transient aplastic crisis, persistent viremia, and pure red cell aplasia. In fetuses, B19V infection can result in nonimmune hydrops fetalis and fetal death. These clinical manifestations of B19V infection are a direct outcome of the death of human erythroid progenitors that host B19V replication. B19V infection induces a DNA damage response that is important for cell cycle arrest at late S phase. Here, we analyzed dynamic changes in cellular gene expression and found that DNA metabolic processes are tightly regulated during B19V infection. Although genes involved in cellular DNA replication were downregulated overall, the cellular DNA replication machinery was tightly associated with the replicating single-stranded DNA viral genome and played a critical role in viral DNA replication. In contrast, the DNA damage response-induced phosphorylated forms of RPA32 were dispensable for viral DNA replication.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[St] Status:In-Data-Review

  10 / 3297 MEDLINE  
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[PMID]: 28453379
[Au] Autor:Han M; Afshar Y; Chon AH; Scibetta E; Rao R; Chmait RH
[Ad] Address:a Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology , University of California , Los Angeles, Los Angeles , California , USA.
[Ti] Title:Pseudoamniotic Band Syndrome Post Fetal Thoracoamniotic Shunting for Bilateral Hydrothorax.
[So] Source:Fetal Pediatr Pathol;36(4):311-318, 2017 Aug.
[Is] ISSN:1551-3823
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Pseudoamniotic band syndrome (PABS) occurs iatrogenically after fetal surgery or amniocentesis due to chorioamniotic membrane separation. Separation of the amnion from the chorion can expand to form fibrous amniotic bands that can envelope fetal limbs or the umbilical cord, with consequences ranging from limb constriction to fetal demise. CASE REPORT: We report a case of bilateral fetal pleural effusions at 27 weeks' gestation treated by bilateral thoracoamniotic shunts. Following shunt placement, the hydrothorax resolved. However, chorioamniotic membrane separation developed resulting in PABS with subsequent umbilical cord strangulation and fetal demise at 32 weeks' gestation. CONCLUSION: PABS has been previously described in the literature following various fetal interventions. This is the first reported case of pseudoamniotic band syndrome after placement of fetal thoracoamniotic shunts. A high index of suspicion is required to diagnose PABS via postoperative ultrasound. Post intervention chorioamniotic membrane separation warrants close surveillance for sonographic evidence of PABS.
[Mh] MeSH terms primary: Amniotic Band Syndrome/etiology
Chylothorax/congenital
Fetal Therapies/adverse effects
Hydrops Fetalis/surgery
[Mh] MeSH terms secundary: Chylothorax/surgery
Female
Fetal Death
Fetus
Humans
Pleural Effusion/surgery
Pregnancy
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[Js] Journal subset:IM
[Da] Date of entry for processing:170429
[St] Status:MEDLINE
[do] DOI:10.1080/15513815.2017.1313915


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