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Erythroblastosis Fetalis [keywords]
- Histopathological analysis of the placental lesions in pregnancies complicated with IUGR and stillbirths in comparison with noncomplicated pregnancies. [Journal Article]
- J Turk Ger Gynecol Assoc 2011; 12(2):75-9.
Placental factors and hypoxemia are the keys to intrauterine growth restriction (IUGR) and stillbirth. The aim of the study is to analyze histological changes in placentas of IUGR fetuses in pregnancies with no apparent etiologic factor and unexplained intrauterine fetal deaths.A total of 110 placentas were collected; 26 placentas of IUGR fetuses with no apparent cause, 58 placentas from unexplained intrauterine deaths over 20 weeks of gestation, and 26 placentas from uncomplicated pregnancies who delivered a healthy live baby. Microscopic examinations of placentas were performed for histopathological analyzes.Gestational age at delivery was 33.67±4.37 weeks, 29.15±8.36 weeks, and 39.0±1.52 weeks in women in group I, group II and group III, respectively (p<0.01). Infarction and intervillous thrombosis are significantly more frequent in placentas of Group I and group II. Chronic villitis occurred in 69%, 63% and 30% of group I, group II, and group III, respectively. Placental intravascular thrombi (Group I, 31% and group II, 26%), perivillous fibrin deposition and fibrinoid necrosis (65% in Group I and 53% in group II), infarction, intervillous thrombosis, chronic villitis, hemorrhagic endovasculitis, placental intravascular thrombi, perivillous fibrin deposition, fibrinoid necrosis, erythroblastosis and villous edema were found in the study group.The results reported here indicate that a relationship exists between morphological changes in the placentas of IUGR and intrauterine fetal deaths.
- 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.
- Neonatal death suspected to be from sepsis was found to be kernicterus with G6PD deficiency. [Case Reports, Journal Article]
- Pediatrics 2013 Dec; 132(6):e1694-8.
We cared for a term male infant born to Burmese immigrants. At about 24 hours a total serum bilirubin (TSB) was 9.3 mg/dL, and phototherapy was begun. It was stopped 48 hours later, with a TSB of 10.9 mg/dL, and he was discharged from the hospital with an appointment for a repeat TSB check 48 hours later. A few hours before the appointment he became listless and apneic, and his parents took him to the emergency department of the regional children's hospital, where sepsis was suspected. The TSB was 41 mg/dL. He died 4 hours later, despite intensive care efforts, with opisthotonus and refractory hypotension. Blood drawn before the exchange transfusion had low glucose-6-phosphate dehydrogenase (G6PD) enzymatic activity, and sequencing of the G6PD gene revealed the G6PD Mahidol mutation (c.487G>A). Cultures and postmortem examination did not demonstrate an infectious process, but kernicterus was present. Acute kernicterus can mimic septic shock.
- [Mirror syndrome: a case report in fetal medicine]. [Case Reports, English Abstract, Journal Article]
- Rev Med Liege 2013 Sep; 68(9):440-3.
Mirror syndrome is a rare entity describing the association of foetal hydrops and maternal symptoms as general oedema and excessive weight gain mimicking preeclampsia. We report the case of a patient who developed symptoms of oedema, weight gain, headache and biological hemodilution associated with foetal hydrops due to a complex congenital heart defect. This symptomatology spontaneously resolved after foetal expulsion. Mirror or Ballantyne's syndrome needs to be identified on time and well differentiated from preeclampsia. Its consequences may involve the maternal and foetal prognosis.
- Investigation and management of non-immune fetal hydrops. [Journal Article, Practice Guideline, Review]
- J Obstet Gynaecol Can 2013 Oct; 35(10):923-38.
To describe the current investigation and management of non-immune fetal hydrops, with a focus on treatable or recurring etiologies.To provide better counselling and management in cases of prenatally diagnosed non-immune hydrops.Published literature was retrieved through searches of PubMed or MEDLINE, CINAHL, and The Cochrane Library in 2011 using key words (non-immune hydrops fetalis, fetal hydrops, fetal therapy, fetal metabolism). Results were restricted to systematic reviews, randomized controlled trials/controlled clinical trials, observational studies, and significant case reports. Additional publications were identified from the bibliographies of these articles. There were no date or language restrictions. Searches were updated on a regular basis and incorporated in the guideline to May 2012. Grey (unpublished) literature was identified through searching the websites of health technology assessment and health technology-related agencies, clinical practice guideline collections, clinical trial registries, and national and international medical specialty societies.These guidelines educate readers about the causes of non-immune fetal hydrops and its prenatal counselling and management. It also provides a standardized approach to non-immune fetal hydrops, emphasizing the search for prenatally treatable conditions and recurrent genetic etiologies.The quality of evidence in this document was rated using the criteria described in the Report of the Canadian Task Force on Preventive Health Care (Table 1).1. All patients with fetal hydrops should be referred promptly to a tertiary care centre for evaluation. Some conditions amenable to prenatal treatment represent a therapeutic emergency after 18 weeks. (II-2A) 2. Fetal chromosome analysis and genetic microarray molecular testing should be offered where available in all cases of non-immune fetal hydrops. (II-2A) 3. Imaging studies should include comprehensive obstetrical ultrasound (including arterial and venous fetal Doppler) and fetal echocardiography. (II-2A) 4. Investigation for maternal-fetal infections, and alpha-thalassemia in women at risk because of their ethnicity, should be performed in all cases of unexplained fetal hydrops. (II-2A) 5. To evaluate the risk of fetal anemia, Doppler measurement of the middle cerebral artery peak systolic velocity should be performed in all hydropic fetuses after 16 weeks of gestation. In case of suspected fetal anemia, fetal blood sampling and intrauterine transfusion should be offered rapidly. (II-2A) 6. All cases of unexplained fetal hydrops should be referred to a medical genetics service where available. Detailed postnatal evaluation by a medical geneticist should be performed on all cases of newborns with unexplained non-immune hydrops. (II-2A) 7. Autopsy should be recommended in all cases of fetal or neonatal death or pregnancy termination. (II-2A) Amniotic fluid and/or fetal cells should be stored for future genetic testing. (II-2B).
- Glycophorin C ligation: another biochemical pathway in red blood cell senescence? [Comment, Editorial]
- Transfusion 2013 Oct; 53(10):2111.
- The Diego blood group system: a review. [Journal Article, Review]
- Immunohematology 2013; 29(2):73-81.
The Diego blood group system (DI) currently encompasses 22 antigens. Three of the antigens are of high prevalence and the other 19 are of low prevalence. The antigens of the Diego blood group system are carried on the erythroid band 3 protein anion exchanger 1 (AE1), the product of a single gene, SLC4A1 (solute carrier family 4, anion exchanger, member 1). AE1 is a member of a family of three anion exchangers or transporters expressed in a variety of tissues. This protein is involved in carbon dioxide transport from tissues to lungs. It is also found in the kidney,where it is involved in acid secretion. Antibodies to Diego system antigens with the exception of anti-Dia, -Dib, -Wra, -ELO and-DISK do not seem to be of clinical significance for transfusion or of importance in hemolytic disease of the fetus and newborn.
- A review of the JR blood group system. [Journal Article, Review]
- Immunohematology 2013; 29(2):63-8.
The JR blood group system (ISBT 032) consists of one antigen,Jra, which is of high prevalence in all populations. The rare Jr(a-) phenotype has been found mostly in Japanese and other Asian populations, but also in people of northern European ancestry, in Bedouin Arabs, and in one Mexican. Anti-Jra has caused transfusion reactions and is involved in hemolytic disease of the fetus and newborn. The Jra antigen is located on ABCG2 transporter, a multipass membrane glycoprotein (also known as the breast cancer resistance protein, BCRP), which is encoded by the ABCG2 gene on chromosome 4q22.1. The Jr(a-) phenotype mostly results from recessive inheritance of ABCG2 null alleles caused by frameshift or nonsense changes.