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Fetal Abnormalities (fetal + abnormality)
Selected AbstractsA review of antiviral therapies in the treatment of cytomegalovirusDERMATOLOGIC THERAPY, Issue 3 2000Adrienne M. Hinkle ABSTRACT: Cytomegalovirus (CMV) is a member of the herpesvirus family that is very prevalent world wide based on serologic testing. In immunocompromised persons CMV produces high rates of morbidity and mortality. Congenital CMV is the leading infectious cause of fetal abnormalities in the United States. Infection of human immunodeficiency virus (HIV) seropositive persons or transplant patients with CMV can produce retinitis, encephalitis, pneumonitis, hepatitis, gastrointestinal ulcerations, and cutaneous lesions. Three intravenous therapies are available for CMV infections: ganciclovir; foscarnet and cidofovir. Most recently a fourth antiviral agent was approved for intravitreal injection. This drug, fomivirsen, is the first antisense oligonucleotide available for therapeutic use. A number of other antiviral drugs and vaccines are currently under study. [source] Ultrafast MRI of the fetusJOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 1 2002Christine M Glastonbury SUMMARY During the last decade there has been increasing interest in MRI for the evaluation of ultrasound-detected fetal abnormalities. Motion artefacts previously precluded detailed imaging, but this is now possible using single-shot rapid acquisition sequences. These ultrafast techniques with subsecond images capture ,snap-shot' views of the fetus. By virtue of the infinitely long relaxation time (TR) these images are heavily T2-weighted so that fluid around and within the fetus delineates the anatomy. Currently, fetal MRI has shown to be most beneficial in the investigation of cerebral abnormalities suspected from sonography, and in the detection of subtle associated anomalies. It clearly has a role in the evaluation of complex somatic abnormalities, and is helpful in the evaluation of fetuses prior to surgery. We present a pictorial review of our experience with single-shot fast spin-echo (SSFSE) imaging, demonstrating normal anatomy of the fetal brain and body. In addition we present cerebral and somatic abnormalities to illustrate cases where we have found fetal MRI to be a useful adjunct to sonography. [source] Dietary Zinc Supplementation Throughout Pregnancy Protects Against Fetal Dysmorphology and Improves Postnatal Survival After Prenatal Ethanol Exposure in MiceALCOHOLISM, Issue 4 2009Brooke L. Summers Background:, We have previously demonstrated that ethanol teratogenicity is associated with metallothionein-induced fetal zinc (Zn) deficiency, and that maternal subcutaneous Zn treatment given with ethanol in early pregnancy prevents fetal abnormalities and spatial memory impairments in mice. Here we investigated whether dietary Zn supplementation throughout pregnancy can also prevent ethanol-related dysmorphology. Methods:, Pregnant mice were injected with saline or 25% ethanol (0.015 ml/g intraperitoneally at 0 and 4 hours) on gestational day (GD) 8 and fed either a control (35 mg Zn/kg) or a Zn-supplemented diet (200 mg Zn/kg) from GD 0 to 18. Fetuses from the saline, saline + Zn, ethanol and ethanol + Zn groups were assessed for external birth abnormalities on GD 18. In a separate cohort of mice, postnatal growth and survival of offspring from these treatment groups were examined from birth until postnatal day 60. Results:, Fetuses from dams treated with ethanol alone in early pregnancy had a significantly greater incidence of physical abnormalities (26%) compared to those from the saline (10%), saline + Zn (9%), or ethanol + Zn (12%) groups. The incidence of abnormalities in ethanol + Zn-supplemented fetuses was not different from saline-treated fetuses. While ethanol exposure did not affect the number of fetal resorptions or pre- or postnatal weight, there were more stillbirths with ethanol alone, and cumulative postnatal mortality was significantly higher in offspring exposed to ethanol alone (35% deaths) compared to all other treatment groups (13.5 to 20.5% deaths). Mice supplemented with Zn throughout pregnancy had higher plasma Zn concentrations than those in un-supplemented groups. Conclusions:, These findings demonstrate that dietary Zn supplementation throughout pregnancy ameliorates dysmorphology and postnatal mortality caused by ethanol exposure in early pregnancy. [source] Zinc Supplementation at the Time of Ethanol Exposure Ameliorates Teratogenicity in MiceALCOHOLISM, Issue 1 2003Luke C. Carey Background: We have previously demonstrated that ethanol teratogenicity in mice is related to the maternal expression of metallothionein (MT), a zinc (Zn)-binding protein. Ethanol induces maternal liver MT, which causes plasma Zn concentrations to decrease as Zn moves into the liver. During pregnancy it is suggested that this change decreases fetal Zn supply and contributes to abnormal development. Here we investigated whether maternal Zn supplementation at the time of ethanol exposure reduces teratogenicity. Methods: Mice were injected with 25% ethanol (0.015 ml/g intraperitoneally at 0 and 4 hr) and ZnSO4 (2.5 ,gZn/g subcutaneously at 0 hr) and were killed over 16 hr to ascertain changes in plasma Zn. Plasma Zn concentrations peaked at 2 hr, where levels were 5-fold normal and then returned toward normal over 14 hr. Pregnant mice were treated in a similar manner on gestation day 8 with saline, saline + Zn, ethanol + Zn, or ethanol alone, and fetal abnormalities were assessed on gestation day 18. Results: External abnormalities were most prevalent in offspring from dams treated with ethanol. Zn treatment at the time of ethanol exposure reduced the incidence of fetal abnormalities to basal levels. Litters from dams treated with ethanol + Zn contained more fetuses and fewer fetal resorption sites compared with those from ethanol-treated dams. Conclusions: These findings demonstrate that Zn supplementation at the time of ethanol exposure significantly negates the deleterious effects of ethanol on the fetus. [source] Complex de novo cryptic subtelomeric rearrangements in a fetus with multiple ultrasonographic abnormalities and a normal karyotype at amniocentesisPRENATAL DIAGNOSIS, Issue 12 2005M. Anwar Iqbal Abstract Objective Prenatal diagnosis is usually offered to the majority of pregnancies with fetal structural abnormalities detected by prenatal ultrasound; however, only a small proportion show an abnormal karyotype. We wanted to detect cryptic subtelomeric rearrangements (CSTR) in a fetus with multiple abnormal ultrasonographic findings that revealed a normal karyotype at amniocentesis. Methods Fetal chromosome analysis was performed from amniotic fluid cells. Parental chromosome analysis was done on PHA stimulated lymphocyte cultures. For fluorescence in situ hybridization (FISH) analysis, ToTelVysion multicolor DNA probe mixture was used to hybridize the p and q telomeres of each chromosome. Results The amniotic fluid chromosome analysis revealed an apparently normal 46,XY karyotype. A follow-up FISH analysis showed three apparently balanced complex translocations involving (1) the chromosome 4p and 22q telomeres (2) 4q and 11q telomeres and (3) 8p, 20p and 20q telomeres. Parental chromosome and subtelomere FISH analysis was found to be normal. Conclusion To our knowledge, this is the first report of complex de novo cryptic translocations in an abnormal fetus. These CSTR identified by FISH with subtelomere-specific probes are not detected by other cytogenetic and/or molecular cytogenetic approaches. However, to confirm the balanced nature of CSTR, array-CGH can be helpful. Further studies are in progress to determine the frequency of CSTR and its significance in the etiology of fetal abnormalities. Copyright © 2005 John Wiley & Sons, Ltd. [source] Fetal cardiac effects of maternal hyperglycemia during pregnancyBIRTH DEFECTS RESEARCH, Issue 6 2009Niamh Corrigan Maternal diabetes mellitus is associated with increased teratogenesis, which can occur in pregestational type 1 and type 2 diabetes. Cardiac defects and with neural tube defects are the most common malformations observed in fetuses of pregestational diabetic mothers. The exact mechanism by which diabetes exerts its teratogenic effects and induces embryonic malformations is unclear. Whereas the sequelae of maternal pregestational diabetes, such as modulating insulin levels, altered fat levels, and increased reactive oxygen species, may play a role in fetal damage during diabetic pregnancy, hyperglycemia is thought to be the primary teratogen, causing particularly adverse effects on cardiovascular development. Fetal cardiac defects are associated with raised maternal glycosylated hemoglobin levels and are up to five times more likely in infants of mothers with pregestational diabetes compared with those without diabetes. The resulting anomalies are varied and include transposition of the great arteries, mitral and pulmonary atresia, double outlet of the right ventricle, tetralogy of Fallot, and fetal cardiomyopathy. A wide variety of rodent models have been used to study diabetic teratogenesis. Both genetic and chemically induced models of type 1 and 2 diabetes have been used to examine the effects of hyperglycemia on fetal development. Factors such as genetic background as well as confounding variables such as obesity appear to influence the severity of fetal abnormalities in mice. In this review, we will summarize recent data on fetal cardiac effects from human pregestational diabetic mothers, as well as the most relevant findings in rodent models of diabetic cardiac teratogenesis. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. [source] The future of prenatal diagnosis: rapid testing or full karyotype?BJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 10 2005An audit of chromosome abnormalities, pregnancy outcomes for women referred for Down's Syndrome testing Objective To assess the implications of a change in prenatal diagnosis policy from full karyotype analysis to rapid trisomy testing for women referred primarily for increased risk of Down's Syndrome. Design Retrospective collection and review of data. Setting The four London Regional Genetics Centres. Population Pregnant women (32,674) in the London area having invasive prenatal diagnosis during a six-year three-month period. Methods Abnormal karyotypes and total number of samples referred for raised maternal age, raised risk of Down's Syndrome following serum screening or maternal anxiety were collected. Abnormal karyotypes detected by molecular trisomy detection were removed, leaving cases with residual abnormal karyotypes. These were assessed for their clinical significance. Pregnancy outcomes were ascertained by reviewing patient notes or by contacting obstetricians or general practioners. Main outcome measures Proportion of prenatal samples with abnormal karyotypes that would not have been detected by rapid trisomy testing, and the outcome of those pregnancies with abnormal karyotypes. Results Results from 32,674 samples were identified, of which 24,891 (76.2%) were from women referred primarily for Down's Syndrome testing. There were 118/24,891 (0.47%) abnormal sex chromosome karyotypes. Of the samples with autosomal abnormalities that would not be detected by rapid trisomy testing, 153/24,891 (0.61%) were in pregnancies referred primarily for Down's Syndrome testing. Of these, 98 (0.39%) had a good prognosis (46/98 liveborn, 3/98 terminations, 1/98 intrauterine death, 1/98 miscarriage, 47/98 not ascertained); 37 (0.15%) had an uncertain prognosis (20/37 liveborn, 5/37 terminations; 12/37 not ascertained) and 18 (0.07%) had a poor prognosis (1/18 liveborn, 2/18 miscarriage, 11/18 terminations, 4/18 not ascertained). Conclusions For pregnant women with a raised risk of Down's Syndrome, a change of policy from full karyotype analysis to rapid trisomy testing would result in the failure to detect chromosome abnormalities likely to have serious clinical significance in approximately 0.06% (1 in 1659) cases. However, it should be noted that this figure may be higher (up to 0.12%; 1 in 833) if there were fetal abnormalities in some of the pregnancies in the uncertain prognosis group for which outcome information was not available. [source] Long-term psychological consequences of pregnancy termination for fetal abnormality: a cross-sectional studyPRENATAL DIAGNOSIS, Issue 3 2005M. J. Korenromp Abstract Objective We examined women's long-term psychological well-being after termination of pregnancy (TOP) for fetal anomaly in order to identify risk factors for psychological morbidity. Methods A cross-sectional study was performed in 254 women, 2 to 7 years after TOP for fetal anomaly before 24 weeks of gestation. We used standardised questionnaires to investigate grief, posttraumatic symptoms, and psychological and somatic complaints. Results Women generally adapted well to grief. However, a substantial number of the participants (17.3%) showed pathological scores for posttraumatic stress. Low-educated women and women who had experienced little support from their partners had the most unfavourable psychological outcome. Advanced gestational age at TOP was associated with higher levels of grief, and posttraumatic stress symptoms and long-term psychological morbidity was rare in TOP before 14 completed weeks of gestation. Higher levels of grief and doubt were found if the fetal anomaly was presumably compatible with life. Conclusion Termination of pregnancy for fetal anomaly is associated with long-lasting consequences for a substantial number of women. Clinically relevant determinants are gestational age, perceived partner support, and educational level. Copyright © 2005 John Wiley & Sons, Ltd. [source] Infection and fetal loss in the mid-second trimester of pregnancyAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 3 2010Ben ALLANSON Introduction:, Chorioamnionitis is a common cause of second trimester pregnancy loss, usually due to ascending infection. This study investigates the prevalence and bacteriology of chorioamnionitis in cases of spontaneous pregnancy loss in previable gestations (16,22 weeks). Methods:, Fetal losses between 16- and 22-week gestation were identified from the institutional database over a three-year period. Cases with an autopsy were identified, pathology reports reviewed, and maternal features noted (clinical symptoms, blood count and vaginal culture results). Second trimester medical termination for fetal abnormality during the same time period served as controls for the confounding influence of labour. Results:, A total of 101 cases of spontaneous non-anomalous non-macerated fetal losses and 103 control cases of induced loss for fetal anomaly were identified. Median gestation of cases was 19 weeks (interquartile range (IQR) 17, 21) and of controls was 20 weeks (IQR 19, 21). Maternal white cell count was higher in cases (median 13.6 IQR 10.8, 16.6) than in controls (9.9 IQR 7.6, 11.5) (P < 0.01). Seventy-eight (77.2%) of 101 cases and no controls had histological chorioamnionitis. A fetal reaction was identified in 48.7% of cases with chorioamnionitis, and the frequency of fetal reaction increased as gestation advanced (5.3% at 16-week gestation vs 33.3% at 22-week gestation). In cases with chorioamnionitis 36/76 (47.4%) were culture positive, whereas 4/25 (16%) without chorioamnionitis were culture positive. Conclusion:, In otherwise normal fetuses, chorioamnionitis is a common finding in mid-trimester pregnancy loss. Routine culture methods have a low sensitivity for isolation of the causative micro-organisms. This inflammatory process seems to predate the onset of labour and appears a primary mechanism in the aetiology of such losses. [source] Mifepristone and second trimester pregnancy termination for fetal abnormality in Western Australia: Worth the effortAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 1 2010Jan E. DICKINSON Objective:, To determine the impact on the process of second trimester medical termination for fetal abnormality following the introduction of adjunctive mifepristone in an Australian tertiary hospital. Methods:, All second trimester medical terminations for fetal abnormality between July 2006 and June 2009 were prospectively identified. Two temporal therapeutic cohorts were created: the first (1 July 2006 to 31 December 2007) using vaginal misoprostol alone and the second (1 January 2008 to 30 June 2009) using mifepristone priming prior to the administration of misoprostol. The primary outcome was to evaluate the impact of mifepristone priming upon the duration of pregnancy termination. Results:, During the study period, 388 women with prenatally recognised fetal anomalies between 14 and 24 weeks gestation underwent medical termination: 189 with misoprostol alone and 199 with mifepristone priming followed by misoprostol. There was no difference between the groups for maternal age, parity or prior caesarean delivery. The median abortion duration was 15.5 h (interquartile ranges (IQR) 11.2,22.7) in the misoprostol group and 8.6 h (IQR 5.6,13.8) in the mifepristone primed group (P < 0.001). In both the groups, nulliparity and advancing gestation were associated with a significant prolongation of the abortion interval. Duration of hospitalisation was significantly longer in the misoprostol alone group (31.5 h (27,48.9) vs 27.2 h (22,31.5), misoprostol vs mifepristone priming, respectively, P < 0.001). Conclusions:, The introduction of mifepristone priming prior to second trimester medical termination with misoprostol has resulted in a significant reduction in the duration of the termination procedure and length of inpatient stay. These observed benefits of mifepristone provide objective support for the decision to permit use of this medication in Australia. [source] | |||||||||||||