Sonographic predictors of postnatal bowel atresia in fetal gastroschisis.

OBJECTIVES: To estimate the association between antenatal bowel dilation and postnatal small-bowel atresia in fetal gastroschisis and to establish a threshold at which the risk of adverse neonatal outcome increases. METHODS: This was a retrospective cohort study of singleton gestations with an antenatal diagnosis of gastroschisis seen in our ultrasound unit from 2001 to 2010. We reviewed stored images from the last ultrasound examination before delivery, blinded to postnatal diagnoses and outcomes. Fetal intra- and extra-abdominal bowel dilation (IABD and EABD, respectively) and bowel-wall thickness were measured. Previously published definitions of bowel dilation, including > 6, > 10, > 14 and > 18 mm, were evaluated for association with the primary outcome of bowel atresia. The optimal threshold to define fetal bowel dilation was determined by evaluating the significance of association as well as test performance characteristics. RESULTS: Of 109 consecutive patients with fetal gastroschisis, there were four cases of intrauterine fetal demise and three neonatal deaths. Of the 94 live births with complete outcome data, 39 (41.5%) had measurable IABD. There were 14 (14.9%) cases of bowel atresia. Using a threshold of > 14 mm, IABD was significantly associated with an increased risk for bowel atresia (relative risk, 3.1 (95% CI, 1.2-8.2)) with a sensitivity of 57.1%, specificity of 75.0%, positive predictive value of 28.6% and negative predictive value of 90.9%. IABD > 14 mm was also associated with a significantly longer stay in neonatal intensive care unit. There was no significant association between EABD and bowel atresia at any of the thresholds evaluated. CONCLUSION: IABD > 14 mm is associated with an increased risk for postnatal bowel atresia in fetal gastroschisis. This finding may be useful in counseling patients regarding the anticipated postnatal course for their neonate.

Placental volume and vascular flow assessed by 3D power Doppler and adverse pregnancy outcomes.

OBJECTIVE: To estimate the utility of first-trimester 3D-placental volume and vascular flow indices in the prediction of adverse pregnancy outcomes. METHODS: A prospective cohort study including women with singleton pregnancies seen between 11 and 14 weeks as part of a screening program for aneuploidy. Placental volume and vascularization indices were obtained using 3D power Doppler imaging and the VOCAL technique. Placental volume (PV), Vascularization Index (VI), Flow Index (FI) and Vascularization Flow Index (VFI) were calculated. The adverse pregnancy outcomes investigated include preeclampsia (PE), gestational hypertension (GH) and small for gestational age (SGA). The predictive ability of each variable was evaluated using receiver-operating characteristic (ROC) curves. RESULTS: Of 388 women included, PE was seen in 30 (7.7%), GH in 37 (9.0%) and SGA in 31 (8.0%). Placental volume was not significantly different between the pregnancies with adverse outcomes and those without. The mean values of the VI and VFI were significantly lower in the pregnancies that developed PE but not in GH or SGA. The area under the ROC curve for the prediction of PE was 0.71, 0.69 and 0.70 for VI, FI and VFI, respectively. CONCLUSION: The study confirms lower 3D power Doppler vascular flow indices in pregnancies that develop PE. The discriminatory ability of using these indices alone for predicting PE appears modest.

Analysis of the relationship between viral infection and autoimmune disease.

The clinical association between viral infection and onset or exacerbation of autoimmune disorders remains poorly understood. Here, we examine the relative roles of molecular mimicry and nonspecific inflammatory stimuli in progression from infection to autoimmune disease. Murine herpes virus 1 (HSV-1 KOS) infection triggers T cell-dependent autoimmune reactions to corneal tissue. We generated an HSV-1 KOS point mutant containing a single amino acid exchange within the putative mimicry epitope as well as mice expressing a TCR transgene specific for the self-peptide mimic to allow dissection of two pathogenic mechanisms in disease induction. These experiments indicate that viral mimicry is essential for disease induction after low-level viral infection of animals containing limited numbers of autoreactive T cells, while innate immune mechanisms become sufficient to provoke disease in animals containing relatively high numbers of autoreactive T cells.