Fetal Superior Mesenteric Artery Peak Systolic Velocity as a Marker of Prenatal Bowel Inflammation in Gastroschisis: A Case-Control Study.
R, J., B, M., M, R.K., D, M., E, S., A, N., & T, M. (2026). Fetal Superior Mesenteric Artery Peak Systolic Velocity as a Marker of Prenatal Bowel Inflammation in Gastroschisis: A Case-Control Study.. Birth defects research. https://doi.org/10.1002/bdr2.70097
R J, B M, M RK, D M, E S, A N, et al. Fetal Superior Mesenteric Artery Peak Systolic Velocity as a Marker of Prenatal Bowel Inflammation in Gastroschisis: A Case-Control Study.. Birth defects research. 2026; doi: 10.1002/bdr2.70097
R J, B M, M RK, et al. Fetal Superior Mesenteric Artery Peak Systolic Velocity as a Marker of Prenatal Bowel Inflammation in Gastroschisis: A Case-Control Study.[J]. Birth defects research. 2026. DOI: 10.1002/bdr2.70097.
@article{r2026,
author = {Jaczyńska R and Mikulska B and Rybak-Krzyszkowska M and Mydlak D and Sawicka E and Nimer A and Maciejewski T},
title = {Fetal Superior Mesenteric Artery Peak Systolic Velocity as a Marker of Prenatal Bowel Inflammation in Gastroschisis: A Case-Control Study.},
journal = {Birth defects research},
year = {2026},
doi = {10.1002/bdr2.70097},
note = {PMID: 42521617},
}
TY - JOUR AU - Jaczyńska R AU - Mikulska B AU - Rybak-Krzyszkowska M AU - Mydlak D AU - Sawicka E AU - Nimer A AU - Maciejewski T TI - Fetal Superior Mesenteric Artery Peak Systolic Velocity as a Marker of Prenatal Bowel Inflammation in Gastroschisis: A Case-Control Study. T2 - Birth defects research PY - 2026 DO - 10.1002/bdr2.70097 AN - PMID:42521617 ER -
OBJECTIVE: This study aimed to evaluate whether peak systolic velocity (PSV) in the fetal extra-abdominal superior mesenteric artery (SMA) is a useful prenatal marker of bowel inflammation in gastroschisis (GS), which manifests postnatally as bowel matting. METHODS: This case-control study included 30 fetuses with gastroschisis who underwent standardized bowel assessment and Doppler measurement of the extra-abdominal SMA-PSV. Postnatal bowel status was classified as normal or inflamed. The primary analysis examined the association between fetal SMA-PSV and bowel inflammation, using linear models and generalized estimating equations for repeated measurements. RESULTS: Among 30 fetuses, bowel matting was identified postnatally in 10 cases (33.3%). These neonates had significantly lower birthweight percentiles (5.5 vs. 50.5; p = 0.002) and more frequent ultrasound inflammatory signs such as bowel wall oedema (80% vs. 15%; p = 0.002), bowel wall stiffness (50% vs. 5%; p = 0.004), and corrugation wall (60% vs. 5%; p = 0.004). PSV was strongly correlated with bowel wall thickness (r = 0.81) and significantly higher in fetuses with postnatally diagnosed bowel matting (p < 0.001). GEE models showed that higher prenatal PSV independently predicted the later occurrence of bowel matting. Incorporating the time × bowel matting interaction significantly improved model fit (adjusted R2 = 0.460). CONCLUSIONS: Fetal SMA-PSV is significantly associated with prenatal/ultrasound and postnatal signs of bowel inflammation in gastroschisis, such as bowel wall thickening and bowel matting. This association appears independent of the simple/complex GS surgical classification, suggesting PSV as a functional marker of intestinal compromise. Although technically demanding, SMA-PSV assessment may aid prenatal evaluation and perinatal planning, particularly in detecting evolving intestinal inflammatory cases.