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Objective <p>Prenatal alcohol exposure (PAE) of the fetus may result in physiognomic alterations and/or impediment of cognitive development, summarized as fetal alcohol spectrum disorders (FASDs). Although alcohol is metabolized in the liver, the effects of PAE on the fetal liver are unknown.</p> Materials and methods <p>For this study, <i>n</i> = 21 prenatal MRIs of fetuses with PAE and <i>n</i> = 45 MRIs of fetuses without PAE were included. To assess macroscopic organ development, liver volumetry was conducted and compared to an established prenatal estimation formula. A texture-based radiomics analysis based on ensemble (random forest) and linear (L2-penalized logistic regression) models was conducted.</p> Results <p>PAE and non-PAE fetuses were age-matched (gestational age 27.4 [IQR 25.1–30.0] vs. 26.7 [25.4–29.3] weeks, <i>p</i> = 0.650). PAE had no effect on liver volume (normalized per gestational week, <i>p</i> = 0.971) or signal intensity (SI) in T1 (<i>p</i> = 0.574) and T2 (<i>p</i> = 0.104). MRI-derived liver volumetry correlated strongly with a gestational age-based volume estimation regardless of PAE (both r &gt; 0.75, <i>p</i> &lt; 0.001). A texture-based radiomics analysis was unable to discern between PAE and no-PAE fetuses (ROC-AUC = 0.43, 95% CI 0.29–0.57 for random forest, ROC-AUC = 0.40, 95% CI 0.31–0.60 for L2-penalized logistic regression).</p> Conclusion <p>PAE had no significant effect on signal intensity of the fetal liver, and gestational-age-adjusted liver volumes did not differ between fetuses with and without PAE, suggesting no relevant effect on organ development. Texture-based radiomics were unable to identify PAE. Hence, alterations of the liver in fetal MRI with known PAE warrant investigations for causes other than alcohol.</p> Key Points <p><Emphasis Type="BoldItalic">Question</Emphasis> <i>Prenatal alcohol exposure can lead to morphological and neurocognitive changes in the fetus. The effect on the fetal liver is unknown</i><i>.</i></p> <p><Emphasis Type="BoldItalic">Findings</Emphasis> <i>No differences in fetal liver volume or signal intensity were found regarding alcohol exposure. Texture-based radiomics analysis was unable to discern between the two groups</i><i>.</i></p> <p><Emphasis Type="BoldItalic">Clinical relevance</Emphasis> <i>Fetal MRI and radiomics analysis were unable to detect effects of alcohol exposure on the fetal liver. Aberrations of the fetal liver on MRI in patients with a history of prenatal alcohol exposure warrant investigation for other causes</i><i>.</i></p> Graphical Abstract <p></p>

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Analysis of fetal MRI data reveals no effect on liver maturation following prenatal alcohol exposure

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月16日

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  • Michael Schwarz,
  • Martin Watzenboeck,
  • Marlene Stuempflen,
  • Katharina Tontsch,
  • Patric Kienast,
  • Julia Binder,
  • Tim Dorittke,
  • Rebecca Sokol,
  • Felix Ragnar Merlin Koenig,
  • Caroline Schwarz,
  • Thomas Reiberger,
  • Daniela Prayer,
  • Gregor Kasprian,
  • Victor Ulrich Schmidbauer

摘要

Objective

Prenatal alcohol exposure (PAE) of the fetus may result in physiognomic alterations and/or impediment of cognitive development, summarized as fetal alcohol spectrum disorders (FASDs). Although alcohol is metabolized in the liver, the effects of PAE on the fetal liver are unknown.

Materials and methods

For this study, n = 21 prenatal MRIs of fetuses with PAE and n = 45 MRIs of fetuses without PAE were included. To assess macroscopic organ development, liver volumetry was conducted and compared to an established prenatal estimation formula. A texture-based radiomics analysis based on ensemble (random forest) and linear (L2-penalized logistic regression) models was conducted.

Results

PAE and non-PAE fetuses were age-matched (gestational age 27.4 [IQR 25.1–30.0] vs. 26.7 [25.4–29.3] weeks, p = 0.650). PAE had no effect on liver volume (normalized per gestational week, p = 0.971) or signal intensity (SI) in T1 (p = 0.574) and T2 (p = 0.104). MRI-derived liver volumetry correlated strongly with a gestational age-based volume estimation regardless of PAE (both r > 0.75, p < 0.001). A texture-based radiomics analysis was unable to discern between PAE and no-PAE fetuses (ROC-AUC = 0.43, 95% CI 0.29–0.57 for random forest, ROC-AUC = 0.40, 95% CI 0.31–0.60 for L2-penalized logistic regression).

Conclusion

PAE had no significant effect on signal intensity of the fetal liver, and gestational-age-adjusted liver volumes did not differ between fetuses with and without PAE, suggesting no relevant effect on organ development. Texture-based radiomics were unable to identify PAE. Hence, alterations of the liver in fetal MRI with known PAE warrant investigations for causes other than alcohol.

Key Points

Question Prenatal alcohol exposure can lead to morphological and neurocognitive changes in the fetus. The effect on the fetal liver is unknown.

Findings No differences in fetal liver volume or signal intensity were found regarding alcohol exposure. Texture-based radiomics analysis was unable to discern between the two groups.

Clinical relevance Fetal MRI and radiomics analysis were unable to detect effects of alcohol exposure on the fetal liver. Aberrations of the fetal liver on MRI in patients with a history of prenatal alcohol exposure warrant investigation for other causes.

Graphical Abstract