Aicardi-Goutières syndrome (AGS) was first described in 1984. 1 It is responsible for a rare autosomal recessive encephalopathy, with clinical and genetic heterogeneity and the presence of interferon αin cerebrospinal fluid as the same marker. 2 Clinically, AGS results in severe intellectual and physical impairment. In most cases, the syndrome appears either in the neonatal period or progressively after a few months of apparently normal development. Such patients generally do not survive beyond adolescence. Six genes have been described to this day: TREX1 (also known by its locus name AGS1) and RNASEH2B (AGS2) are responsible for 73% of the known forms; then come RNASEH2C (AGS3), RNASEH2A (AGS4), SAMHD1 (AGS5), and ADAR1 (AGS6). 3,4 Only 2 cases have been prenatally diagnosed and reported 5,6 to the best of our knowledge.Our patient was a North African 23-year-old primigravida whose husband was a first-degree cousin. Neither had a specific medical history. Routine maternal serologic screening revealed immunity for rubella virus and negative results for toxoplasmosis, human immunodeficiency virus, syphilis, and hepatitis B and C. First-trimester sonographic findings were normal, with a nuchal translucency of 1.0 mm and a crown-rump length of 70 mm (0.59 multiple of the median [MoM]). The trisomy 21 combined risk was 1:3225 (pregnancy-associated plasma protein A, 1.13 MoM; human chorionic gonadotropin, 2.37 MoM). At the routine second-trimester sonographic examination (22 weeks of pregnancy), cerebral white matter hyper echogenicity and a hyperechoic bowel were detected. An additional more precise sonographic examination showed fetal growth restriction (fifth percentile estimation of fetal weight), microcephaly (head circumference of 215 mm at 24 weeks of pregnancy), microencephaly with enlargement of pericerebral spaces, delayed closure of the sylvian fissure, parenchymal punctate calcifications, and bilateral periventricular cavitations inside a bilateral periventricular halo (Figure 1, A and B). 7 The lateral ventricles were normal and measured 9 mm at the atrial level. In addition to cerebral abnormalities, a grade 3 hyperechoic bowel with dotted contents and hepatosplenomegaly were found. The fetus was female, and an enlarged placenta with normal echogenicity was noted. These findings were suggestive of congenital cytomegalovirus (CMV) infection, but maternal CMV serologic testing was performed and yielded negative results: immunoglobulin G positive and immunoglobuliln M negative with avidity of 86%. Nonetheless, amniocentesis was performed at 24 weeks of pregnancy, and CMV polymerase chain reaction results were negative, invalidating the hypothesis of CMV infection. The fetal karyotype was normal (46,XX). Fetal magnetic resonance imaging (MRI) performed at 26 weeks of pregnancy (Figure 1C) confirmed brain damage plus ventriculomegaly (10 and 11 mm at the right and left atria, respectively), periventricular punctuate hypersignals on T1-weighted sequences and hyposignals on T2-weighted sequences, and millimetr...

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Background Literature focusing on migration and maternal health inequalities is inconclusive, possibly because of the heterogeneous definitions and settings studied. We aimed to synthesize the literature comparing the risks of severe maternal outcomes in high-income countries between migrant and native-born women, overall and by host country and region of birth. Methods and findings Systematic literature review and meta-analysis using the Medline/PubMed, Embase, and Cochrane Library databases for the period from January 1, 1990 to April 18, 2023. We included observational studies comparing the risk of maternal mortality or all-cause or cause-specific severe maternal morbidity in high-income countries between migrant women, defined by birth outside the host country, and native-born women; used the Newcastle–Ottawa scale tool to assess risk of bias; and performed random-effects meta-analyses. Subgroup analyses were planned by host country and region of birth. The initial 2,290 unique references produced 35 studies published as 39 reports covering Europe, Australia, the United States of America, and Canada. In Europe, migrant women had a higher risk of maternal mortality than native-born women (pooled risk ratio [RR], 1.34; 95% confidence interval [CI], 1.14, 1.58; p < 0.001), but not in the USA or Australia. Some subgroups of migrant women, including those born in sub-Saharan Africa (pooled RR, 2.91; 95% CI, 2.03, 4.15; p < 0.001), Latin America and the Caribbean (pooled RR, 2.77; 95% CI, 1.43, 5.35; p = 0.002), and Asia (pooled RR, 1.57, 95% CI, 1.09, 2.26; p = 0.01) were at higher risk of maternal mortality than native-born women, but not those born in Europe or in the Middle East and North Africa. Although they were studied less often and with heterogeneous definitions of outcomes, patterns for all-cause severe maternal morbidity and maternal intensive care unit admission were similar. We were unable to take into account other social factors that might interact with migrant status to determine maternal health because many of these data were unavailable. Conclusions In this systematic review of the existing literature applying a single definition of “migrant” women, we found that the differential risk of severe maternal outcomes in migrant versus native-born women in high-income countries varied by host country and region of origin. These data highlight the need to further explore the mechanisms underlying these inequities. Trial Registration PROSPERO CRD42021224193.