PubMed · 8635300
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R S Howe. 1996. Early pregnancy: normal and abnormal.. https://doi.org/10.1097/00003081-199603000-00019
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The mesonephrogenic cord disintegrates into approximately 35-40 provesicular cell masses which are in close contact with the mesonephric (Wolffian) duct (WD) on their lateral side. Here, the epithelium of the WD is columnar and shares a common basal lamina with the provesicular cell masses. This in turn gives rise to a sickle-shaped pseudostratified epithelium. The concavity of the sickle is filled by spherical cells, the transition of which into the surrounding connective tissue is continuous. The sickle is transformed into a distillation flask and becomes separated from the mesonephric duct while the spherical cells maintain a connection to it by a-for the time being-solid outlet pipe. The columnar epithelium of the mesonephric duct becomes a multilayered cone, whose surface is in contact with the outlet tube. Shortly after, a continuous lumen is formed in the cone and the outlet pipe which is delimited by cells becoming columnar and forming a basal lamina. The epithelial anlage of the nephron is clearly separated from the surrounding mesenchyma by these processes. The flask eventually becomes a corpusculum, the outlet pipe a secretory (proximal) as well as collecting tubule, and the cone of the mesonephric duct a mesoureter. The various sections display differentially differentiated epithelia that are clearly distinct from each other. The mesoureter behaves differently during differentiation of epi- and paragenitale: in the epigenitale, it is short and runs into the collecting tubules of the nephrons at the lateral side of the convolved tubules, whereas a long mesoureter crosses the dorsal side of the convolved tubules and joins the corresponding collecting tubules at the far end of the mesonephros in the paragenitale.
OBJECTIVE: To determine the likelihood ratio for trisomy 21 in fetuses with tricuspid regurgitation at the 11 to 13 + 6-week scan. METHODS: Fetal echocardiography was carried out by specialist pediatric cardiologists in 742 singleton pregnancies at 11 to 13 + 6 weeks' gestation and pulsed wave Doppler was used to ascertain the presence or absence of tricuspid regurgitation. To avoid confusion with other adjacent signals, a strict definition of tricuspid regurgitation was used, in that it had to occupy at least half of systole and reach a velocity of over 80 cm/s. The fetal crown-rump length (CRL) and the nuchal translucency (NT) thickness were measured and the presence of any congenital heart abnormality noted. Follow-up of the pregnancy was carried out to determine the presence of chromosomal abnormalities. The likelihood ratio for trisomy 21 in fetuses with and without tricuspid regurgitation was determined. RESULTS: The tricuspid valve was successfully examined in 718 (96.8%) cases. Tricuspid regurgitation was present in 39 (8.5%) of the 458 chromosomally normal fetuses, in 82 (65.1%) of the 126 with trisomy 21, in 44 (53.0%) of the 83 with trisomy 18 or 13, and in 11 (21.6%) of the 51 with other chromosomal defects. The prevalence of tricuspid regurgitation was also associated with fetal CRL, delta NT and the presence of cardiac defects. Logistic regression analysis, irrespective of cardiac defects, demonstrated that in the chromosomally normal fetuses significant independent prediction of the likelihood of tricuspid regurgitation was provided by fetal delta NT (odds ratio (OR), 1.26; 95% CI, 1.34-1.41; P < 0.0001), while in trisomy 21 fetuses prediction was provided by CRL (OR, 0.94; 95% CI, 0.89-0.99; P = 0.021). The likelihood ratio for trisomy 21 for tricuspid regurgitation was derived by dividing the likelihood in trisomy 21 by that in normal fetuses. In the chromosomally normal fetuses, the prevalence of tricuspid regurgitation in those with cardiac defects was 46.9% and 5.6% in those without cardiac defects, and the likelihood ratio of tricuspid regurgitation for cardiac defects was 8.4. CONCLUSION: At 11 to 13 + 6 weeks' gestation, there is a high association between tricuspid regurgitation and trisomy 21, as well as other chromosomal defects. The prevalence of tricuspid regurgitation increases with fetal NT thickness and is substantially higher in those with, than those without, a cardiac defect.
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