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We performed a scanning electron microscopic study of fimbrial biopsies from two patients with Rokitansky's syndrome and from three fertile patients in the same period of the menstrual cycle as controls. In the patient samples we observed irregular running and frequent conglutination of the mucosal folds. Ciliated cells appeared reduced in number compared with controls, and cilia were often agglutinated. Some areas contained nonciliated cells, dome-shaped or giant as observed in the menopause, with rare microvilli, suggesting disturbances of cellular growth and trophism of the tubes in patients with Rokitanskys syndrome.

The endometrium of an infertile patient with Kartagener's syndrome showed initial secretory phase characteristics at SEM, whereas TEM analysis demonstrated several alterations in the central and peripheral microtubular distribution in 87% of the cilia examined. Such aspects seemed appropriate for a normal implantation, but the ciliary immotility or dyskinesia could cause an altered flow of the endometrial secretions and compromise the upstream movement of the spermatozoa.

Objective: To assess hematologic and biochemical blood variables in growth-restricted fetuses and relate them to biophysical measurements. Methods: Blood was sampled from 22 growth-restricted fetuses. All had normal karyotypes and no congenital infections. Venous pH, partial pressure of oxygen, hematocrit, glucose, uric acid, urea, creatinine, total protein, total and direct bilirubin, aspartate aminotransferase, alanine aminotransferase, γ-glutamyltransferase, alkaline phosphatase, lactic dehydrogenase, amylase, pseudocholinesterase, creatinine kinase, triglycerides, and cholesterol were measured and compared with our reference range. Results: Ultrasound measurements of abdominal circumference correlated with fetal pH (r = 0.64), partial pressure of oxygen (r = 0.52), glucose (r = 0.67), total bilirubin (r = −0.54), lactic dehydrogenase (r = −0.48), and triglyceride levels (r = −0.65). Compared with fetuses with present end-diastolic velocities in the umbilical artery, the eight with absent end-diastolic velocities had lower pH (median z score −4.31), partial pressure of oxygen (median z score = −2.39), glucose (median z score = −2.01), and cholesterol (median z score = −2.34), and higher γ-glutamyltransferase (median z score = 2.43), lactic dehydrogenase (median z score = 3.75), urea (median z score = 1.33), creatinine (median z score = 1.23), and triglyceride levels (median z score = 1.71). Only triglycerides correlated with abdominal circumference, independent of Doppler results. Conclusion: Growth-restricted fetuses with absent end-diastolic velocities in the umbilical artery had more marked acidemia, hypoxemia, hypoglycemia, and abnormal liver function than those with end-diastolic velocities. Triglyceride levels were inversely related to fetal size independent of Doppler results. High triglyceride levels might reset fetal homeostatic mechanisms, leading to disturbances of lipid metabolism in later life.

OBJECTIVE: Because individuals with Down syndrome appear to be protected from the development of atherosclerosis, we aimed to assess whether blood lipid and lipoprotein concentrations are different from controls in fetuses with trisomy 21. STUDY DESIGN: Eighteen fetuses with trisomy 21 and seven with trisomy 18 undergoing blood sampling at 18 to 36 weeks' gestation were matched by gestational age and size with an equal number of controls. Cholesterol and triglycerides were assayed in all fetuses and compared with the reference range constructed from 157 normal fetuses. High-density lipoproteins and apoproteins A and B were assayed in eight fetuses with trisomy 21, four with trisomy 18, and an equivalent number of controls. RESULTS: When compared with the reference range, fetuses with trisomy 21 had significantly increased cholesterol levels (median Z score 2.31, 95% confidence interval 1.57 to 3.08, p = 0.0001). Cholesterol and apoprotein A concentrations were also significantly higher than in fetuses with normal karyotypes matched by gestational age and size at sampling, whereas other lipids and lipoproteins were similar. There were no differences between fetuses with trisomy 18 and their matched controls. A value of fetal cholesterol ≥85 mg/dl had a sensitivity of 72% and specificity of 95% in detecting fetuses with trisomy 21. CONCLUSIONS: Fetuses with trisomy 21 have abnormalities of lipid metabolism that are specific and may be genetically determined. The finding of high cholesterol levels in fetuses undergoing blood sampling for indications other than karyotyping should prompt investigation of fetal chromosomes because of the increased risk of trisomy 21. The mechanism through which high levels of cholesterol during prenatal life are not leading to increased risk of atherosclerosis remains to be elucidated.(Am J Obstet Gynecol 1997;176:540-3

To construct reference ranges for fetal pH, oxygen pressure (PO2), and hematologic and biochemical blood constituents, which can be used to analyze changes with gestation and differences with maternal values, thus elucidating some aspects of fetal biology and the effects of the maternal and placental environments.We assayed venous pH, PO2, hematocrit, glucose, uric acid, urea, creatinine, total protein, total and direct bilirubin, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase, alkaline phosphatase, lactic dehydrogenase, amylase, pseudocholinesterase, creatine kinase, triglycerides, and cholesterol concentrations in 157 fetuses and 134 mothers who underwent fetal blood sampling from 18 to 37 weeks' gestation. None of the fetuses was infected or had chromosomal, hematologic, or hormonal abnormalities.All the variables analyzed were similar in fetuses sampled at the placental cord insertion (n = 125) or at the intrahepatic vein (n = 32). Maternal and fetal concentrations of glucose (r = 0.79, P.001), urea (r = 0.96, P.001), creatinine (r = 0.83, P.001), and uric acid (r = 0.94, P.001) correlated significantly, and their differences exhibited significant changes: the maternal-fetal differences of glucose and urea increased, whereas those of uric acid and creatinine decreased with advancing gestation. Fetal pH and PO2 decreased with gestational age, whereas hematocrit increased, similar to what has been described previously. All of the other variables, with the exception of amylase and cholesterol, changed significantly during the investigated period of pregnancy. Gestational age explained at least 40% of the variance in values of fetal total protein, pseudocholinesterase, alanine aminotransferase, creatine kinase, and triglycerides, but only 3-25% of the variation in the remainder. Most enzymes were higher in the fetus than in the maternal circulation, and all except alkaline phosphatase increased with gestational age. The maternal-fetal glucose difference correlated significantly with hematocrit, pH, and PO2, independent of gestational age and independent of each other.With the exception of aspartate aminotransferase, all of the analyzed fetal variables were different from the maternal values, and most changed with gestational age. The mechanisms leading to these fetal specificities remain mostly uncertain, but the provision of reference ranges for several blood constituents may be useful in the differential diagnosis of fetal disease.