According to common understanding of sexual differentiation, the formation and development of a penile clitoris in female spotted hyaenas requires the presence of naturally circulating androgens during fetal life. The purpose of the present study was to determine potential source(s) of such fetal androgens by investigating the timing of urogenital development and placental production of androgen during early and mid-gestation. Fetuses determined to be female by molecular techniques (lack of SRY gene) at days 33 and 48 of gestation had undifferentiated gonads, but the clitoris was already 'masculinized' and was generally similar to the phallus of a 50-day-old male fetus. Wolffian and Müllerian ducts terminated at the urogenital sinus in both sexes and a urethra was present along the entire length of the clitoris and penis. The adrenal gland was large and histologically differentiated at 33 days. Steroid gradients across the uterus (a drop in delta 4-androstenedione, with increases in oestrogen and androgen), and high androstenedione in ovarian veins indicated that ovarian androstenedione was metabolized and secreted as testosterone by the placenta throughout gestation. In vitro, whole or homogenized placentae at days 48 and 58 of gestation (110 days total) metabolized radiolabelled androstenedione into testosterone and oestradiol; the specific enzymatic activity of early placental tissues was higher than at later stages. A human placental homogenate had higher aromatase activity but did not produce testosterone unless aromatase was inhibited. Infusion of labelled androstenedione into the uterine arteries of hyaenas demonstrated the conversion of this substrate into testosterone and oestradiol and their secretion into the fetal circulation. Evidently, androgen is produced by the placenta and secreted into the fetal circulation from early in pregnancy when masculinization is first evident, before differentiation of the fetal ovary.
Gastroschisis is a rare congenital anomaly characterized by the herniation of fetal intestines directly through an abdominal wall defect. It is associated infrequently with chromosomal or other nonbowel defects and can be treated surgically after delivery, with survival rates reported to be between 87 and 100%. We reviewed 21 cases of prenatally diagnosed gastroschisis to ascertain the effect of fetal growth retardation on perinatal outcome. Ten of the 21 fetuses (48%) were identified prenatally as growth retarded, although only seven of these ten truly had birth weights less than the 10th percentile. Three additional fetuses that had not been identified prenatally as growth retarded did, in fact, have birth weights less than the 10th percentile, for a total frequency of growth retardation at birth of 48% (10/21 fetuses). When compared to non‐growth‐retarded fetuses with gastroschisis, fetuses who were growth retarded, although more likely to have been delivered by emergency cesarean section, had shorter hospitalization times, were more likely to have undergone primary closure on the first day of life, and had fewer major complications. We conclude that growth retardation is common in fetuses with gastroschisis and the postnatal outcome in gastroschisis is not poorer for fetuses who are growth retarded.
Sonograms of fetuses at risk for congenital lethal osteogenesis imperfecta (osteogenesis imperfecta type II) were retrospectively reviewed blindly and correlated with pregnancy outcomes. Six of eight cases of type II osteogenesis imperfecta were correctly diagnosed with use of the proposed criteria of multiple fractures, demineralization of the calvaria, and femoral length more than 3 standard deviations below the mean for gestational age. The two cases not diagnosed had sonographic abnormalities but did not meet all three criteria. Among 18 pregnancies genetically at risk for the disease but with normal outcomes, all sonograms were normal, meeting none of the proposed criteria. Among an additional 25 fetuses with osteochondrodysplasias, no case satisfied all three of the proposed diagnostic criteria. With use of strict standards for the diagnosis of type II osteogenesis imperfecta, this disease can be distinguished from other fetal skeletal abnormalities. In a pregnancy at risk for recurrence of osteogenesis imperfecta, a normal sonogram after 17 weeks excludes this lethal condition.
In an attempt to predict histologic fetal renal dysplasia among fetuses with obstructive uropathy, three antenatal sonographic features (presence of renal cortical cysts, echogenicity of renal parenchyma, and degree of hydronephrosis) were studied. Identification of renal cortical cysts in the kidneys of fetuses with obstructive uropathy enabled accurate prediction of renal dysplasia. Of 49 fetal kidneys with obstructive uropathy, all 15 kidneys with sonographically visible cortical cysts had severe but not necessarily lethal dysplasia (accuracy of positive prediction = 100%). Of 15 obstructed but nondysplastic fetal kidneys, none had sonographically visible cysts (specificity = 100%). The absence of fetal renal cysts on antenatal sonography, however, did not exclude the presence of dysplasia. Assessment of the echogenicity of renal parenchyma and the degree of hydronephrosis are of only limited value in predicting whether an obstructed fetal kidney will show histologic dysplasia.
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