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Whether pregnant women with insulin-dependent diabetes mellitus have an increased risk of spontaneous abortion is controversial. To address this question, we enrolled 386 women with insulin-dependent diabetes and 432 women without diabetes before or within 21 days after conception and followed both groups prospectively. Sixty-two diabetic women (16.1 percent) and 70 control women (16.2 percent) had pregnancy losses (odds ratio, 0.99; 95 percent confidence interval, 0.67 to 1.46). After adjustment for known risk factors for spontaneous abortion, the rate was still not significantly higher in the diabetic group (odds ratio, 0.91; 95 percent confidence interval, 0.59 to 1.40). Nonetheless, among the diabetic women, most of whom had good metabolic control, those who had spontaneous abortions had higher fasting and postprandial glucose levels in the first trimester than those whose pregnancies continued to delivery (P = 0.01 for fasting glucose levels and P = 0.005 for postprandial levels). In the small subgroup of diabetic women with poor control, who had elevated values for glycosylated hemoglobin in the first trimester, each increase of 1 SD above the normal range was associated with an increase of 3.1 percent in the rate of pregnancy loss (95 percent confidence interval, 0.6 to 5.6). We conclude that diabetic women with good metabolic control are no more likely than nondiabetic women to lose a pregnancy, but that diabetic women with elevated blood glucose and glycosylated hemoglobin levels in the first trimester have a significantly increased risk of having a spontaneous abortion.

We classified 106 stillborn and live-born infants with anencephaly, meningomyelocele, meningocele and encephalocele according to the recognized causes of these malformations. Six different causes were identified, including both genetic and nongenetic disorders; 12 per cent had nongenetic disorders, a chromosome abnormality, or an encephalocele as part of the autosomal recessive Meckel syndrome. Therefore, for this 12 per cent genetic counseling normally provided for isolated anencephaly, meningomyelocele or encephalocele would have been incorrect. If all infants were considered together regardless of cause, the precurrence and recurrence rates of similar malformations in the sibs were 5.2 and 1.7 per cent respectively. However, if infants with other disorders, especially the Meckel syndrome, were excluded, the precurrence and recurrence rates for isolated anencephaly, meningomyelocele and encephalocele among white infants were only 1.7 per cent and 0 per cent. These rates are much lower than the risk of 5 per cent currently being used in genetic counseling in the United States.

In attempting to differentiate early-onset Group B streptococcal infection from hyaline-membrane disease we found features of severe Group B infection to be rupture of the membranes for more than 12 hours before delivery (four or eight versus one of nine), gram-positive cocci in the gastric aspirate (four or four versus none of one), apnea and shock in the first 24 hours of life (seven of eight versus none of nine), and the generation of lower peak inspiratory pressures on avolume-cycled respirator (mean of 36.5 +/- 2.8 versus 63.9 +/- 6.2 cm of water; P = 0.005). In eight fatal cases of Group B infection, four patients had radiographic features indistinguishable from hyaline-membrane disease whereas the other cases were consistent with neonatal pneumonia. Seven of the eight infected infants had no histologic evidence of coexisting hyaline-membrane disease. Microscopical features of Group B infection included cocci in unevenly distributed hyaline membranes and minimal atelectasis. Group B streptococcal infection differs clinically and pathologically from hyaline-membrane disease. Differentiating clinical features include early apnea and shock and lower inspiratory pressures on mechanical ventilation.

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The acid ethanol extractable insulin content of pancreases from thirty-seven infants and three early fetuses of diabetic and control mothers has been measured and their islet cell histology was studied. In general there was good agreement between these two parameters. Pancreatic insulin could be detected in one of two twelve-week old fetuses examined and in the pancreas of a fourteen-week old fetus of a diabetic mother. The remaining thirty-seven pancreases were obtained from fetuses of gestational age twenty weeks to term, nine of whom were offspring of diabetic mothers. The latter contained more insulin than the corresponding control group. The possible mechanisms are discussed; the hyperglycemic hypothesis is favored.

Eighteen term placentas from a middle-class North American urban population were examined by stereologic techniques and an image quantizer. The trimmed placental weight averaged 469 g, of which 339 g was Ê»functional parenchyma’ and 130 g Ê»nonparenchymal tissue’ (decidual and chorionic plates and large vessels and pathological components such as infarcts). Microscopically, the parenchyma was divided into villi and intervillous space. The volume of intervillous space was, at 110 cm³, significantly larger than that of the villous capillaries, which measured 30 cm³. The mass of the chorionic villi averaged 214 g and comprised 168 g of peripheral and 46 g of stem villi. Most of the 60 g of trophoblast and of the 31.5 g of fibroblasts, and a significant fraction of the 91 g of collagenous stroma were present in the peripheral villi. The longest diameter of the peripheral villi averaged 74 µm and their cross-sectional area 1,100 µm². The surface area of the peripheral villi was 16 m² and that of the corresponding xillous capillaries 12 m². A model for estimating placental oxygen diffusion capacity (Dpo₂) was constructed on the basis of these stereologic measurements. The resistance to oxygen diffusion from maternal to fetal red cells in the placenta was attributed to five serial compartments i.e. (1) the oxygen-hemoglobin interactions in the maternal red cells in the intervillous space; (2) the maternal blood plasma in the intervillous space; (3) the villous membrane comprising syncytiotrophoblast, basement membrane, connective tissue and fetal capillary wall; (4) the fetal blood plasma, in the villous capillaries and (5) the oxygen-hemoglobin interactions in the fetal red cells present in the villous capillaries. The diffusion capacity of the placental membrane (D_M), comprising (2–4), was 3.256 and that of the total placenta 3.086 ml oxygen min^––1 · mm Hg^––1. The corresponding specific diffusion capacities per 100 g of placenta were 0.694 for the placental membrane (D_M/w) and 0.658 ml. min^––1 · mm Hg^––1 for the whole placenta (D_P/_w). The resistance of the villous membrane was consequently the limiting factor in oxygen diffusion, both when considering the 110-ml maternal and 30-ml fetal blood volumes as the effective exchangers or when considering a single capillary transit for oxygen with 10 ml in each of the maternal and fetal compartments.

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