11beta-Hydroxysteroid dehydrogenase type 2 (11beta-HSD2) inactivates cortisol to cortisone. In the placenta 11beta-HSD2 activity is thought to protect the fetus from the deleterious effects of maternal glucocorticoids. Patients with apparent mineralocorticoid excess owing to mutations in the 11beta-HSD2 gene invariably have reduced birth weight, and we have recently shown reduced placental 11beta-HSD2 activity in pregnancies complicated by intrauterine growth restriction. This is reflected in the literature by evidence of hypercortisolemia in the fetal circulation of small babies. In this study we have determined the levels of placental 11beta-HSD2 mRNA expression across normal gestation (n = 86 placentae) and in pregnancies complicated by intrauterine growth restriction (n = 19) and evaluated the underlying mechanism for any aberrant 11beta-HSD2 mRNA expression in intrauterine growth restriction. 11beta-HSD2 mRNA expression increased more than 50-fold across gestation, peaking at term. Placental 11beta-HSD2 mRNA levels were significantly decreased in intrauterine growth restriction pregnancies when compared with gestationally matched, appropriately grown placentae [e.g. at term DeltaCt (11beta-hydroxysteroid dehydrogenase type 2/18S) 12.8 +/- 0.8 (mean +/- SE) vs. 10.2 +/- 0.2, respectively, P < 0.001]. These differences were not attributable to changes in trophoblast mass in intrauterine growth restriction placentae, as assessed by parallel analyses of cytokeratin-8 mRNA expression. No mutations were found in the 11beta-HSD2 gene in the intrauterine growth restriction cohort, and imprinting analysis revealed that the 11beta-HSD2 gene was not imprinted. Although the underlying cause is unknown, 11beta-HSD2 gene expression is reduced in intrauterine growth restriction pregnancies. These data highlight the important role of 11beta-HSD2 in regulating fetal growth, a known factor in determining fetal morbidity but also the subsequent development of cardiovascular disease in adulthood.

A retrospective study of the complications of cone biopsy showed that among 9 15 women examined between t h e years 1976 and 1982, 121 (13%) had primary or secondary haemorrhage, 153 (17%) cervical stenosis and 39 (4%) subsequent infertility or an abnormal pregnancy. Cervical stenosis was commonest among women who had had long cones removed. Stenosis occurred more often in the group of women who had been assessed by colposcopy before operation but this was due t o the fact that prior colposcopy selected a favourable group of patients with lesions of limited extent that were susceptible to treatment by local destructive therapy, so that prior colposcopic assessment resulted in the removal of longer cones.

A study was carried out to determine the incidence of maternal ketoacidosis in 635 insulin-treated diabetic pregnancies managed in a combined antenatal/diabetic clinic between 1971 and 1990. A total of 11 episodes occurred, representing 1.73% of diabetic pregnancies of which 9 were in the antenatal period. Overall fetal loss including spontaneous abortion was 22%, but there was only one fetal death in the seven episodes of ketoacidosis in the second and third trimesters. Ketoacidosis is an infrequent occurrence in diabetic pregnancy managed in a combined clinic and is not associated with a high fetal loss after the first trimester.

SummaryIn 58 consecutive pregnancies in insulin-dependent diabetic women, glycosylated haemoglobin levels were abnormally high in 78% at the time of booking for antenatal care.Spontaneous abortion was the outcome in 15 pregnancies, 10 occurring before the 15th week of gestation. Glycosylated haemoglobin levels were significantly higher in those women who aborted spontaneously than in women who delivered successfully (128 ±+ 1.8% v. 112 ±+ 2.3%, mean ± s.d.). These results emphasise the inadequacy of diabetic control in the first trimester and lend further support to the importance of good control at this critical time in insulin-dependent diabetes.

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