Women with polycystic ovarian syndrome (PCOS) often have insulin resistance and hyperinsulinaemia and may therefore be at an increased risk for gestational diabetes mellitus (GDM). Hyperinsulinaemia may also be associated with pre-eclampsia. Information concerning outcome of pregnancies in PCOS women is scanty and somewhat controversial. Therefore, 99 pregnancies were retrospectively evaluated in women with PCOS and the findings were compared with an unselected control population. The average body mass index (BMI) in PCOS patients was greater than that in controls (25.6 versus 23.0) (P < 0.0001), and PCOS patients were more often nulliparous than controls (76 versus 42%) (P < 0.001). The multiple pregnancy rate was 9.1% in PCOS patients and 1.1% in controls [odds ratio (OR) 9.0; 95% confidence interval (CI) 3.5-23.3]. GDM developed in 20% of the PCOS patients and in 8.9% of the controls (P < 0.001). After logistic regression analysis, BMI >25 seemed to be the greatest predictor for GDM (adjusted OR 5.1; CI 3.2-8.3), while PCOS remained as another independent predictor (adjusted OR 1.9; CI 1.0-3.5). In contrast, PCOS was not a significant predictor for pre-eclampsia, which was merely associated with nulliparity. Premature delivery (16.1% in PCOS and 6.5% in controls) was explained to a large extent by multiple pregnancies and marginally by nulliparity and PCOS. In singleton pregnancies, there was no difference in birth weights, Apgar scores or perinatal morbidity of infants. In conclusion, PCOS slightly increases the risk for GDM, but does not have an important effect on the rate of premature delivery and pre-eclampsia.

The incidence of congenital malformations is reportedly two to four times higher in pregnancies of women with Type I (insulin-dependent) diabetes mellitus than in normal pregnancies [1,2]. Hyperglycaemia in early pregnancy has been most often implied as the reason because an association between maternal HbA 1 c in early pregnancy and the frequency of fetal malformations has been reported.Although it has been suggested that the risk of fetal malformations in women with Type I diabetes increases only when HbA 1 c is above a certain value, e. g. 8 or 10 SD units above the non-diabetic mean [3,4], existence of such thresholds has recently been challenged. It is still not clear whether only slightly impaired glycaemic control during early pregnancy in women with Type I diabetes is teratogenic.We assessed the risk of fetal malformations in women with Type I diabetes and compared it with that in a background population. We also related this risk to glycaemic control in early pregnancy as determined by HbA 1 c . Diabetologia (2000) Abstract Aims/hypothesis. To assess the relation between glycaemic control in early pregnancy and the risk of congenital malformations in offspring of mothers with Type I (insulin-dependent) diabetes mellitus. Methods. From 1988±1997, we prospectively collected data from 691 pregnancies and 709 offspring of 488 women with Type I diabetes in a specific geographic area in Southern Finland. Glycated haemoglobin A 1 c at less than 14 weeks of gestation was used as the indicator of glycaemic control. The malformations were diagnosed either by ultrasonography in pregnancy or during the neonatal period. We also studied 729 non-selected control pregnancies in women without diabetes. Results. The numbers of major fetal malformations were 30 (4.2 %) in patients with Type I diabetes and 10 (1.2 %) in the control subjects (relative risk 3.1; 95 % confidence interval: 1.6 to 6.2). Even women whose HbA 1 c was only slightly raised (5.6 to 6.8 %, ie 2.0 to 5.9 standard deviation units) showed a relative risk of 3.0 (95 % confidence interval: 1.2 to 7.5). Haemoglobin A 1 c retained its statistically significant association with the occurrence of malformations after adjusting for White's class, age at onset of diabetes, duration of diabetes, parity, smoking and participation in pre-pregnancy counselling. Conclusions/interpretation. Even a slightly raised HbA 1 c during early pregnancy in women with Type I diabetes carries an increased risk for fetal malformations. Therefore normoglycaemia should be strived for during early pregnancy. [Diabetologia (2000) 43: 79±82]

It has long been known that Type I (insulin-dependent) diabetes mellitus considerably increases the risk of pre-eclampsia and maternal and fetal co-morbidity [1±3]. The most important risk factor of pre-eclampsia in women with diabetes is nephropathy (White's class F) [1]. Even incipient nephropathy substantially increases the risk [4]. In addition, retinopathy and long duration of diabetes also increase the risk of pre-eclampsia [5±8].Although an association between poor glycaemic control in early pregnancy and pre-eclampsia has been reported [4, 7±11], it has not been observed by all [12]. It is not clear to what extent glycaemic control in early pregnancy might exert an effect on the occurrence of pre-eclampsia. Diabetic women with HbA 1 c values greater than 8 % could be at a greater risk of pre-eclampsia than those with values less than 8 % [10]. It is not known whether the risk of pre-eclampsia in diabetic women with relatively good gly- Abstract Aims/hypothesis. To investigate the association between glycaemic control and hypertensive pregnancy complications. Methods. From 1988 to 1997, we followed up 683 consecutive non-selected pregnancies in women with Type I (insulin-dependent) diabetes mellitus. Glycaemic control was assessed by assay of HbA 1 c . Pre-eclampsia was defined as diastolic blood pressure of 90 mmHg or more at the end of pregnancy after an increase of 15 mmHg or more, combined with proteinuria of 0.3 g or more for 24 h. Pregnancy-induced hypertension was defined similarly but without proteinuria. The same criteria were applied to a control group of 854 non-selected non-diabetic women. Results. Pre-eclampsia developed in 12.8 % of the women with diabetes (excluding those with nephropathy before pregnancy) and in 2.7 % of the control women (odds ratio 5.2; 95 % CI 3.3±8.4). In multiple logistic regression, glycaemic control, nulliparity, retinopathy and duration of diabetes emerged as statistically significant independent predictors of pre-eclampsia. The adjusted odds ratios for pre-eclampsia were 1.6 (95 % CI 1.3±2.0) for each 1 % increment in the HbA 1 c value at 4±14 (median 7) weeks of gestation and 0.6 (0.5±0.8) for each 1 % decrement achieved during the first half of pregnancy. Changes in glycaemic control during the second half of pregnancy did not significantly alter the risk of pre-eclampsia. Unlike pre-eclampsia, the risk of pregnancy-induced hypertension was not associated with glycaemic control. Conclusion/interpretation. In women with Type I diabetes, poor glycaemic control is associated with an increased risk of pre-eclampsia but not with a risk of pregnancy-induced hypertension. [Diabetologia (2000

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The relationship between pregnancy-induced hypertension (and pre-eclampsia) and gestational glucose intolerance was examined prospectively in 81 women with gestational diabetes mellitus. A borderline group consisted of 203 women with a single abnormal value on an oral glucose tolerance test. Controls consisted of 327 healthy women with normal glucose tolerance test at 28-32 weeks of gestation. The women with gestational diabetes were older (p < 0.01) and their prepregnancy weight and body mass index were higher (p < 0.001) than those in the control group. Also the women in the borderline group had higher prepregnancy weight (p < 0.01) and body mass index (p < 0.001) than the women in the control group. However, the pregnancy weight gain was lower in the gestational diabetics than in the control women (p < 0.001). Birth weight, birth trauma, low Apgar scores and hypoglycemia did not differ between the groups. However, hyperbilirubinemia occurred more frequently (28.4% vs. 3.7%, p < 0.001) in the gestational diabetics than in the controls. The frequency of both chronic hypertension (2.5% vs. 0.3%, p < 0.05) and pregnancy induced hypertension and pre-eclampsia (19.8% vs. 6.1%, p < 0.001) were higher in the gestational diabetes group, but not in the borderline group when compared with the controls.