Obstetric outcome in women with polycystic ovarian syndrome.

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.

Resistance of Trichomonas vaginalis to metronidazole: report of the first three cases from Finland and optimization of in vitro susceptibility testing under various oxygen concentrations.

Trichomonas vaginalis is a globally common sexually transmitted human parasite. Many strains of T. vaginalis from around the world have been described to be resistant to the current drug of choice, metronidazole. However, only a few cases of metronidazole resistance have been reported from Europe. The resistant strains cause prolonged infections which are difficult to treat. T. vaginalis infection also increases the risk for human immunodeficiency virus transmission. We present a practical method for determining the resistance of T. vaginalis to 5-nitroimidazoles. The suggested method was developed by determining the MICs and minimal lethal concentrations (MLCs) of metronidazole and ornidazole for T. vaginalis under various aerobic and anaerobic conditions. Using this assay we have found the first three metronidazole-resistant strains from Finland, although the origin of at least one of the strains seems to be Russia. Analysis of the patient-derived and previously characterized isolates showed that metronidazole-resistant strains were also resistant to ornidazole, and MLCs for all strains tested correlated well with the MICs. The suggested MICs of metronidazole for differentiation of sensitive and resistant isolates are >75 microg/ml in an aerobic 24-h assay and >15 microg/ml in an anaerobic 48-h assay.

Glycaemic control during early pregnancy and fetal malformations in women with type I diabetes mellitus.

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 A1c 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 HbA1c was only slightly raised (5.6 to 6.8%, i.e. 2.0 to 5.9 standard deviation units) showed a relative risk of 3.0 (95% confidence interval: 1.2 to 7.5). Haemoglobin A1c 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 HbA1c 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.

Glycaemic control is associated with pre-eclampsia but not with pregnancy-induced hypertension in women with type I diabetes mellitus.

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 HbA1c. 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 HbA1c 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.

Hypertension and pre-eclampsia in women with gestational glucose intolerance.

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.

Effect of interferon gamma on the sensitivity of bovine-papilloma-virus(BPV1)-transformed cell lines to cell-mediated cytotoxicity.

The effect of interferon gamma (IFN gamma) on the immunogenicity and immunosensitivity of mouse cell lines transformed by bovine papillomavirus type 1 (BPV1) DNA was examined in a syngeneic mouse model. The overnight incubation of BPV1-transformed cell lines with 100 IU/ml IFN gamma did not affect their ability to induce the generation of cytotoxic effector cells but it clearly increased their sensitivity to lysis by interleukin-2-induced lymphokine-activated killer (LAK) cells and by non-specific LAK-type effector cells induced by BPV-1-transformed cell lines. The treatment of two allogeneic lymphoid tumour cell lines, P815X2 and YAC-1, with IFN gamma either decreased or had no effect on their sensitivity to LAK-cell-mediated lysis.

Correlation of HbA1C, glycated serum proteins and albumin, and fructosamine with the 24-h glucose profile of insulin-dependent pregnant diabetics.

To assess the value of various methods for long-term follow-up of diabetic patients, we compared the concentrations of fructosamine in serum with those of various glycated proteins: hemoglobin (HbA1C), total serum proteins (G-prot), and albumin (G-alb), assayed in 30 pregnant insulin-dependent diabetics every two weeks after initial determination of a 24-h blood glucose profile. HbA1C correlated best with the 24-h glucose profile during the succeeding 10-35 days (r = 0.65-0.68, P less than 0.001). G-prot and G-alb correlated nearly as well as HbA1C 10-20 days after the glucose profile (r = 0.54-0.64, P less than 0.01-0.001), but only weakly after 25-35 days. Values for fructosamine did not correlate significantly with the glucose profile 10-35 days after it (r = 0.23-0.36). Evidently the fructosamine assay is not an adequate alternative to HbA1C, G-alb, or G-prot as an index to long-term control of blood glucose in such patients.

Vaginal and abdominal delivery increases maternal urinary 6-keto-prostaglandin F1 alpha excretion.

To study the role of the antiaggregatory and vasodilatory prostacyclin (PGI2) during human delivery, serial urine samples collected from 13 women delivered vaginally and from eight delivered abdominally were assayed for 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha, a breakdown product of PGI2) by high-performance-liquid-chromatography and radioimmunoassay. In women delivered vaginally the mean urinary 6-keto-PGF1 alpha concentration was 41.9 (SE 8.3) ng/mmol creatinine, before the onset of labour and increased progressively to a maximum of 186.5 (SE 47.6) ng/mmol creatinine 2 h after delivery irrespective of the use of oxytocin and epidural analgesia. In women delivered by caesarean section under epidural anaesthesia, the urinary 6-keto-PGF1 alpha rose from 33.4 (SE 4.2) ng/mmol creatinine to 2153 (SE 314) ng/mmol creatinine 2 h after section. In both groups the increased levels had fallen by 24 h postpartum to levels below those found before delivery. In neonatal urine 6-keto-PGF1 alpha concentrations were some 12-30 times higher than those in postpartum urine. Thus, vaginal and abdominal delivery is accompanied by significant increases in maternal PGI2 release, perhaps in the myometrium and/or intrauterine tissues. This may be of significance in the regulation of fetoplacental blood flow and in the prevention of intra- and postpartum thrombosis.