Early random capillary glucose level screening and multidisciplinary antenatal teamwork to improve outcome in gestational diabetes mellitus

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1 Acta Obstetricia et Gynecologica. 2007; 86: ORIGINAL ARTICLE Early random capillary glucose level screening and multidisciplinary antenatal teamwork to improve outcome in gestational diabetes mellitus MARIE BERG 1,2, ANNIKA ADLERBERTH 3, BO SULTAN 2, MARGARETA WENNERGREN 2 & GUNNAR WALLIN 2 1 The Institute of Health and Care Sciences, Sahlgrenska Academy, Göteborg University, Göteborg, Sweden, 2 Department of Obstetrics and Gynaecology, The Institute of Clinical Sciences, Sahlgrenska University Hospital, Göteborg, Sweden, and 3 The Institute of Medicine, Sahlgrenska University Hospital, Göteborg, Sweden Abstract Background. This study describes maternal and neonatal characteristics and delivery outcome in women with gestational diabetes mellitus [GDM], compared to a control. Methods. A retrospective observational study of 719 women with GDM was undertaken in a Swedish urban district. All other parturients at the same hospital served as the control. GDM was diagnosed using random capillary glucose levels at fixed intervals, beginning early in pregnancy. An oral glucose tolerance test was performed at glucose levels ]/7.0 mmol/l (127.8 mg/dl). Data was analysed according to glucose levels at diagnosis, ie, mild or severe GDM. Results. GDM was diagnosed in 2.28% of the women who were older and had higher Body Mass Index [BMI]. A high proportion was of non-nordic origin (44.5%); they had severe GDM more often (49.1%) than the Nordic (33.1%). The GDM-mild had less complications and abnormalities, compared to the GDM-severe, although both s differed from the control in this respect. Delivery was spontaneous in 70.2% of GDM-mild, 65.7% of GDMsevere and 81.0% of the control. LGA (/2 SD) was found in 4.8, 10.5 and 3.2%, respectively. Conclusion. Early nonfasting random universal screening and multidisciplinary antenatal teamwork intervention seems to be favourable, with low rates of excessive fetal growth, instrumental vaginal delivery and caesarean section. Key words: Gestational diabetes mellitus, maternal-fetal outcome, random blood glucose, oral glucose tolerance test Abbreviations: AGA: average for gestational age, BMI: body mass index, GDM: gestational diabetes mellitus, LGA: large for gestational age, MBR: the Medical Birth Register, NS: not significant, NA: not applicable, OGTT: oral glucose tolerance test, OOOW: obstetrical outpatient observation ward, OR: odds ratio, RCG: random capillary whole blood glucose, SD: standard deviation, SGA: small for gestational age, SUH: Sahlgrenska University Hospital, WHO: World Health Organisation, 2-h OGTT: two-hour capillary blood glucose OGTT Introduction Gestational diabetes mellitus [GDM] is defined as any abnormal glucose tolerance first diagnosed during pregnancy and caused by insulin resistance connected with pregnancy-related defects in insulin secretion. Occurrence of GDM during early pregnancy may indicate abnormal metabolism preceding pregnancy. GDM is associated with adverse pregnancy outcome, such as pre-eclampsia, macrosomia, brachial plexus palsy, neonatal hypoglycaemia and jaundice (15). There is also an increased risk of developing diabetes mellitus, mainly type 2, later in life (6). No definite knowledge exists about at what level the impairment in glucose metabolism will affect obstetric outcome (7). Globally, a multitude of diagnostic criteria and treatments are available. The 75-g oral glucose tolerance test [OGTT], proposed by the World Correspondence: M Berg, Institute of Health and Caring Sciences, Sahlgrenska Academy, Göteborg University, Box 457, SE , Göteborg, Sweden. marie.berg@fhs.gu.se (Received 3 March 2006; accepted 4 November 2006) ISSN print/issn online # 2007 Taylor & Francis DOI: /

2 284 M. Berg et al. Health Organization [WHO] (8), is utilised for diagnosis in many centres. OGTT may be administered to all pregnant women at a certain gestational age or only to those with risk factors for gestational diabetes. Another option is non-fasting random blood glucose sampling only once or at regular intervals during pregnancy to select women for OGTT (9,10). The aim of this study was to examine maternal and neonatal characteristics and delivery outcomes associated with a new antenatal care regimen for GDM, including early non-fasting random capillary whole blood glucose [RCG] level screening and multidisciplinary antenatal teamwork. Material and methods In connection with an organisational change in maternity care in the western part of Sweden, including concentration of maternity care to Sahlgrenska University Hospital [SUH], the routines for detecting and treating GDM were changed. The WHO recommendation (11), suggesting early intervention, was followed. All pregnant non-diabetic women attending the antenatal clinics were offered non-fasting RCG tests, at fixed gestational ages, but at random times during the day. Tests were taken at the first visit, at gestational week 812, and every 46 weeks, beginning from gestational week 24, a total of 5 6 tests during pregnancy. Women with RCG ]/11.1 mmol/l (203 mg/dl), or with a fasting glucose level ]/6.1 mmol/l (111 mg/dl) preceding OGTT, were diagnosed as GDM. If RCG was ]/7.0 mmol/l (128 mg/dl) and B/11.1 mmol/l (203 mg/dl), OGTT, with 75 g anhydrous glucose dissolved in 300 ml of water, was performed after an overnight fast. Both RCG and blood tests for the OGTT were analysed in a Hemocue using 5 ml capillary whole blood (Hemocue AB, Ängelholm, Sweden). A 2-h capillary blood glucose level (2-h OGTT) ]/7.8 mmol/l (142 mg/dl) during the OGTT led to a diagnosis of GDM. This is in agreement with the 1998 WHO classification criteria (11). After diagnosis, the woman attended the hospital s obstetrical outpatient observation ward [OOOW] and met a specially trained diabetes midwife. The model of care stressed the importance of the woman s participation in and responsibility for her treatment, aimed at normalising blood glucose levels, and consisted of individual adjusted diet and physical activities. She received a blood glucose monitor and was instructed to test glucose levels at least three times pre-prandially and 1 h postprandially daily. Dietary advice included a balanced diet with slow carbohydrates without caloric restriction and regular food intake, including three meals and two or three snacks. To avoid hyperglycemia before noon, breakfast was commonly divided into smaller portions. The slow carbohydrate diet included dietary fibres, eg, whole-grain sourdough bread instead of white, sweetened bread, fruit instead of juice, no milk in liquid form, fibre rich legumes as carrots and not only lettuce, tomatoes or cucumbers. Information was given on the positive effects of physical activity to lower blood glucose level and daily walks were proposed as exercise. The target glucose level was 46 mmol/l (73109 mg/l) preprandially, and B/8 mmol/l (146 mg/dl) postprandially. Follow-up was scheduled at the OOOW some days later, including a visit to an obstetrician who also performed an ultrasound in cases /28 gestational weeks. The blood glucose levels, changed diet regimen and physical activities were followed up and revised in dialogue between the woman and the diabetes midwife. When lifestyle changes were sufficient to normalise blood glucose levels, the woman continued her visits to the primary antenatal clinic. Twice a week, she monitored blood glucose levels six times daily as prescribed above, and had telephone contact with the diabetes midwife at the OOOW every other week in order to follow up glucose levels, be given additional advice on diet and physical activities and engage in dialogue according to her needs. Ultrasound, including estimation of weight and amniotic fluid index, was performed every 4 weeks, beginning from 28 gestational weeks. If treatment with diet and physical activities was insufficient, insulin treatment was added and the woman terminated her contact with the primary antenatal clinic. Her antenatal care, including the GDM treatment, was taken over by a multidisciplinary team consisting of a diabetes midwife, a diabetologist, and an obstetrician specially trained in diabetology, at the hospital s antenatal specialist outpatient department. Mealtime insulin (human insulin or analogue) was initiated at postprandial glycemic increases of /2 mmol/l (target value B/8 mmol/l), and bedtime insulin (Neutral Protamine Hagedon; NPH) was prescribed if fasting glucose levels were /6 mmol/l. If there were problems normalising preprandial blood glucose levels, treatment with NPH insulin was also given in the morning. At term, the woman saw the obstetrician in order to review the pregnancy and plan for delivery. The first choice was spontaneous vaginal delivery at a special high-risk delivery ward. After birth, roomingin was the norm and early breastfeeding/supplementary formula, and strict blood glucose monitoring of the neonate were routine. The woman returned to

3 Gestational diabetes; antenatal teamwork 285 her ordinary diet and checked blood glucose levels after at least 24 h to ensure a normal range. The study population consisted of all women with GDM identified and treated according to the routines described above during the period July to June , who gave birth at SUH. Among the included women, 15 gave birth twice during the study period. (n/607) were treated with diet only and 15.6% (n / 112) were also treated with insulin. The mean gestational age at GDM diagnosis was 27 weeks and 5 days, 59.8% (n/430) were diagnosed as GDMmild and 40.2% (n / 289) as GDM-severe. Significantly more women, 26.0% (n / 75), with GDMsevere needed insulin treatment compared to 8.6% (n / 37) in the GDM-mild (p B/ 0.001). Analysis Maternal, delivery and neonatal outcomes in the study were compared with a control consisting of all other women (without signs of GDM) giving birth during the same period at the same hospital (SUH controls). Data was available from hospital records and the Swedish Medical Birth Register [MBR] (12). The European Pregnancy Study Group (10) has suggested a 2-h OGTT ]/9.0 mmol/l (165 mg/dl) as the diagnostic criterion for GDM. We, therefore, stratified the GDM subjects into two subs for analysis, according to the blood glucose level at diagnosis, ie, (1) GDM-mild: fasting glucose B/6.1 mmol/l (111 mg/dl) and 2-h OGTT mmol/ L ( mg/dl), and (2) GDM-severe: RCG ]/ 11.1 mmol/l (203 mg/dl), or fasting glucose 6.1 / mmol/l (111 mg/dl) preceding OGTT, or 2-h OGTT ]/9 mmol/l (165 mg/dl). For the sake of completeness, we also present the GDM-composite. Statistical analyses were performed using the statistical software package (SPSS). Descriptive statistics were performed for all variables. The x 2 - test (Pearson x 2 ), odds ratio with 95% confidence interval were applied for analyse categorical variables. Analysis of variance [ANOVA] was used for continuous variables, as well as the t-test when assumptions of normality were met. Otherwise, the Wilcoxon test was performed. The Bonferroni adjustment procedure was used to control for multiple testing. p-values B/0.05 were regarded as significant. Body mass index [BMI] was calculated from height and weight at the first visit to the antenatal clinic. Results Prevalence and week for diagnosis During the observational period, 31,542 deliveries, resulting in 32,176 children, took place at SUH. GDM was diagnosed in 719 women (699 singleton mothers) resulting in 741 children, corresponding to 2.28% of the whole population. Of these, 84.4% Maternal characteristics and delivery outcome Maternal characteristics and delivery outcomes are presented in Tables I IV. Many of the women with GDM were of non-nordic origin (44.5%, n / 320), and significantly more women in this had GDM-severe, 49.1% (n / 157) compared to 33.1% (n/132) (pb/0.001) among the Nordic women. No information concerning ethnic origin in the SUH control was available, but 25.3% of women of fertile age (age 1545) were of non-nordic origin in the city of Göteborg (the main geographic area of the study) at the time (Personal communication, Marianne Tedeholm, Göteborg Statistics). Women with GDM were older and of higher parity than those in the. Obesity was more frequent in the GDM-mild and GDM-severe s than in the control (18.5 and 29.6% versus 8.3%). The need for insulin treatment increased with increasing BMI. Among women with normal weight (BMI B/25 kg/m 2 ), 9.6% (n/33) required insulin, compared to 31.9% (n / 52) in the obese (p B/ 0.001). Pre-eclampsia, induction of labour and elective caesarean section in both s was more frequent than in the control. Neonatal characteristics Neonatal characteristics are presented in Tables V and VI. There was a significant difference in mean birth weight when dividing in weight classes based on growth standards for a Swedish population (13), including small for gestational age [SGA] defined as B/ 2 SD and large for gestational age [LGA] defined as /2 SD. Both GDM s had lower frequency of average weight for gestational age [AGA]. The LGA frequency was 10.5% in the GDM-severe, and 7.1% in the GDM-composite, compared to 3.2% in the control. There were significantly more infants with Apgar scores B/7 at 5 min in the GDM-severe than in the control (2.7 versus 0.8%, OR: 3.25) and well as in the GDM-composite (1.8 versus 0.8%, OR: 2.10). There were two stillbirths in the GDM-mild (chromosome fault and abruption of placenta), and none in the GDM-severe

4 286 M. Berg et al. Table I. Maternal characteristics according to glucose level at diagnosis. GDM-mild (n/ 430) GDM-severe (n/ 289) (n/ 30823) $ p-value GDM-mild/SUHcontrol GDM-severe/SUHcontrol B/0.001 NA NA B/0.001 NA NA Maternal age (years) 31.89/ / /5.0 (n/30793) $$ BMI* (kg/m 2 ) 26.79/ / /4.0 (n/19758) $$ BMI B/25 kg/m (217) 43.6 (125) 67.7 (13384) (n/ 19758) B/ (0.40, 0.59) 0.36 (0.29, 0.46) 255/BMIB/30 kg/m (126) 26.8 (77) 24.0 (4742) (n/ 19758) (1.1, 1.62) 1.15 (0.89, 1.50) BMI / 30 kg/m (78) 29.6 (85) 8.3 (1632) (n/ 19758) B/ (1.92, 3.16) 4.63 (3.58, 6.00) Parity** (No.) 2.09/ / /0.9 B/ NA NA (n/31291) $$ Smoking* 3.8 (16) 8.2 (23) 10.6 (3104) B/ (n/ 419) (n/ 281) (n/29159) $$ (0.20, 0.55) (0.49, 1.15) Pre-pregnancy 0.5 (2) 0.7 (2) 0.3 (99) NS hypertension (n/31514) $$ (0.37, 6.03) (0.54, 9.01) Pregnancy-induced 1.9 (8) 1.4 (4) 0.5 (169) hypertension (n/31514) $$ (1.72, 7.19) (0.96, 7.06) Pre-eclampsia 5.1 (22) 6.6 (19) 2.9 (920) (n/31514) $$ B/ (1.16, 2.77) 2.34 (1.46, 3.74) $ The GDM is excluded except for parity, pre-pregnancy hypertension, pre-pregnancy hypertension and pre-eclampsia. $$ From the MBR. Personal communication, Frida Lundblad, MBR, September *BMI and smoking at first visit at the antenatal clinic. BMI B/25 kg/m 2 /normal weight, 255/BMIB/30 kg/m 2 /overweight, BMI ]/30 kg/ m 2 /obesity. **Parity: after the present delivery. Data are given as mean9/sd, or rate% (n). Significance test p/ B/0.05 (x 2 or variance test) for all three s., compared to 157 among the controls. Unfortunately, data on neonatal complications such as jaundice and hypoglycemia, was not available due to insufficient hospital records. Discussion In this observational retrospective study, it was concluded that the pregnancy outcome of women with GDM differs from that of a control of women from the same unit. This is in agreement with other studies in which GDM women, despite various treatments, are more likely to suffer maternal and fetal complications (3,14,15). Our choosing to analyse the results in two subs, GDM-mild and GDM-severe, seems appropriate as earlier studies (14,16) suggest that women with 2-h OGTT ]/ mmol/l ( mg/dl) (GDM-mild) should not be the objects of intervention. More knowledge is needed concerning the glucose level at which metabolic disorders affect mother and child, knowledge which will hopefully evolve from the Hyperglycemia and Adverse Pregnancy Outcome study (17). One of the most important outcomes in our study is the low frequency of LGA and macrosomia. It is considerable lower compared to data 10 years ago, when we used another model of treatment (unpublished data). First, we compare our result with studies on untreated GDM. In Swedish studies by Nord et al. (16) and Östlund et al. (18), using the same criterion for LGA (/2 SD), the frequency of LGA infants was 10.8% in a with 2-h OGTT ]/ ( mg/dl) (16), and 25% in a with 2-h OGTT ]/ ( mg/ dl) (18). In our study, the frequency of LGA neonates was 4.8 and 10.5% in the with 2-h OGTT ]/ mmol/l (GDM-mild), and ]/9.0 (GDM-severe), respectively. In the composite GDM-, the frequency was 7.1%. As the definition of LGA varies globally, frequency of macrosomia may be a useful variable when comparing different studies. In a large Danish cohort study by Jensen et al. (14), 33.9% of the infants born to the of women with 2-h OGTT ]/ ( mg/dl) and with no intervention had birth weights over 4000 g. This can be compared to 14.3% for the corresponding of women who were the objects of active intervention in our study (GDM-mild). In the Swedish study by Östlund et al. (18), 33% had macrosomia compared to 21.8% in our corresponding (GDM-severe).

5 Gestational diabetes; antenatal teamwork 287 Table II. Delivery outcomes according to glucose level at diagnosis. GDM-mild (n/ 430) GDM-severe (n/ 289) (n/ 30,823) p-value GDM-mild/ GDM-severe/ Delivery gestational age (weeks) 39.49/ / /2.2 (n/ 28,849) Premature delivery 8.4 (36) 6.9 (20) 8.0 (2315) B/37 week (n/ 28,847) Induction of labour 16.7 (72) 17.0 (49) 10.7 (3297) Spontaneous delivery 70.2 (302) 65.7 (190) 81.0 (24,963) Vaginal delivery, 77.7 (334) 73.7 (213) 79.2 (24,418) non-instrumental (n/ 30, 820) Instrumental vaginal 6.5 (28) 5.9 (17) 5.5 (1681) delivery Emergency caesarean 7.0 (30) 8.3 (24) 8.6 (2664) section Elective caesarean 8.8 (38) 12.1 (35) 6.5 (1993) section B/ NA NA NS 1.05 (0.74, 1.48) B/ (1.30, 2.17) B/ (0.45, 0.68) (0.73, 1.15) NS 1.21 (0.82, 1.78) NS 0.79 (0.55, 1.15) B/ (1.00, 1.96) 0.85 (0.54, 1.35) 1.70 (1.25, 2.32) 0.45 (0.35, 0.58) 0.73 (0.57, 0.96) 1.08 (0.66, 1.77) 0.96 (0.63, 1.46) 1.99 (1.40, 2.85) Data are given as mean9/sd, or rate% (n). Significance test p/ B/0.05 (x 2 or variance test) for all three s. This comparison indicates that treatment of GDM reduces macrosomia/lga, as has been shown in other studies. Furthermore, we have compared our results with studies on treated GDM. In a large casecontrol study (19), the frequency of LGA and macrosomia and composite neonatal outcome in treated cases of GDM approached that in the of non-diabetic subjects, in contrast to untreated cases. The frequency of macrosomia was 7% in the treated, compared to 17% in the untreated (19). It is difficult to compare this with the results of our study, as the study s differ. The criteria for diagnosis of GDM differ and there are considerable differences in ethnicity; 86% of the subjects in the above-mentioned study were Hispanic. A randomised, multi-centre, study with similar inclusion criteria as in our GDM-composite (2-h OGTT mmol; mg/dl) has recently been presented (20). The frequency of macrosomia in the treatment was 10%, compared with 17.3% in our GDM-composite. The difference may be due to diverse study populations, eg, 19% of Asian origin compared to 44.5% of non-nordic origin in our study. Moreover, Table III. Maternal characteristics in GDM-composite versus. GDM-composite (n/ 719) (9802) (n/ 30,823) $ p-value GDM-composite / Maternal age (years) 31.99/ /5.0 (n/ 30,793) $$ NA BMI* (kg/m 2 ) 27.19/ /4.0 (n/ 19,758) $$ NA BMI B/25 kg/m (342) 67.7 (13,384) (n/ 19,758) (0.37, 0.50) 255/BMIB/30 kg/m (203) 24.0 (4742) (n/ 19,758) (1.06, 1.47) BMI ]/30 kg/m 2 23 (163) 8.3 (1632) (n/ 19,758) (2.72, 3.91) Parity** (No.) 2.19/ /0.9 (n/ 31,291) $$ NA Smoking* 5.6 (39) (n/700) 10.6 (3104) (n/ 29,159) $$ (0.35, 0.67) Pre-pregnancy hypertension 0.6 (4) 0.3 (99) (n/ 31,514) $$ NS 1.78 (0.65, 4.84) Pregnancy-induced hypertension 1.7 (12) 0.5 (169) (n/ 31,514) $$ (1.75, 5.68) Pre-eclampsia 5.7 (41) 2.9 (920) (n/ 31,514) $$ (1.46, 2.78) $ The GDM is excluded except for parity, pre-pregnancy hypertension, pre-pregnancy hypertension and pre-eclampsia. *BMI and smoking at first visit at the antenatal clinic. BMI B/25 kg/m 2 /normal weight, 255/BMIB/30 kg/m 2 /overweight, BMI ]/30 kg/ m 2 /obesity. **Parity: after the present delivery. $$ From the MBR. Personal communication, Frida Lundblad, MBR, September Data are given as mean9/sd or rate% (n). Significance test p/ B/0.05 (x 2 or t-test).

6 288 M. Berg et al. Table IV. Delivery outcomes in GDM-composite versus. GDM composite (n/ 719) (n/ 30,823) p-value GDM composite / Delivery gestational age (weeks) 39.39/ /2.2 (n/ 28,849) NA Premature delivery B/37 week 7.8 (56) 8.0 (2315) (n/ 28,847) NS 0.97 (0.74, 1.28) Induction of labour 16.8 (121) 10.7 (3297) (1.39, 2.06) Spontaneous delivery 68.4 (492) 81.0 (24,963) (0.43, 0.60) Vaginal delivery, non-instrumental 76.1 (547) 79.2 (24,418) (0.70, 0.99) Instrumental vaginal delivery 6.3 (45) 5.5 (1681) NS 1.16 (0.85, 1.57) Emergency caesarean section 7.5 (54) 8.6 (2664) NS 0.86 (0.65, 1.14) Elective caesarean section 10.2 (73) 6.5 (1993) (1.28, 2.09) Data are given as mean9/sd or rate% (n). Significance test p/ B/0.05 (x 2 or t-test). different frequencies of insulin treatment (20 versus 15.6%) cannot be ruled out as an explanation for the lower macrosomia frequency in their study. We found a significantly increased rate of induction of labour in the GDM-mild and -severe s compared to the controls (16.7 and 17.0%, respectively, versus 10.7%) (Table II). The rates of elective caesarean section were also increased in both s (8.8 and 12.1%, respectively, versus 6.5%). One may speculate that the obstetrician s knowledge of GDM diagnosis makes him/her more inclined to intervene. However, the total caesarean rate, including emergency and elective procedures, of 17.6% for the composite GDM and 15.1% for the SUH control is much lower than that generally described (18,20), and points to the fact that Sweden, in an international perspective, still has a comparably low caesarean section rate. Different models of treatment of GDM are proposed in the literature. Bonomo et al. (21) has shown, in a randomised trial study, that flexible ultrasound-based approach to the treatment of GDM is more effective than conventional management focusing glycemia. They used fetal abdominal circumference, showing indirect evidence of fetal hyperinsulinisation, as an indication for the use of insulin treatment. However, Schaeffer et al. (22), in their randomised trial study, has found that GDM management, based on strict maternal glycemia criteria alone, provides outcomes equivalent to Table V. Neonatal characteristics, according to glucose level at diagnosis. Mode of delivery GDM-mild (n/ 443) GDM-severe (n/ 298) (n/ 31,435) p -Value GDM-mild/ GDMsevere/ Birth weight (g) / / /619.7 (n/ 28,959) Birth weight ]/4000 g 14.3 (62) 21.8 (64)* 16.9 (4812) (n/ 28,958) Birth weight ]/4500 g 2.7 (12) 6.4 (19)* 3.2 (922) (n/ 28,958) Birth weight ]/5000 g 0.5 (2) 0.3 (1) 0.4 (121) (n/ 28,958) LGA //2 SD 4.8 (21) 10.5 (31)* 3.2 (900) (n/ 28,535) SGA B/ 2 SD 5.3 (23) 3.7 (11) 3.5 (1008) (n/ 28,535) AGA ]/ 2SD, 5//2 SD 89.9 (391)* 85.7 (252)* 93.3 (26627) (n/ 28,535) Apgar score B/4 at 5 min 0.9 (4)* 0.7 (2) 0.3 (93) (n/ 31,435) Apgar score B/7 at 5 min 1.1 (5) 2.7 (8)* 0.8 (265) (n/ 31,435) $ NA NA (0.62, 1.07) (0.48, 1.51) NS 1.08 (0.27, 4.39) B/ (0.98, 2.38) NS 1.50 (0,98, 2,29) B/ (0.40, 0.72) (1.13, 8.40) (0.55, 3.27) 1.37 (1.04, 1.81) 2.07 (1.30, 3.31) 0.80 (0.11, 5.76) 3.57 (2.44, 5.20) 1,05 (0,57, 1,92) 0.39 (0.29, 0.54) 2.28 (0.56, 9.30) 3.25 (1.59, 6.63) $ The adjusted Bonferroni p-value is not significant. *Statistical significant difference comparing sub- versus. Data are given as mean9/sd, or rate% (n). Significance test p/ B/0.05 (x 2 or variance test) for all three s.

7 Table VI. Neonatal characteristics in the GDM composite versus. Gestational diabetes; antenatal teamwork 289 Mode of delivery GDM-composite (98 02) (n/ 741) (n/ 31,435) p-value GDM-composite / Birth weight (g) / /619.7 (n/ 28,959) NS NA Birth weight ]/4000 g 17.3 (126) 16.9 (4812) (n/ 28,958) NS (0.847, 1.248) Birth weight ]/4500g 4.3 (31) 3.2 (922) (n/ 28,958) NS (0.921, 1.914) Birth weight ]/5000 g 0.4 (3) 0.4 (121) (n/ 28,958) NS (0.307, 3.053) LGA //2 SD 7.1 (52) 3.2 (900) (n/ 28,535) (1.735, 3.096) SGA B/ 2 SD 4.6 (34) 3.5 (1008) (n/ 28,535) NS (0.926, 1.863) AGA ]/ 2SD, 5//2 SD 88.2 (643) 93.3 (26627) (n/ 28,535) (0.378, 0.584) Apgar score B/4 at 5 min 0.8 (6) 0.3 (93) (n/ 31,435) (1.201, 6.302) Apgar score B/7 at 5 min 1.8 (13) 0.8 (265) (n/ 31,435) (1.198, 3.683) Data are given as mean9/sd, or rate;% (n). Significance test p/ B/0.05 (x 2 or t -test). management based on fetal growth combined with high glycemic criteria. The treatment in our study was based on strict maternal glycemic criteria, but also included a high degree of women s participation in and responsibility for their own treatment. This increased their consciousness of relationship between lifestyle (diet and physical activities) and blood glucose level. They were also informed about the increased risk for future type 2 diabetes and were encouraged to continue the healthy lifestyle and strive for normal weight as a tool to prevent type 2 diabetes. Our study included early universal screening for GDM, which is found beneficial as it is associated with a decrease in adverse fetal outcomes (23,24). As a consequence of early screening and diagnosis, a larger proportion of pregnant women in our study started their treatment early compared with other studies. This provided more time for intervention before term, in contrast to a screening procedure and intervention late in pregnancy. It has been shown that early diagnosis of GDM is a predictor of adverse maternal and neonatal outcome (23,25), and that early intervention to improve glucose homeostasis may prevent some complications commonly related to pregestational diabetes (23). It is well-known that GDM covaries with higher BMI. The rising incidence of obesity in society is apparent and frequently discussed and, furthermore, one would expect a rising incidence of GDM in the population. Moreover, the need for insulin treatment was found to be much higher in obese patients in our study. It has been suggested that intense insulin treatment improves outcome in this (26,27). Our impression is that early screening, early intervention and out-patient treatment by a multidisciplinary team, including specially trained diabetes midwives and a participative woman, is highly beneficial. This model of care yields low rates of excessive fetal growth, instrumental vaginal delivery and caesarean section, comparable to those found in other studies. Acknowledgements The study was supported by grants from Swedish Diabetes Association. References 1..Östlund I, Haglund B, Hanson U. Gestational diabetes and preeclampsia. Eur J Obstet Reprod Biol. 2004;/15:/ Pollack RN, Buchman AS, Yaffe H, Divon MY. Obstetrical brachial palsy: pathogenesis, risk factors and prevention. Clin Obstet Gynecol. 2000;/43:/ Persson B, Hanson U. Neonatal morbidities in gestational diabetes mellitus. Diabetes Care. 21 Suppl. 1998;/2:/B Hod M, Rabinerson D, Peled Y. Gestational diabetes mellitus: is it a clinical entity? Diabetes Rev. 1995;/3: / Stenninger E, Schollin J, Aman J. Neonatal macrosomia and hypoglycaemia in children of mothers with insulin-treated gestational diabetes mellitus. Acta Paediatr Scand. 1991;/80:/ Damm P, Kühl C, Bertelsen A, Molsted-Pedersen L. Predictive factors for the development of diabetes mellitus in women with previous gestational diabetes mellitus. Am J Obstet Gynecol. 1992;/167:/ Åberg A, Rydhström H, Fried A. Impaired glucose tolerance associated with adverse pregnancy outcome: a populationbased study in southern Sweden. Am J Obstet Gynecol. 2001;/ 184:/ WHO Expert Committee on Diabetes Mellitus. Technical report series. Report No 1980: 646. Geneva, Switzerland: World Health Organization, Östlund I, Hansson U. Repeated random blood glucose measurements as universal screening test for gestational diabetes mellitus. Acta Obstet Gynecol Scand. 2004;/83:/ 4651.

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