help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2007-2301
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kautzky-Willer, A.
Right arrow Articles by Lechleitner, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kautzky-Willer, A.
Right arrow Articles by Lechleitner, M.
Related Collections
Right arrow Pediatric Endocrinology
Right arrow Diabetes and Insulin
Right arrow Female Endocrinology
The Journal of Clinical Endocrinology & Metabolism Vol. 93, No. 5 1689-1695
Copyright © 2008 by The Endocrine Society

The Impact of Risk Factors and More Stringent Diagnostic Criteria of Gestational Diabetes on Outcomes in Central European Women

A. Kautzky-Willer, D. Bancher-Todesca, R. Weitgasser, T. Prikoszovich, H. Steiner, N. Shnawa, G. Schernthaner, R. Birnbacher, B. Schneider, Ch. Marth, M. Roden and M. Lechleitner

Departments of Endocrinology and Metabolism (A.K.-W., T.P.), Obstetrics and Gynecology (D.B.-T.), Neonatology (R.B.), and Statistics (B.S.), Medical University of Vienna, Vienna, Austria; First Department of Medicine (R.W.) and Department of Obstetrics and Gynecology (H.S.), Paracelsus Private Medical University Salzburg, Salzburg, Austria; Department of Internal Medicine I (N.S., G.S.), Rudolfstiftung Vienna, Vienna, Austria; First Department of Medicine (M.R.), Hanusch-Krankenhaus, Vienna, Austria; and Department of Internal Medicine (C.M., M.L.), University of Innsbruck, Innsbruck, Austria, for The Austrian Gestational Diabetes Study Group

Address all correspondence and requests for reprints to: Alexandra Kautzky-Willer, M.D., Associate Professor of Medicine, Department of Internal Medicine III, Division of Endocrinology and Metabolism, Medical University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna; Austria. E-mail: alexandra.kautzky-willer{at}meduniwien.ac.at.


    Abstract
 Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Objectives: In the face of the ongoing discussion on the criteria for the diagnosis of gestational diabetes (GDM), we aimed to examine whether the criteria of the Fourth International Workshop Conference of GDM (WC) select women and children at risk better than the World Health Organization (WHO) criteria.

Design and Setting: This was a prospective longitudinal open study in five tertiary care centers in Austria.

Patients and Outcome Measures: The impact of risk factors, different thresholds (WC vs. WHO), and numbers of abnormal glucose values (WC) during the 2-h, 75-g oral glucose tolerance test on fetal/neonatal complications and maternal postpartum glucose tolerance was studied in 1466 pregnant women. Women were treated if at least one value according to the WC (GDM-WC1) was met or exceeded.

Results: Forty-six percent of all women had GDM-WC1, whereas 29% had GDM-WHO, and 21% of all women had two or three abnormal values according to WC criteria (GDM-WC2). Eighty-five percent of the GDM-WHO were also identified by GDM-WC1. Previous GDM [odds ratio (OR) 2.9], glucosuria (OR 2.4), preconceptual overweight/obesity (OR 2.3), age 30 yr or older (OR 1.9), and large-for-gestational age (LGA) fetus (OR 1.8) were the best independent predictors of the occurrence of GDM. Previous GDM (OR 4.4) and overweight/obesity (OR 4.0) also independently predicted diabetes postpartum. GDM-WC1 had a higher rate of obstetrical complications (LGA neonates, neonatal hypoglycemia, cesarean sections; P < 0.001) and impaired postpartum glucose tolerance (P < 0.0001) than GDM-WHO.

Conclusion: These results suggest the use of more stringent WC criteria for the diagnosis of GDM with the initiation of therapy in case of one fasting or stimulated abnormal glucose value because these criteria detected more LGA neonates with hypoglycemia and mothers with impaired postpartum glucose metabolism than the WHO criteria.


    Introduction
 Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Considerable controversy exists regarding the thresholds and the numbers of the plasma glucose values considered for diagnosis of gestational diabetes (GDM) during oral glucose tolerance testing (1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11). In addition, it is not known whether general screening for GDM in all pregnancies is preferable to selective screening of groups at increased risk for glucose intolerance. GDM is the most frequent single complication of pregnancy, causing increased fetal mortality and perinatal morbidity (12, 13, 14), leaving both mother and child at an increased risk to develop diabetes mellitus and/or obesity in later life (15, 16, 17, 18). On the other hand, recent studies showed that strict metabolic control is able to reduce perinatal complications (19, 20).

The 75-g, 2-h oral glucose tolerance test (oGTT) is widely accepted for the diagnosis of large for gestational age (LGA) in Central Europe, and the diagnostic criteria are either recommended by the World Health Organization (WHO) (2 h > 140 mg/dl) or following the Fourth International Workshop Conference on Gestational Diabetes (WC) (modified Carpenter/Coustan criteria). The latter are also supported by the American Diabetes Association as an alternative to the 100-g oGTT (8, 10) if at least two values meet or exceed the glucose thresholds (GDM-WC2: fasting 95 or greater; 1 h, 180 or greater; 2 h, 155 mg/dl or greater). The general use of 75-g oGTTs in pregnant and nonpregnant women seems to be preferable for simplicity and better comparison in the pre- and/or postpregnant state. However, because maternal and fetal morbidity is even increased in women with borderline GDM (21, 22, 23, 24), the diagnostic criteria during pregnancy need to be lowered, compared with those for impaired glucose tolerance in the nonpregnant state. To aim at an ideal test for identification of both children at risk for macrosomia and mothers at risk for diabetes at follow-up, the German and Austrian Diabetes Association adopted the criteria of the WC for the 75-g, 2-h oGTT (fasting 95 or greater; 1 h, 180 or greater; 2 h, 155 mg/dl or greater) with the exception that one abnormal plasma glucose value would be sufficient for diagnosis of GDM impaired glucose tolerance (IGT) (GDM-WC1) and subsequent treatment (25).

Thus, the primary objectives of our observational prospective multicenter national study were to evaluate the diagnostic efficacy of the different criteria (WC vs. WHO) to detect: 1) LGA and neonatal hypoglycemia; 2) impaired maternal glucose metabolism early after delivery; and 3) to compare the relationship of the three glucose values (oGTT) with fetal and maternal outcome. The secondary objective was to evaluate the predictive value of risk factors for fetal growth as well as the occurrence of GDM, the need of subsequent insulin therapy, and postpartum glucose tolerance in these women.

We hypothesized that the GDM-WC1 criteria would detect more LGA newborns and better identify women with impaired glucose metabolism early postpartum. In addition, we hypothesized that each glucose value (oGTT) independently relates to maternal and fetal/neonatal complications.


    Subjects and Methods
 Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
This prospective open multicenter study was conducted in five hospitals with suitable infrastructure including an intensive care unit for neonates in different parts of Austria (Vienna, Salzburg, Steyr, and Innsbruck) from 2001 until 2004. All women gave informed consent before participation in this study. The study was performed according to the most recent version of the Helsinki declaration.

Risk assessment

At an initial contact, which occurred between 11 and 13 wk gestation, a broad risk assessment of conventional and nonconventional risk factors for GDM was carried out, and each subject at risk was scheduled for a full diagnostic oGTT (75 g, 2 h) between 24 and 28 gestational weeks. Conventional risk factors were history of GDM or history of prediabetes (26) [IGT or impaired fasting glucose (IFG)]; intrauterine fetal death, birth weight of previous child greater than 4000 g, malformation, or previous recurrent abortion (>3 in previous pregnancies); ethnic group at high risk for type 2 diabetes (Hispanics, African, Asian, or Indian origin); moderate overweight or obesity before [body mass index (BMI) ≥ 27 kg/m2] or during pregnancy (weight gain ≥ 10 kg in first trimester); age 30 yr or older; history of first- and second-degree relative with type 2 diabetes; clinical markers: glucosuria and LGA fetus (ultrasound: abdominal circumference > 90th percentile of reference group) (27); other risk factors: hypertension (≥140/90 mm Hg), preconceptual dyslipidemia (triglycerides > 150 mg/dl or cholesterol > 200 mg/dl); and previous preterm delivery (<37 gestational wk). Another group of women without any of these risk factors, but referred to the hospitals for booking, were also tested between 24 and 28 gestational weeks by oGTT to serve as reference group (n = 171). Women presenting with type 1 diabetes, women screened positive for GAD autoantibodies, and women with known pregestational type 1 or type 2 diabetes were excluded from this study.

Children with a birth weight greater than the 90th percentile on the basis of actual local growth standard curves were defined as LGA newborns [analysis of the newborns from 1999 to 2004 in Austria (2007); http://dx.doi.org/10.1007/s00112–007-1545–2].

Diagnostic criteria and oGTT

All women were on an isocaloric diet containing 200 g of carbohydrates per day at least 3 d before the oGTT. oGTTs were performed after a 10- to 12-h overnight fasting period. All women ingested 75 g of glucose solution within 2 min, and venous plasma samples were collected for glucose measurements at fasting and 1 and 2 h after glucose loading. Glucose measurements were done on a Hitachi modular system (Hitachi Ltd., Tokyo, Japan) by a hexokinase method (Roche Diagnostics, Basel, Switzerland). Gestational diabetes was diagnosed according to the criteria of the WC adapted by the German and Austrian Diabetes Association, which suggest treatment in women in case of at least one (GDM-WC1) abnormal value (oGTT, 75 g; plasma glucose fasting ≥ 95, 1 h ≥ 180, 2 h ≥ 155 mg/dl) (25). The subgroup of women with two or more abnormal values are defined as GDM-WC2, whereas women with diagnosis of GDM according to WHO criteria are called GDM-WHO. GDM-WC1 were referred to dietary counseling (three main meals and three snacks corresponding to 25–30 kcal/kg per day; in case of BMI greater than 30 kg/m2 30% caloric restriction was recommended) and advised to measure blood glucose levels four times daily until delivery. If self-measured blood glucose levels exceeded the treatment targets (5.0 mmol/liter at fasting and 7.2 mmol/liter 1 h postprandially), insulin therapy was started and the insulin dose was adjusted accordingly (see Table 4Go). In GDM women mean fasting and postprandial glucose concentrations were within the target range (data not shown). All GDM-WC1 were examined every 2–3 wk and, if necessary, in weekly intervals.


View this table:
[in this window]
[in a new window]

 
TABLE 4. Obstetric characteristics of women with GDM-WC1 (one or more abnormal values; n = 672), those with GDM-WC2 (two or more abnormal values; n = 309), and those with GDM according to WHO criteria (GDM-WHO; n = 428)

 
All women with impaired glucose tolerance during pregnancy (GDM-WC1 or GDM-WHO) were invited to a follow-up investigation 6–12 wk after delivery for reclassification (75 g, 2 h oGTT/WHO criteria), which is performed in 55% of the population.

Statistical analysis

All data are expressed as means ± SEM. Comparisons between groups were performed using ANOVA for parameters with means following normal distribution. Nonparametric Kruskal Wallis test was carried out if appropriate. For multiple group comparison, the Tukey post hoc test was applied. Predictors for the occurrence of gestational diabetes were obtained by stepwise logistic regression analysis. Odds ratios are reported including 95% confidence intervals (CIs). To compare the different oGTT criteria the McNemar test was applied. For all analyses the SAS Package 9.1.3 (Cary, NC) was used.


    Results
 Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Diagnostic criteria and oGTT

Twenty-one percent of the 1466 pregnant women had GDM-WC2, whereas 46% had GDM-WC1. Twenty-nine percent would have been diagnosed by WHO criteria and 85% of these GDM-WHO women were also identified as GDM-WC1.

Of note, 31% of all women had an elevated 1-h value, 26% had an increased fasting value, and only 18% a 2-h glucose value above normal range.

There was no significant difference in the relative proportion of women with impaired glucose tolerance within the various centers. In the reference group with no apparent risk factors, 9% had GDM-WC2, 25% GDM-WC1, and 15% would have been diagnosed as GDM-WHO.

Studying the relationship between fasting, the 1- and the 2-h glucose value during the oGTT as well as fetal and maternal outcome, it turned out that the fasting glucose was the best predictor for birth weight [P < 0.003, odds ratio (OR) 1.01 (1.004–1.018)], LGA newborns [P < 0.002, OR 1.023 (1.01–1.04)] as well as impaired glucose metabolism [P < 0.0001; OR 1.3 (1.2–1.4)] or overt diabetes [P < 0.0001; OR 1.16 (1.1–1.2)] early after delivery. On the other hand, 1 h glucose best predicted neonatal hypoglycemia [P < 0.003, OR 1.009 (1.003–1.014)] and 2 h glucose the rate of cesarean sections [P < 0.0001, OR 1.007 (1.004–1.01)] and neonates with a birth weight of more than 4500 g [P < 0.0001, OR 1.018 (1.009–1.27)].

Risk factors

Characteristics (Table 1Go) GDM-WC1 women featured the phenotype of the metabolic syndrome. Ninety-two percent of the women were Caucasians and 8% were of Asian origin.


View this table:
[in this window]
[in a new window]

 
TABLE 1. Clinical characteristics of women with GDM-WC1 (n = 672; one or more abnormal values) and those with NGT during pregnancy (n = 794)

 
There was the same percentage of women (13%) with a diabetic father or a diabetic mother, which was higher than for the women with normal glucose tolerance (NGT: 8.5% for father, P < 0.002, and 7.8% for mother, P < 0.0009). More GDM-WC1 women had a sibling with type 2 diabetes (2.5%), compared with those with NGT (0.8%, P < 0.01).

Logistic regression analysis revealed that maternal type 2 diabetes was the best independent predictor [OR 1.78 (1.26–2.51), P < 0.0005]. Family history in total explained only 2.5% of the occurrence of GDM-WC1.

Distribution and predictive value of risk factors (Table 2Go) Twenty-four percent of the pregnant women had only one risk factor; the most common risk factor was age above 30 yr.


View this table:
[in this window]
[in a new window]

 
TABLE 2. Distribution of risk factors and their specificity and sensitivity to detect GDM-WC1 (n = 672) (one or more abnormal values) including the subgroups with one (n = 363), two (n = 208), or three (n = 101) abnormal glucose values, compared with NGT (n = 794)

 
We calculated the detection rate for the BMI cutoff value of 27 kg/m2, which was used in our study as risk factor for overweight/obese GDM, as well as the BMI cutoff value of 25 kg/m2, which is used to define overweight. Indeed the relationship between sensitivity and specificity seems to favor the cutoff value of 27 kg/m2 in this study (BMI 25 kg/m2: sensitivity/specificity: 0.60/0.53; BMI 27 kg/m2: sensitivity/specificity: 0.54/0.70). Moreover, using the specific set of risk factors no GDM woman without any of these risk factors would have been detected by lowering the BMI cutoff value to 25 kg/m2.

Logistic regression analysis revealed that the risk factors previous GDM [2.32 (1.8–3.0), P < 0.0001], glucosuria [2.42 (1.8–3.2), P < 0.0001], overweight/obesity [2.92 (1.8–4.7), P < 0.0001], age 30 yr or older [1.85 (1.4–2.3), P < 0.0001], LGA fetus [1.8 (1.1–2.9), P < 0.01], and ethnicity [1.6 (1.2–2.2), P < 0.005] independently predicted the occurrence of GDM-WC1.

The best independent predictors for subsequent need of insulin therapy were the risk factors previous GDM (OR 4.1; CI 2.6–6.5), previous IGT/IFG (OR 6.0; CI 2.5–14.6), glucosuria (OR 2.7; CI 2.0–3.7), ethnicity (OR 2.4; CI 1.7–3.5), preconceptional overweight/obesity (OR 1.9; CI 1.4–2.6), and age (OR 1.7; CI 1.3–2.3) (all P < 0.0001).

Obstetric characteristics (Table 3Go)

In GDM patients with three abnormal glucose values, the highest rate of obstetric complications was observed, but even the group with one abnormal glucose value had a higher rate of neonatal hypoglycemia than women with NGT. The rate of small-for-gestational age neonates did not differ between groups (12.3 vs. 11.3%, GDM-WC1 vs. NGT, respectively). Induction of labor was more frequent in GDM, compared with NGT (22 vs. 15%, P < 0.01).


View this table:
[in this window]
[in a new window]

 
TABLE 3. Obstetric characteristics of GDM-WC1 (one or more abnormal values; n = 672), including the subgroups with one (n = 363), two (n = 208), or three (n = 101) abnormal glucose values, compared with NGT (n = 794)

 
A birth weight of 4.5 kg or greater was independently predicted by the risk factors previous child with a birth weight of 4.5 kg or greater [OR 7.8 (CI 3.2–18.8), P < 0.001], previous GDM [OR 4.0 (1.5–11.0), P < 0.04] or weight gain of 10 kg in the first trimester [OR 3.2 (CI 1.1–9.2), P < 0.03]. When comparing these outcome variables between the different diagnostic criteria (oGTT), it became evident that if two or more abnormal glucose values were required or if the WHO criteria were used, only a quarter or, at best, half of the neonates with complications would be identified (Table 4Go). Dividing the groups with complications according to the presence of risk factors revealed that worse obstetric outcome occurred in the women with risk factors in both the GDM-WC1 (97%: neonatal hypoglycemia, cesarean section or LGA neonates including those with a birth weight of 4.5 kg or greater by 100%) and the NGT (87%: cesarean section; 89%: LGA neonates and 95%: neonatal hypoglycemia) women. Less than 5% of the GDM-WC1 without risk factors had such complications.

Postpartum glucose tolerance (Table 5Go)

Mean hemoglobin a1c values were 5.4 ± 0.03% and mean triglycerides were 122.7 ± 4.7 mg/dl in GDM women 3 months after delivery. A quarter of GDM-WC1 with persistent impairment of glucose metabolism early postpartum had only one abnormal glucose value (oGTT) during pregnancy. Twenty percent of the women with persistent type 2 diabetes would have been missed by the WHO criteria and 10% if two or more glucose values (oGTT) were required.


View this table:
[in this window]
[in a new window]

 
TABLE 5. Postpartum glucose metabolism in comparison between GDM-WC1 (one or more abnormal values; n = 368) and those with GDM-WC2 (two or more abnormal values; n = 108), and women with GDM-WHO (n = 230)

 
The risk factors independently predicting diabetes were previous GDM [OR 4.4 (1.2–15.9); P < 0.02] and preconceptual overweight/obesity [OR 4.0 (1.1–15.6); P < 0.05], whereas excessive weight gain [OR 2.7 (1.2–6.1);P < 0.01] and birth weight greater than 4000 g in a previous pregnancy [OR 2.1 (1.08–4.5); P < 0.05] predicted IFG. LGA fetus [OR 3.7 (1.3–10.7); P < 0.01], previous prediabetes [OR 10.6 (2.9–39.2); P < 0.0005], and Asian origin [OR 3.5 1(.4–8.8); P < 0.01] predicted combined IFG and IGT. Any impairment of glucose metabolism early after delivery was independently predicted by glucosuria [P < 0.01; OR 1.8 (1.1–2.9)] and preconceptual obesity (P < 0.03; OR 1.7 [1.07–2.7]). Interestingly, none of the women screened positive by the WHO criteria but negative by GDM-WC1 had overt diabetes, and only three had persistent IGT early postpartum.


    Discussion
 Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
This study detected a high rate of pregnant women with at least one abnormal glucose value (GDM-WC1) and with two or more abnormal glucose values (GDM-WC2), which may be attributed to the fact that only tertiary care centers with mostly preselected women participated in this study. Interestingly, the rates found in our study were similar to those recently reported in Italian women using the 3-h, 100-g oGTTs after an abnormal prescreening test (28).

Our study tried to evaluate the criteria proposed by the Fourth International Workshop Conference on Gestational Diabetes for the 75-g, 2-h oGTT, but treatment was already initiated in case of one single abnormal value according to the recommendations of the German and the Austrian Diabetes Association (25). Previous studies showed that one value in the oGTT is already associated with impaired insulin secretion and sensitivity (28), increased perinatal complications, such as LGA neonates or cesarean delivery (22), as well as fetal hyperinsulinemia, neonatal obesity and placental immaturity (24). In our study, women with one abnormal value did not differ from those with two abnormal values in their obstetric outcome, which supports the arguments for a strict surveillance of such women. However, the risk of earlier delivery and LGA infants including those with a birth weight greater than 4.5 kg was highest in GDM women with three abnormal values as was the rate of previous obstetric complications in general. Therefore, three abnormal values seem to hint at preexisting disturbances of maternal glucose metabolism, which is also supported by the observation that these women had the highest rate of overt diabetes postpartum.

We also found that, although fasting glucose was the strongest predictor of birth weight and glucose tolerance postpartum, each of the three glucose values measured during the oGTT independently related to and predicted maternal or fetal/neonatal complications, which is a new finding of the study. This further argues for the consideration of each glucose value for diagnosis and subsequent therapy. The final proof of the concept that there is a linear relationship between all glucose values across a broad range during the 75-g, 2-h oGTT and perinatal outcome independently of ethnicity can be expected from the Hyperglycemia and Adverse Pregnancy Outcome study (29).

In our observational study, all GDM-WC1 patients were treated to target with dietary modification and if necessary insulin therapy. Two recent studies with similar targets for glycemic control during pregnancy as in our study, one prospective, randomized, controlled study conducted in women diagnosed by the WHO criteria (20) and one study using the WC criteria (two or more abnormal values) (19) proved the efficacy of strict therapy in GDM on perinatal outcome. In the present study, we found similar rates of complications in the GDM-WC1 or GDM-WC2 women as in the treated women of these studies. Interestingly, although all women were closely monitored and on strict metabolic control, even the group with one single increased glucose value still had higher rates of complications. Therefore, it is questionable whether strict metabolic control alone is able to normalize perinatal complications. One might hypothesize that additional unmodified factors will contribute to the increased risk. These factors could be variations in circulating adipocytokines like decreased adiponectin levels (30, 31) or alterations of lipid metabolism and body fat content like increased intramyocellular lipids as previously shown in women with GDM (32).

Of note, Asian origin and family history of type 2 but not type 1 diabetes were associated with an increased risk of GDM-WC1, confirming the assumption that GDM-WC1 and type 2 share the same genetic background. Maternal type 2 diabetes was the most important independent risk factor regarding first-degree relatives, but family history in total explained only a very low number of cases. This finding further outlines the influence of the maternal intrauterine environment for the risk of diabetes in the offspring and the importance of acquired risk factors.

The 3.5-fold increased risk for recurrence of GDM-WC1 and the high rate of women with impaired glucose metabolism at the postpartum oGTT outlines the need for an oGTT early after delivery and regular follow-up, even in women with subclinical GDM.

The risk factors, previous gestational diabetes, pregestational overweight/obesity, and glucosuria, increased age and LGA independently predicted occurrence of GDM-WC1 with subsequent need of insulin therapy and fetal and maternal complications supporting a risk assessment in pregnancy independently of their glucose tolerance.

The results of our study propose that diagnosis of GDM-WC1 leads to an additional dietary treatment necessity for 20% of all women and could identify another 10% requiring insulin therapy during pregnancy to maintain normoglycemia, compared with GDM-WC2 or GDM-WHO.

In summary, each of three glucose values measured during the oGTT is independently associated with perinatal complications and should be considered for diagnosis of impaired glucose tolerance during pregnancy. Initiation of therapy, even in case of one abnormal glucose value according to WC criteria (GDM-WC1), detected a higher rate of LGA newborns with neonatal hypoglycemia, and in addition, more women with impaired glucose metabolism early after delivery than the WHO criteria. Pregnancy is a good opportunity to change lifestyle and many women will continue a healthy diet after delivery, which is important for public health facing the epidemic of obesity. The higher costs of insulin therapy and dietary counseling during pregnancy should be justified by the better detection of newborns at risk and potentially fewer long-term complications of mothers and children.


    Acknowledgments
 
We are indebted to our coworkers M. Politor, M. Hofmann, B. Gappmayer, C. Garstenauer, G. Hasenöhrl, T. Kann, and M. Olechowsky.


    Footnotes
 
This work was supported by a clinical research project award of the Austrian Diabetes Association (to A.K.-W.).

Disclosure Statement: The authors have nothing to disclose.

First Published Online February 19, 2008

Abbreviations: BMI, Body mass index; CI, confidence interval; GDM, gestational diabetes; IFG, impaired fasting glucose; IGT, impaired glucose tolerance; LGA, large for gestational age; NGT, normal glucose tolerance; oGTT, oral glucose tolerance test; OR, odds ratio; WC, Fourth International Workshop Conference of GDM.

Received October 15, 2007.

Accepted February 8, 2008.


    References
 Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

  1. Pendergrass M, Fazioni E, DeFronzo R 1995 Non-insulin-dependent diabetes mellitus and gestational diabetes mellitus: same disease, another name? Diabetes Rev 3:566–583
  2. Buchanan TA, Metzger BE 1993 Gestational diabetes mellitus. In: Mazzaferri EL, Bar RS, eds. Advances in endocrinology and metabolism. Chicago: Mosby Yearbook; 29–46
  3. Ramus RM, Kitzmiller JL 1994 Diagnosis and management of gestational diabetes. Diabetes Rev 2:43–52
  4. Jovanovic-Peterson L 1995 The diagnosis and management of gestational diabetes. Feature article. Clinical Diabetes 32–39
  5. McCance DR, Hanson RL, Pettitt DJ, Bennett PH, Hadden DR, Knowler WC 1997 Diagnosing diabetes mellitus—do we need new criteria? Diabetologia 40:247–255[CrossRef][Medline]
  6. 2004 Gestational diabetes mellitus. Diabetes Care 27(Suppl 1):S88–S90
  7. Naylor CD, Sermer M, Chen E, Farine D 1997 Selective screening for gestational diabetes mellitus. Toronto Trihospital Gestational Diabetes Project Investigators. N Engl J Med 337:1591–1596[Abstract/Free Full Text]
  8. 1997 Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 20:1183–1197
  9. 1979 Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. National Diabetes Data Group. Diabetes 28:1039–1057
  10. 1985 Diabetes mellitus. Report of a WHO Study Group. World Health Organ Tech Rep Ser 727:1–113
  11. Deerochanawong C, Putiyanun C, Wongsuryrat M, Serirat S, Jinayon P 1996 Comparison of National Diabetes Data Group and World Health Organization criteria for detecting gestational diabetes mellitus. Diabetologia 39:1070–1073[Medline]
  12. Ogata ES 1995 Perinatal morbidity in offspring of diabetic mothers. Diabetes Rev 3:625–657
  13. Blank A, Grave GD, Metzger BE 1995 Effects of gestational diabetes on perinatal morbidity reassessed. Report of the International Workshop on Adverse Perinatal Outcomes of Gestational Diabetes Mellitus, December 3–4, 1992. Diabetes Care 18:127–129[Medline]
  14. Schaefer UM, Songster G, Xiang A, Berkowitz K, Buchanan TA, Kjos SL 1997 Congenital malformations in offspring of women with hyperglycemia first detected during pregnancy. Am J Obstet Gynecol 177:1165–1171[CrossRef][Medline]
  15. Metzger BE, Cho NH, Roston SM, Radvany R 1993 Prepregnancy weight and antepartum insulin secretion predict glucose tolerance five years after gestational diabetes mellitus. Diabetes Care 16:1598–1605[Abstract]
  16. Kjos SL, Peters RK, Xiang A, Henry OA, Montoro M, Buchanan TA 1995 Predicting future diabetes in Latino women with gestational diabetes. Utility of early postpartum glucose tolerance testing. Diabetes 44:586–591[Abstract]
  17. Pettitt DJ, Aleck KA, Baird HR, Carraher MJ, Bennett PH, Knowler WC 1988 Congenital susceptibility to NIDDM. Role of intrauterine environment. Diabetes 37:622–628[Abstract]
  18. Silverman BL, Purdy LP, Metzger BE 1996 The intrauterine environment: Implications for the offspring of diabetic mothers. Diabetes Rev 4:21–35
  19. Langer O, Yogev Y, Most O, Xenakis EM 2005 Gestational diabetes: the consequences of not treating. Am J Obstet Gynecol 192:989–997[CrossRef][Medline]
  20. Crowther CA, Hiller JE, Moss JR, McPhee AJ, Jeffries WS, Robinson JS 2005 Effect of treatment of gestational diabetes mellitus on pregnancy outcomes. N Engl J Med 352:2477–2486[Abstract/Free Full Text]
  21. Naylor CD 1989 Diagnosing gestational diabetes mellitus. Is the gold standard valid? Diabetes Care 12:565–572[Abstract]
  22. Sacks DA, Abu-Fadil S, Greenspoon JS, Fotheringham N 1989 Do the current standards for glucose tolerance testing in pregnancy represent a valid conversion of O’Sullivan’s original criteria? Am J Obstet Gynecol 161:638–641[Medline]
  23. Langer O, Brustman L, Anyaegbunam A, Mazze R 1987 The significance of one abnormal glucose tolerance test value on adverse outcome in pregnancy. Am J Obstet Gynecol 157:758–763[Medline]
  24. Schafer-Graf UM, Dupak J, Vogel M, Dudenhausen JW, Kjos SL, Buchanan TA, Vetter K 1998 Hyperinsulinism, neonatal obesity and placental immaturity in infants born to women with one abnormal glucose tolerance test value. J Perinat Med 26:27–36[Medline]
  25. Kautzky-Willer A, Bancher-Todesca D, Birnbacher R 2004 Gestational diabetes mellitus. Acta Med Austriaca 31:182–184[Medline]
  26. American Diabetes Association 2008 Position Statement: diagnosis and classification of diabetes mellitus. Diabetes Care 31(Suppl 1):S55–S60
  27. Hadlock FP, Deter RL, Harrist RB, Park SK 1984 Estimating fetal age: computer-assisted analysis of multiple fetal growth parameters. Radiology 152:497–501[Abstract/Free Full Text]
  28. Di Cianni G, Seghieri G, Lencioni C, Cuccuru I, Anichini R, De Bellis A, Ghio A, Tesi F, Volpe L, Del Prato S 2007 Normal glucose tolerance and gestational diabetes mellitus: what is in between? Diabetes Care 30:1783–1788[Abstract/Free Full Text]
  29. HAPO Study Cooperative Research Group 2002 The Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study. Int J Gynaecol Obstet 78:69–77[CrossRef][Medline]
  30. Winzer C, Wagner O, Festa A, Schneider B, Roden M, Bancher-Todesca D, Pacini G, Funahashi T, Kautzky-Willer A 2004 Plasma adiponectin, insulin sensitivity, and subclinical inflammation in women with prior gestational diabetes mellitus. Diabetes Care 27:1721–1727[Abstract/Free Full Text]
  31. Worda C, Leipold H, Gruber C, Kautzky-Willer A, Knofler M, Bancher-Todesca D 2004 Decreased plasma adiponectin concentrations in women with gestational diabetes mellitus. Am J Obstet Gynecol 191:2120–2124[CrossRef][Medline]
  32. Kautzky-Willer A, Krssak M, Winzer C, Pacini G, Tura A, Farhan S, Wagner O, Brabant G, Horn R, Stingl H, Schneider B, Waldhausl W, Roden M 2003 Increased intramyocellular lipid concentration identifies impaired glucose metabolism in women with previous gestational diabetes. Diabetes 52:244–251[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
J. Clin. Endocrinol. Metab.Home page
R. Retnakaran, Y. Qi, M. Sermer, P. W. Connelly, A. J. G. Hanley, and B. Zinman
The Antepartum Glucose Values that Predict Neonatal Macrosomia Differ from Those that Predict Postpartum Prediabetes or Diabetes: Implications for the Diagnostic Criteria for Gestational Diabetes
J. Clin. Endocrinol. Metab., March 1, 2009; 94(3): 840 - 845.
[Abstract] [Full Text] [PDF]


Home page
Eur J EndocrinolHome page
S. Kralisch, H. Stepan, J. Kratzsch, M. Verlohren, H.-J. Verlohren, K. Drynda, U. Lossner, M. Bluher, M. Stumvoll, and M. Fasshauer
Serum levels of adipocyte fatty acid binding protein are increased in gestational diabetes mellitus
Eur. J. Endocrinol., January 1, 2009; 160(1): 33 - 38.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kautzky-Willer, A.
Right arrow Articles by Lechleitner, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kautzky-Willer, A.
Right arrow Articles by Lechleitner, M.
Related Collections
Right arrow Pediatric Endocrinology
Right arrow Diabetes and Insulin
Right arrow Female Endocrinology


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals