Maternal low birth weight and gestational hyperglycemia.

We aimed to investigate whether birth weight could predict the subsequent risk of gestational diabetes and impaired glucose tolerance. Consecutive women with a singleton pregnancy and gestational diabetes (n = 50), impaired glucose tolerance (n = 50) and normoglycemia (n = 200) were included in the study. Birth data were collected from original hospital records of the women. Women with gestational hyperglycemia were significantly older and heavier than those with normoglycemia. Maternal birth weights significantly declined for each class of glucose tolerance (3389 +/- 644; 3184 +/- 583 and 3077 +/- 661, respectively for women with normoglycemia, impaired glucose tolerance and gestational diabetes). After adjustment for age, gestational age and weight gain, maternal diabetes, and pre-pregnancy body mass index, maternal birth weight was negatively related to impaired glucose tolerance (OR 0.88, 95% CI 0.81-0.97) and to gestational diabetes (OR 0.82, 95% CI 0.74-0.91) in a multiple logistic regression model. These findings suggest that women with low birth weight constitute a group at increased risk for both gestational impaired glucose tolerance and diabetes.

Clinical characteristics and outcome of pregnancy in women with gestational hyperglycaemia with and without antibodies to beta-cell antigens.

AIMS: To evaluate the prevalence of beta-cell autoantibodies in women with gestational diabetes and impaired glucose tolerance, and identify clinical characteristics differentiating hyperglycaemic patients with and without autoantibodies. METHODS: One hundred and twenty-three pregnant patients with gestational diabetes, 84 with impaired glucose tolerance and 290 with normoglycaemia were evaluated for anti-islet cell antibodies, glutamic acid decarboxylase (GAD) autoantibodies, and the components of the metabolic syndrome. RESULTS: Autoantibody positivity was 8.9%, 17.9% and 0.3% in patients with diabetes, impaired tolerance and normoglycaemia, respectively. Hyperglycaemic patients with autoantibodies had lower body mass index, waist, weight gain at the time of the screening test and a lower percentage of previous pregnancies than those without autoantibodies. In addition, their fasting insulin values were significantly lower and inversely related to the presence of autoantibodies (odds ratio (OR) = 0.64; 95% confidence interval (CI) 0.42-0.96), the lowest values being found in anti-GAD+ patients. Autoantibody-positive women with diabetes were more frequently treated with insulin than negative patients (OR = 7.21; 95% CI 1.85-28.08). CONCLUSIONS: Autoantibody-positive women with gestational hyperglycaemia displayed fewer features of insulin resistance and required more frequent insulin therapy than negative women and presumably had presymptomatic Type 1 diabetes. If this conclusion is corroborated by the follow-up of larger series, clinical and immunological distinction of types of gestational hyperglycaemia would be useful.