ABSTRACT
BACKGROUND: Fetal overgrowth is the most important complication of gestational (GDM) and pregestational diabetes mellitus. METHODS: We correlated maternal glucose profiles, as detected by continuous glucose monitoring (CGM), with fetal growth parameters for 80 pregnant women (32 with type 1 diabetes, 31 with GDM, and 17 healthy controls). Glucose profiles were monitored in the first, second, and third trimesters of pregnancy for type 1 diabetes women and in the second and third trimesters for GDM women and controls. To analyze glycemic variability, we considered the mean amplitude of glycemic excursion, mean glycemia, the continuous overlapping net glycemic action (CONGA), the SD, the High Blood Glucose Index (HBGI), the Low Blood Glucose Index, and the interquartile range (IQR). RESULTS: Mean age was the same for the three groups. Prepregnancy body mass index was higher for the women with diabetes (GDM and type 1) than for controls. The newborn's mean birth weight and ponderal index were higher, although not significantly so, for the women with diabetes than for controls. For the type 1 diabetes patients, ponderal index correlated with the HBGI in the first trimester, CONGA1 and IQR in the second, and mean glycemia and SD in the third. For GDM patients, ponderal index correlated with mean glycemia and the HBGI in the second trimester. CONCLUSIONS: Fetal exposure to glycemic variability and hyperglycemia seems to be important in determining fetal overgrowth in pregnant women with diabetes. Optimal glucose control and less glucose variability are needed as early as possible in both type 1 diabetes and GDM patients to ensure normal fetal growth.
Subject(s)
Blood Glucose/metabolism , Diabetes Mellitus, Type 1/blood , Diabetes, Gestational/blood , Pregnancy in Diabetics/blood , Adult , Birth Weight/physiology , Blood Glucose/analysis , Blood Glucose Self-Monitoring , Female , Humans , Infant, Newborn , Linear Models , PregnancyABSTRACT
The aim of the present cohort study is the assessment of treatment failure rates in patients on monotherapy with metformin or insulin secretagogues, observed in a routine clinical setting. A cohort of patients without any pharmacological treatment was also observed. A retrospective observational cohort study was performed on a consecutive series of 2,020 type 2 diabetic patients receiving monotherapy with an oral agent (metformin or insulin secretagogue, n = 1,126) or drug-naive (n = 894). HbA1c and prescribed hypoglycemic therapy were recorded yearly. Patients were followed until death, change of residence, failure to treatment, or up to 48 months. The mean duration of follow up was 34.8 ± 18.0 months. In a Cox regression analysis, metformin was associated with a significant reduction, and insulin secretagogues with a significant increase, in the risk of failure to therapy during follow up. When duration of diabetes and baseline BMI were added to the model, insulin secretagogues, but not metformin, were still associated with increased risk of failure. In conclusion, insulin secretagogues are associated with increased failure rate in comparison with metformin. This difference could be due to detrimental effect of secretagogues, rather than to a beneficial action of metformin.