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AimsStudies to prevent gestational diabetes (GDM) have shown the best results when lifestyle measures have been applied early in pregnancy. We aimed to investigate whether first-trimester fasting plasma glucose (FPG) could predict GDM risk and adverse pregnancy outcomes. MethodsA retrospective analysis of prospectively collected data from singleton pregnancies who were attended at our hospital between 2008 and 2018 (n = 27,198) was performed. We included patients with a recorded first-trimester FPG and complete pregnancy data (n = 6845). Patients under 18, with pregestational diabetes or reproductive techniques, were excluded. First-trimester FPG was evaluated as a continuous variable and divided into quartiles. GDM was diagnosed by NDDG criteria. The relationship between first- and second-trimester glucose > 92 mg/dL was also investigated. The relationship between FPG and pregnancy outcomes was assessed in 6150 patients who did not have GDM.ResultsMaternal age was 34.2 ± 3.9 years, BMI 23.1 ± 3.7 kg/m2 and mean FPG 83.0 ± 7.3 mg/dL. Glucose quartiles were: ≤ 78, 79–83, 84–87 and ≥ 88 mg/dL. First-trimester FPG predicted the risk of GDM (7%, 8%, 10.2% and 16% in each quartile, p < 0.001) and the risk of second-trimester glucose > 92 mg/dL (2.6%, 3.8%, 6.3% and 11.4% in each quartile, p < 0.001). FPG was significantly associated with LGA (8.2%, 9.3%, 10% and 11.7% in each quartile, p = 0.011) but not with other obstetrical outcomes. In a multivariate analysis including age, BMI, tobacco use, number of pregnancies and weight gained during pregnancy, first-trimester FPG was an independent predictor of LGA. ConclusionsFirst-trimester FPG is an early marker of GDM and LGA.

Aims The hyperglycemia and adverse pregnancy outcome study demonstrated a continuous association between fasting plasma glucose (FPG) levels below those diagnostic of diabetes and adverse neonatal outcomes. We aimed to investigate whether the same association was found in a Mediterranean population. Methods A retrospective analysis of singleton pregnancies attended at our Hospital between 2008 and 2015 ( n  = 5203). FPG was evaluated in the second trimester, and it was divided into 7 categories ( 1  < 75, 2 75–79, 3 80–84, 4 85–89, 5 90–94, 6 95–99 and 7 100–124 mg/dL). Pregnancy outcomes included elective cesarean delivery, gestational hypertensive disorders (GHD), large for gestational age (LGA), small for gestational age (SGA), macrosomia, prematurity, severe prematurity and APGAR at 1 min <7. Results Maternal age was 33.8 ± 3.8 years, and BMI at first antenatal visit was 22.9 ± 3.5 kg/m 2 ; mean FPG was 79 ± 7 mg/dL. A positive association was observed between FPG and LGA ( p  < 0.001), GHD ( p  = 0.004) and prematurity both <37 and <34 weeks of gestation ( p  = 0.001 and p  = 0.004). FPG and SGA were inversely related ( p  = 0,038). FPG was not significantly related to rate of C-section or APGAR. Adjusted odds ratios associated with 1 standard deviation increase in the fasting plasma glucose (7 mg/dL) were 1.26 (1.15 to 1.37) for LGA, 1.28 (1.09 to 1.49) for GHD and 0.83 (0.74–0.93) for SGA. In a multivariate analysis controlling for confounders, FPG remained associated with LGA. Conclusions We found an association between FPG levels, below those diagnostic of gestational diabetes according to our guidelines, and adverse maternal and neonatal outcomes in a Mediterranean population.

Effects of nicotinamide and intravenous insulin therapy in newly diagnosed type 1 diabetes. J Vidal , M Fernández-Balsells , G Sesmilo , E Aguilera , R Casamitjana , R Gomis and I Conget Endocrinology and Diabetes Unit, Institut d'Investigacions Biomèdicas August Pi i Sunyer, Hospital Clínic i Universitari, Barcelona, Spain. Abstract OBJECTIVE: To investigate the effect of intravenous insulin therapy combined with nicotinamide in the metabolic control and beta-cell function of newly diagnosed type 1 diabetic subjects in comparison with intensive insulin therapy and nicotinamide alone. RESEARCH DESIGN AND METHODS: A total of 34 newly diagnosed type 1 diabetic patients were included. After the correction of initial metabolic disturbances, subjects were randomly assigned to the following three groups within 72 h after admission: 1) intensive insulin therapy + placebo (C) (n = 12); 2) intensive insulin therapy + nicotinamide, 700 mg three times a day (NIC) (n = 11); and 3) 72-h intravenous insulin followed by intensive insulin therapy + nicotinamide, 700 mg three times a day (NIV) (n = 11). The subjects were monitored for 12 months. GAD, tyrosine phosphatase antibodies, and insulin autoantibodies were measured. C-peptide was measured basally and after 2, 4, 6, 8, and 10 min of 1 mg intravenous glucagon. HbA1c, glucagon, and antibody measurements were determined initially and at 1, 3, 6, 9, and 12 months. RESULTS: HbA1c values declined to normal after treatment was initiated in all groups and remained not significantly different during the follow-up period. We did not find differences between experimental (NIC and NIV) and placebo (C) groups in terms of beta-cell function, considering basal or glucagon-stimulated C-peptide (maximal stimulated C-peptide and area under the curve [AUC] of C-peptide) values during the follow-up period. After pooling data from the NIC and NIV groups (both including nicotinamide) and comparing it with data from the C group, the results remained unchanged. At diagnosis, GAD positivity was observed in 10 of 12, 8 of 11, and 10 of 11 subjects (NS) in the C, NIC, and NIV groups, respectively, and IA2 positivity was observed in 3 of 12, 4 of 11, and 4 of 11 subjects (NS) in the C, NIC, and NIV groups, respectively. Antibody titers displayed a similar behavior in all groups during the follow-up period. CONCLUSIONS: Our pilot study failed to demonstrate that the addition of 72-h intravenous insulin and nicotinamide to conventional intensive insulin therapy produces any beneficial effect in newly diagnosed type 1 diabetic subjects in terms of beta-cell function and metabolic control.

There have recently been reports of a limited number of laparoscopic procedures in patients with clinically manifest hyperinsulinism. However, the precise role of laparoscopy remains unknown. Between January 1998 and September 2003, 11 consecutive patients (10 women and 1 man; mean age, 40 years; age range, 22–66 years) with sporadic insulinoma and two female patients (25 and 40 years old) with multiple insulinomas associated with multiple endocrine neoplasia type 1 (MEN-1) were operated on using the laparoscopic approach. Endoscopic ultrasonography was used to localize the tumor preoperatively in 90% of patients with sporadic insulinoma. In patients with MEN-1, computed tomography and octreoscan- 111In demonstrated multiple tumors. Laparoscopic ultrasonography (LapUS) was performed in all patients for operative decision-making. Of 11 patients with sporadic insulinoma, laparoscopic enucleation (LapEn) was planned in 8 patients, but in 1 patient, the use of LapUS missed the tumor and the patient was converted to open surgery. Mean operating time after LapEn (seven patients) was 180 minutes, and the mean blood loss was 200 ml. The mean hospital stay was 5 days. In three of the 11 patients, laparoscopic spleen-preserving distal pancreatectomy (LapSPDP) was performed; the mean operative time was 240 minutes, and the mean blood loss was 360 ml. Postoperative complications occurred in three of seven patients after LapEn (three pancreatic fistulas managed conservatively, and one case of bleeding requiring reoperation). LapSPDP was performed in both patients with MEN-1; in one patient with splenic vessel preservation (SVP), the operating time was 210 minutes and blood loss was 650 ml, with a hospital stay of 6 days. In another patient without SVP, the operating time was 150 minutes and blood loss was 300 ml. The latter patient developed a 4-cm splenic infarct managed conservatively, and the hospital stay was 14 days. LapEn and LapSPDP are feasible and safe and achieved cure in patients with sporadic insulinoma and multiple insulinomas associated with MEN-1. However, the risk of pancreatic leakage after LapEn remains high, and LapSPDP without SVP may be associated with splenic infarct.