The incidence of gestational diabetes (GDM) continues to rise and requires management by a multidisciplinary diabetes antenatal team. Multiple national and international guidelines exist on the management of hyperglycaemia in pregnancy which are not concordant and may lead to confusion in clinical practice. Limited studies have been conducted examining prescribing habits for hyperglycaemia in GDM.Our survey examined the prescribing practices relating to oral antihyperglycaemic agents (OAHAs, unlicensed for use in pregnancy but widely prescribed) by health care professionals within the UK caring for women with GDM. Although metformin is widely used, our survey highlights heterogeneity in the use of OAHAs with respect to drug choice, timing of introduction, dosage and escalation of glucose lowering therapy. The cause of this heterogeneity appears multi-factorial. Copyright (C) 2016 John Wiley & Sons.

Introduction Individuals with non-alcoholic fatty liver disease (NAFLD) have a significantly increased risk of cardiovascular (CV) disease independent of other cardiometabolic risk factors. We explored the relationship between endothelial function, oxidative stress, vascular inflammation and insulin resistance in patients with NAFLD. Method Patients with proven NAFLD but without cirrhosis were recruited into the study and the following parameters were assessed: Endothelial function – change in reflective index post salbutamol using digital plethysmography, urine albumin:creatinine ratio, plasma vascular cell adhesion molecule-1 (VCAM-1) and plasma cyclic guanosine monophosphate (cGMP) Oxidative stress – blood glutathione ratio (GSH:GSSG), plasma total anti-oxidant status and plasma lipid hydroperoxides Inflammation – highly-sensitive plasma CRP Insulin resistance – HOMA-IR Results We studied 42 patients: 31 males and 11 females. We found 79% had T2DM or impaired fasting glucose. Mean age was 58 ± 8 years, BMI 33.2 ± 5.5 kg/m2, BP 133/82 ± 12/7 mmHg, duration of NAFLD diagnosis 1.0 ± IQR 3.4 years, HbA1c 53 ± 13 mmol/mol, total cholesterol 4.43 ± 1.14 mmol/l, HDL 1.06 ± 0.32 mmol/l, LDLc 2.51 ± 1.02 mmol/l, and triglycerides 1.93 ± 0.85 mmol/l. There was moderate correlation between VCAM-1 and hsCRP (Spearman’s rho=0.392,p = 0.01); moderate correlation between hsCRP and blood glutathione ratio (Spearman’s rho=0.325, p = 0.04) and moderate correlation between HOMA-IR and aspartate aminotransferase [AST] (Spearman’s rho=0.489, p = 0.001). Conclusion Markers of both vascular (VCAM-1) and systemic low grade inflammation (hsCRP) were associated with evidence of endothelial dysfunction and oxidative stress, whilst insulin resistance was associated with AST in non-cirrhotic patients with NAFLD. VCAM-1 as a marker of endothelial activation may be a potential CV risk predictor in this group of patients. Disclosure of interest None Declared.

OBJECTIVES:The effect of aspirin upon platelet function is well documented although experimental studies suggest that aspirin may also affect oxidative stress, vascular inflammation, endothelial dysfunction and dysglycaemia. The optimal dose of aspirin for cardiovascular protection in type 2 diabetes is still debated. We examined the effects of different doses of aspirin upon these novel markers of cardiovascular risk and any association between aspirin-mediated changes in these markers.METHODOLOGY:Subjects with type 2 diabetes attended for baseline evaluation including BMI, glycaemic and lipid markers, endothelial function (photoplethysmography), insulin resistance (HOMA), inflammation (sVCAM-1 and Hs-CRP) and markers of oxidative stress [total anti-oxidant status (TAOS and FRAP), whole blood total glutathione (GSH) assays]. Subjects then received in random, sequential, blinded fashion aspirin 75 mg day(-1) , aspirin 300 mg day(-1) , aspirin 3.6 g day(-1) or placebo for 2 weeks with a 2-week washout. The above investigations were repeated after each intervention. Aspirin-related changes compared with placebo were analysed using repeated measures ANOVA.RESULTS:Subjects = 17 (M - 12; F - 5), mean age - 57.4 ± 9.1 years (mean ± 1 SD), HbA1c - 63 ± 13 mmol mol(-1) (7.9 ± 1.2%), total cholesterol 4.57 ± 1.01 mmol l(-1) . At baseline TAOS value was 59.3 ± 9.7 μM AEAC (Ascorbate Equivalent Anti-oxidant Concentration), glutathione 302.2 ± 183.3 mmol l(-1) and FRAP 0.86 ± 0.23 mM FeII. None of the aspirin doses had a significant impact upon BMI, blood pressure, lipid parameters, insulin sensitivity (HOMA), FRAP, TAOS, GSH, endothelial function, glycaemic control (fructosamine) or inflammation (sVCAM-1 and HsCRP).CONCLUSIONS:Aspirin exhibited no significant dose-dependent effect on markers of vascular inflammation, oxidative stress, insulin resistance and endothelial function (photoplethysmography) when used in type 2 diabetes over a 2-week period. (CLINICAL TRIALS REGISTRATION:NCT00898950, EUDRACT:2004-001418-14).