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With type 2 diabetes (T2D) progression, patients require insulin, but insufficient titration often leads to poor glycemic control. A higher insulin starting dose may reduce the optimal dose deficit, but whether this procedure increases hypoglycemia risk is unknown. This open-label, multicenter trial (NCT02836704) evaluated safety and efficacy of a high (0.3 U/kg) vs. standard (0.2 U/kg) starting dose of glargine 100 U/ml (Gla-100) followed by titration over 16 weeks to achieve self-monitored FBG 4.4-5.6 mmol/L using the same algorithm in each group. Overall, 892 patients with overweight/obesity (BMI 25-40 kg/m2) and uncontrolled T2D (HbA1c 7.5-11.0%; lab FPG >9.0 mmol/L) on stable doses of 2-3 OADs were randomized to receive a high (n=444) or standard (n=448) starting dose of Gla-100. At week 16, 92% of patients completed the study and 866 were analyzed. The primary endpoint (percentage of patients with ≥1 confirmed hypoglycemia, BG <3.9 mmol/L) met the pre-specified threshold (upper bound 95% CI <10%) for non-inferiority of Gla-100 0.3 U/kg vs. 0.2 U/kg with 11.0% and 8.6% in the respective groups (log-binomial regression estimated difference 2.1%; 95% CI: −1.68%, 5.89%). At week 16, symptomatic (9.8% vs. 7.0%, p=0.13) and nocturnal hypoglycemia (2.7% vs. 1.2%, p=0.10), percentage of patients achieving HbA1c <7.0% without hypoglycemia (37.1% vs. 37.1%), and percentage of patients achieving lab FPG targets <5.6 mmol/L (15.9% vs. 16.3%), <6.1 mmol/L (27.6% vs. 26.1%), or <7.0 mmol/L (48.8% vs. 48.3%) were all similar in both groups. However, time to achieve first self-monitored FBG <5.6, <6.1, or <7 mmol/L was 6, 9, and 7 days shorter in the 0.3 U/kg group (all p<0.01). In conclusion, among patients with overweight/obesity and T2D, a higher Gla-100 starting dose was as safe as a standard Gla-100 starting dose and achieved FBG targets earlier during the course of therapy. Disclosure: L. Ji: Advisory Panel; Self; AstraZeneca. Consultant; Self; AstraZeneca, Bayer AG, Boehringer Ingelheim International GmbH, Bristol-Myers Squibb Company, Eli Lilly and Company, Merck KGaA, Merck Sharp & Dohme Corp., Novartis AG, Novo Nordisk A/S, Roche Pharma, Sanofi, Takeda Pharmaceutical Company Limited. Research Support; Self; AstraZeneca, Bristol-Myers Squibb Company, Eli Lilly and Company, Merck Sharp & Dohme Corp., Novartis AG, Roche Pharma, Sanofi. H. Wan: None. B. Wen: None. X. Wang: None. J. Wang: Research Support; Self; Sanofi. R. Bian: None. W. Pang: None. W. Feng: Employee; Self; Sanofi. X. Zhang: None. N. Cui: Employee; Self; Sanofi. Funding: Sanofi China [ABSTRACT FROM AUTHOR]

Objective: To investigate the temporal changes of serum interleukin-37 (IL-37) concentration following acute ST-segment elevation myocardial infarction (ASTEMI) and the relationship between IL-37 and C-reactive protein (CRP) in patients with ASTEMI., Methods: This analysis was conducted in a cohort of 20 patients with an established diagnosis of ASTEMI and 26 patients admitted for chest pain but with normal findings in coronary angiography (control) between June 2012 and December 2013. Venous blood was collected at days 1, 3, 5, and 7 after myocardial infarction for measurement of serum IL-37 and CRP levels using enzyme-linked immunosorbent assay (ELISA)., Results: Compared with the control group, the patients in ASTEMI group showed a significant acute elevation of IL-37 level on day 1 following myocardial infarction; IL-37 level reached the peak on day 3 and began to decrease on day 5, followed by a significant decrease on day 7. The time course of post-infarction CRP changes was consistent with that of IL-37 variations and showed a positive correlation the latter (r=0.63, P<0.05)., Conclusion: IL-37 may participate in the inflammatory responses in ASTEMI.