Only a few reports have examined vascular endothelial function before and after educational hospitalization and the factors that affect it in patients with type 2 diabetes mellitus (T2DM). The aim of this study was to assess vascular endothelial function before and after educational hospitalization and identify factors that affect it. In 65 patients with T2DM who underwent peripheral arterial tonometry (EndoPAT) before and after hospitalization, vascular endothelial function (reactive hyperemia index [RHI]), glucose metabolism, lipid metabolism, and blood pressure were assessed before and after hospitalization. The primary endpoint was hospitalization-induced changes in vascular endothelial function. Educational hospitalization significantly improved the natural logarithmically scaled RHI (L_RHI) from 0.555 ± 0.212 to 0.625 ± 0.245 (p = 0.012). Multivariable logistic regression analysis identified hypoglycemia during hospitalization as the single factor that significantly altered vascular endothelial function (p = 0.019). The odds of achieving normal vascular endothelial function were 0.08 times lower (95% confidence interval, 0.01–0.67) for each episode of hypoglycemia. Furthermore, multivariable analysis identified hypoglycemia during hospitalization as the single factor that worsened L_RHI. Our study showed that educational hospitalization of patients with T2DM improved vascular endothelial function, and that the development of hypoglycemic episodes had a significant negative impact on normalization of vascular endothelial function.

Among the side effects of methimazole (MMI) for the treatment of Graves’ disease, MMI-induced acute pancreatitis (MIP) is a rare adverse reaction, with only seven cases being reported to date. However, two large-scale population-based studies recently revealed that the risk of MIP was significantly higher, ranging between 0.02 and 0.56%. Although MIP is common in middle-aged and elderly Asian women, its pathogenesis remains largely unknown. We herein present a case of a 72-year-old Japanese woman with Graves’ disease who developed MIP 12 days after the initiation of MMI. MMI was discontinued, the patient was switched to propylthiouracil (PTU) therapy, and pancreatitis gradually resolved. Serological human leukocyte antigen (HLA) typing identified HLA-DRB1*08:03:02. This HLA allele was previously detected in a patient with MIP, and is one of the major risk factors for agranulocytosis induced by antithyroid drugs, including PTU as well as MMI. In cases of MIP, PTU is being considered as an alternative to MMI; however, its safety needs further investigation and close monitoring after the switch to PTU. Further studies are warranted, particularly on the relationship between MIP and the presence of HLA alleles causing antithyroid drug-induced agranulocytosis.

The aim of this study was to evaluate the efficacy of canagliflozin in reducing the required insulin dose and the risk of hypoglycaemia in type 2 diabetes (T2D). This study was conducted in patients with T2D treated with insulin. They were randomly assigned to the control (n = 17) and canagliflozin (n = 17, plus 100 mg/day canagliflozin) groups. In both groups, a defined insulin dose adjustment protocol was applied to achieve the same level of glycaemic control. The change from baseline in daily insulin dose was significantly smaller in the canagliflozin group (3.9 units/day) than in the control group (13.4 units/day; P = 0.040). Low blood glucose index and predicted % of blood glucose (BG) <70 mg/dL, which are hypoglycaemia-related variables, worsened significantly in the control group but both remained unchanged in the canagliflozin group. The standard deviation for night-time BG levels improved significantly only in the canagliflozin group. Supplementation of insulin therapy with 100 mg canagliflozin in patients with T2D reduced the required insulin dose and hypoglycaemic risk and flattened night-time glycaemic fluctuations while maintaining the same level of glycaemic control. K E Y W O R D Scanagliflozin, continuous glucose monitoring, hypoglycaemia, insulin therapy, type 2 diabetes

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Background: Tofogliflozin (TOFO) has the highest selectivity to sodium-glucose co-transporter 2 (SGLT2) relative to SGLT1 (2900 times) and does not promote urinary glucose excretion at hypoglycemia compared with phlorhizin and does not enhance further lowering of glucose. To compare the impact of TOFO and ipragliflozin (IPR) on hypoglycemia in patients with T2DM, treated with sulfonylureas. Methods: 30 patients were allocated to either 20 mg TOFO or 50 mg IPR and wore a continuous glucose monitoring (CGM, ipro2®) for 5 days at 3 times in a cross-over manner. The primary outcome measure was proportion of time over 24 hours with glucose less than 70 mg/dl detected by CGM and this was compared between two SGLT2 inhibitors. Results: The percent time spent at glucose less than 70 mg/dl was 0.48, 2.77 and 0.06%, before treatment with SGLT2 inhibitors and treatment with IPR and TOFO (p=0.1135, between SGLT2 inhibitors). The addition of either IPR or TOFO to sulfonylureas markedly and significantly improved other CGM-derived parameters including average glucose, standard deviation of glucose, mean postprandial glucose excursion, percent time with glucose &gt;140, &gt;180 and &gt;200 mg/dl, area over the curve &lt;70, area under the curve &gt;140, &gt;180 and &gt;200, maximum glucose. However, there were no significant differences in these parameters between the SGLT2 inhibitors. We also conducted a sub-analysis in 16 patients who received DPP-4 inhibitors. The results showed the percent time at glucose level &lt;70 mg/dl (p=0.1118, between SGLT2 inhibitors) and the area over the curve &lt;70 (p=0.0631, between SGLT2 inhibitors), tended to be lower in patients treated with TOFO. Conclusion: Based on the CGM the addition of TOFO to sulfonylureas tended to decrease the percent time spent in hypoglycemia in T2DM. The addition of SGLT2 inhibitors to sulfonylureas improved the average glucose level and reduced glucose fluctuations without increasing hypoglycemia. Disclosure A. Kurozumi: None. Y. Okada: None. Y. Goshima: None. T. Otsuka: None. M. Narisawa: None. K. Torimoto: None. Y. Tanaka: None.