Diabetic neuropathy, defined as peripheral neuropathy of the lower limbs, was significantly associated with symptoms of constipation. Peripheral neuropathy of the lower limbs is not a direct risk factor for constipation but may be a useful criterion when assessing whether constipation is associated with DM.
Patients with end stage renal disease frequently show indigestion symptoms as a result of uremia. However, the association between the indigestion symptoms and the earlier stage of diabetic nephropathy is unclear. Therefore we conducted a multicenter study using self-administered questionnaires: the Gastrointestinal Symptom Rating Scale (GSRS).Patients were type1 or type 2 DM between 20-85 years old treated in 2 hospitals and 3 clinics in Yokohama and Tokyo during June 2016 to January 2017. We excluded patients if they were either 1) pregnant or 2) suffering from malignant disease or digestive disease. We defined diabetic nephropathy as stage 3 or later and clinically significant indigestion symptoms (CSIS) as GSRS≧3. We analyzed the association between diabetic nephropathy and CSIS.In total of 722 patients, 430 (61%) were male and 36 (5%) were Type 1 DM. Mean age was 65 years old, mean BMI was 25.0, mean HbA1c was 7.5% and mean duration of DM was 155 months. As for diabetic microangiopathy, 177 (26%) had nephropathy, 186 (30%) had peripheral neuropathy, 180 (29%) had retinopathy. GLP-1 receptor agonists were used in 62 (8.8%) patients. In comparison between patients with and without CSIS, age, BMI, HbA1c were not different. Duration of DM was longer in CSIS (193 ± 19 vs. 153 ± 5 months, p=0.046). Presence of diabetic nephropathy was associated with CSIS (OR=2.08, 95% CI: 1.10-3.91), in contrast, that of neuropathy and retinopathy was not. In multivariate analysis adjusting age, BMI, HbA1c and use of GLP-1 receptor agonist, CSIS were significantly associated with longer duration of DM (β=0.003, SD=0.001, p=0.01), and diabetic nephropathy (OR=1.95, 95% CI:1.01-3.71). Neuropathy and retinopathy had no significant association with CSIS. Our results suggest that not only in the end stage renal disease, earlier stage of diabetic nephropathy with proteinuria might be the risk of indigestion symptoms in patients with diabetes mellitus. Disclosure Y. Namiki: None. E. Yamada: None. Y. Takano: None. H. Takamine: None. H. Sasaki: None. K. Inazumi: None. T. Minami: None. S. Ito: None. N. Mantani: None. T. Iwasaki: None. M. Yamada: None. A. Nakajima: None. Y. Terauchi: Research Support; Self; MSD K.K.. Speaker's Bureau; Self; MSD K.K.. Advisory Panel; Self; MSD K.K.. Research Support; Self; Ono Pharmaceutical Co., Ltd.. Speaker's Bureau; Self; Ono Pharmaceutical Co., Ltd.. Research Support; Self; Novartis Pharma K.K., Boehringer Ingelheim GmbH. Speaker's Bureau; Self; Boehringer Ingelheim GmbH. Advisory Panel; Self; Boehringer Ingelheim GmbH. Research Support; Self; Mitsubishi Tanabe Pharma Corporation. Speaker's Bureau; Self; Mitsubishi Tanabe Pharma Corporation. Advisory Panel; Self; Mitsubishi Tanabe Pharma Corporation. Research Support; Self; Daiichi Sankyo Company, Limited. Speaker's Bureau; Self; Daiichi Sankyo Company, Limited. Advisory Panel; Self; Daiichi Sankyo Company, Limited. Research Support; Self; Sanwa Kagaku Kenkyusho Co., Ltd.. Speaker's Bureau; Self; Sanwa Kagaku Kenkyusho Co., Ltd.. Research Support; Self; Novo Nordisk Inc.. Speaker's Bureau; Self; Novo Nordisk Inc.. Advisory Panel; Self; Novo Nordisk Inc.. Research Support; Self; Eli Lilly and Company. Speaker's Bureau; Self; Eli Lilly and Company. Advisory Panel; Self; Eli Lilly and Company. Research Support; Self; Sanofi. Speaker's Bureau; Self; Sanofi. Advisory Panel; Self; Sanofi. Research Support; Self; Sumitomo Dainippon Pharma Co., Ltd.. Speaker's Bureau; Self; Sumitomo Dainippon Pharma Co., Ltd.. Research Support; Self; Shionogi & Co., Ltd.. Speaker's Bureau; Self; Shionogi & Co., Ltd., Bayer Yakuhin, Ltd., Astellas Pharma US, Inc., AstraZeneca. Advisory Panel; Self; AstraZeneca, Teijin Pharma Limited. U.N. Osada: None.
Effectiveness of real time continuous glucose monitoring (RT-CGM) compared with intensive self-monitoring of blood glucose (SMBG) is not clear. To analyze the effectiveness of RT-CGM, retrospective CGM and, intensive SMBG in adults with type 2 diabetes, we conducted a randomized, open-labelled clinical trial. Patients were type 2 diabetes adults admitted to our hospital from August 2016 to August 2017. Patients of age over 85 years, pregnant, admission less than 1 week were excluded. Patients were randomized to SMBG with RT-CGM using the Medtronic MiniMed 620G, SMBG with retrospective CGM using Medtronic iPro2, or SMBG alone. Both CGMs were worn for 6 days. SMBG was done 6 times a day at every pre-meal and 2 hours post-meal. Primary outcome was the change in HbA1c from baseline to 12weeks. As the secondary outcomes, change in mean glucose level from the admission day to discharge day, and frequency of in-hospital hypoglycemia were evaluated. We also evaluated patients’ satisfaction to treatment using Diabetes Treatment Satisfaction Questionnaire (DTSQ). As the result, 111 patients were enrolled and 33 patients were allocated to RT-CGM group, 26 to retrospective CGM group, and 52 to SMBG group. Among these 111 patients, 63 (56.8%) were male, mean age was 65.1 years, diabetes duration was 8.3 years, BMI was 26.3 kg/m^2, and HbA1c was 9.1%. Overall, glycemic control was improved after treatment for both HbA1c and the mean glucose level; HbA1c from 9.1±1.7% to 6.8±1.0%, mean glucose level from 189±56mg/dl to 137±19mg/dl. However, the changes were not significantly different between the groups. As the safety profile, 34 hypoglycemia was seen during hospitalization with no difference in frequency between the groups (P=0.11). There were no differences in patients’ satisfaction to treatment assessed by DTSQ, either. In conclusion, among adults with type 2 diabetes, intensive SMBG may have the equivalent effect to RT-CGM and retrospective CGM. Disclosure Y. Takano: None. Y. Namiki: None. H. Hiiragi: None. T. Yamada: None. H. Sasaki: None. Y. Murohashi: None. H. Takamine: None. K. Inazumi: None. Y. Terauchi: Research Support; Self; MSD K.K.. Speaker's Bureau; Self; MSD K.K.. Advisory Panel; Self; MSD K.K.. Research Support; Self; Ono Pharmaceutical Co., Ltd.. Speaker's Bureau; Self; Ono Pharmaceutical Co., Ltd.. Research Support; Self; Novartis Pharma K.K., Boehringer Ingelheim GmbH. Speaker's Bureau; Self; Boehringer Ingelheim GmbH. Advisory Panel; Self; Boehringer Ingelheim GmbH. Research Support; Self; Mitsubishi Tanabe Pharma Corporation. Speaker's Bureau; Self; Mitsubishi Tanabe Pharma Corporation. Advisory Panel; Self; Mitsubishi Tanabe Pharma Corporation. Research Support; Self; Daiichi Sankyo Company, Limited. Speaker's Bureau; Self; Daiichi Sankyo Company, Limited. Advisory Panel; Self; Daiichi Sankyo Company, Limited. Research Support; Self; Sanwa Kagaku Kenkyusho Co., Ltd.. Speaker's Bureau; Self; Sanwa Kagaku Kenkyusho Co., Ltd.. Research Support; Self; Novo Nordisk Inc.. Speaker's Bureau; Self; Novo Nordisk Inc.. Advisory Panel; Self; Novo Nordisk Inc.. Research Support; Self; Eli Lilly and Company. Speaker's Bureau; Self; Eli Lilly and Company. Advisory Panel; Self; Eli Lilly and Company. Research Support; Self; Sanofi. Speaker's Bureau; Self; Sanofi. Advisory Panel; Self; Sanofi. Research Support; Self; Sumitomo Dainippon Pharma Co., Ltd.. Speaker's Bureau; Self; Sumitomo Dainippon Pharma Co., Ltd.. Research Support; Self; Shionogi & Co., Ltd.. Speaker's Bureau; Self; Shionogi & Co., Ltd., Bayer Yakuhin, Ltd., Astellas Pharma US, Inc., AstraZeneca. Advisory Panel; Self; AstraZeneca, Teijin Pharma Limited. U.N. Osada: None.
To clarify the safe and effective conversion ratio from continuous intravenous insulin infusion (II) to subcutaneous long-acting insulin injection (SI) in diabetic ketoacidosis (DKA) or hyperosmolar hyper glycemic state (HHS), we conducted single center, retrospective, cohort study. Based on electronic medical records at our hospital from inception through September 2017, we extracted the subjects with DKA/HHS diagnosis. Other inclusion criteria were 1) no intermission between II and SI, 2) co-administered II and SI within 3 hours, and 3) aged ≥18 years old. We defined II requirement (IR) as the total II dose within 24 hours before conversion to SI. Then we divided subjects into 4 groups according to the percentage of SI to IR [group stratification: 0-39% (Q1), 40-69% (Q2), 70-89% (Q3), ≥90% (Q4)], and compared primary outcome which was the percentage achieving glycemic target of 80-180 mg/dl within 24 hours after the conversion. As the result, 44 subjects were included (male 52%, mean age 59 years old, mean HbA1c 11.6%, DKA 75%, median serous-CPR (CPR) 0.17 ng/ml). Median IR and the percentage of SI to IR were in inverse correlation; Q1=51 units (U), Q2=25.2U, Q3=27.2U, and Q4=7.1U (p=0.0001). In primary analysis, the median percentage achieving the glycemic target was highest with 67.5% in Q4, and was comparatively lower in the other groups; Q1=13.4% (p=0.01), Q2=16.7% (p=0.01), Q3=40% (p=0.089). In multivariate analysis adjusted with age, BMI, CPR and IR, ≥90% (β=14.6, SE=5.7, p=0.01) and ≥70% (β=9.1, SE=4.4, p=0.04) but not ≥40% were the significant factor to achieve the glycemic target. Hypoglycemia ≤70 mg/dl occurred only in 2% of entire subjects, and the incident rate were not different between the groups. In summary, our result indicated that at least 70% of the conversion ratio was required for the safe and effective conversion from SI to II in DKA/HHS. Disclosure H. Takamine: None. Y. Namiki: None. H. Hiiragi: None. T. Yamada: None. Y. Takano: None. U.N. Osada: None.
Background: Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a new class of antihyperglycemic drugs that enhances insulin-independent urinary glucose excretion. Recent studies have suggested that SGLT2 inhibitors possess a renoprotective property in type 2 diabetes patients. However, evidence of the effects of SGLT2 inhibition on glomerular and tubular damage markers is lacking. The aim of this study was to examine the effect of SGLT2 inhibitors on renal function, especially on glomerular and tubular damage markers in patients with type 2 diabetes. Methods:We retrospectively analyzed data from 81 patients who used SGLT2 inhibitors. Next, we investigated whether treatment with SGLT2 inhibitors affected urinary damage markers including N-acetyl-β-D-glucosaminidase (NAG), liver-type fatty acid-binding protein (L-FABP), type IV collagen, and β2-microglobulin (β2MG) in patients with type 2 diabetes. Results:In the retrospective study, SGLT2 inhibition reduced the estimated glomerular filtration rate (eGFR) at 4 and 12 weeks in a manner that was correlated with the baseline eGFR. In the longitudinal study, SGLT2 inhibition tended to increase the urinary damage marker levels with an accompanying decrease in eGFR after 1 month of use. The observed changes in eGFR and urinary damage markers were reversed at 3 months, even though both the HbA1c level and blood pressure were further improved. Conclusions:These results indicated that SGLT2 inhibition reduces the eGFR in a manner depending on the baseline eGFR levels and transiently increased the glomerular and tubular damage markers in patients with type 2 diabetes.
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