BackgroundHypertension is the prime risk factor for stroke, and primary aldosteronism (PA) is the most common cause of secondary hypertension. The prevalence of PA in stroke patients has never been reported. The aim of this study was to elucidate the prevalence of PA.MethodsA total of 427 consecutive patients with acute stroke were prospectively enrolled for this study. The screening tests were performed at the initial visit and a week after admission by measuring plasma aldosterone concentration and plasma renin activity. The rapid adrenocorticotropic hormone (ACTH) test was performed as the confirmatory test when both screening tests were positive. The primary endpoint was a final diagnosis of PA.ResultsThe sensitivity of the dual screening system for the diagnosis of PA was 88.2 %, and PA was finally diagnosed in 4.0 % of acute stroke patients and in 4.9 % of stroke patients with a history of hypertension. Patients with PA were less likely to be male and have diabetes, and they had higher blood pressure at the initial visit, lower potassium concentration, and more intracerebral hemorrhage. The rapid ACTH test was performed safely even in acute stroke patients.ConclusionsThe prevalence of PA is not low among acute stroke patients. Efficient screening of PA should be performed particularly for patients with risk factors.Trial registrationUMIN-CTR; UMIN000011021. Trial registration date: June 23, 2013 (retrospectively registered).
Aims/Introduction Liraglutide and empagliflozin suppress cardiovascular events. However, reports on their long‐term combined use with insulin therapy or direct comparisons of these drugs are limited. Materials and Methods This open‐label, parallel‐group, randomized controlled trial compared the effects of liraglutide and empagliflozin combined with insulin therapy in type 2 diabetes patients . Adult type 2 diabetes outpatients undergoing stable insulin therapy with glycated hemoglobin levels of 7.0–9.5% were enrolled. Participants received 0.9 mg/day liraglutide or 10 mg/day empagliflozin for 24 weeks. The primary end‐point was the change in glycated hemoglobin levels from week 0 to 24. Body composition was assessed by dual‐energy X‐ray absorptiometry. Results A total of 64 insulin‐treated patients were randomized to receive liraglutide or empagliflozin. We analyzed 61 patients (30 liraglutide and 31 empagliflozin) who could be followed up. Liraglutide induced greater changes in glycated hemoglobin and glycated albumin than empagliflozin (glycated hemoglobin −1.24 ± 0.15% vs −0.35 ± 0.11%, P < 0.0001; glycated albumin −4.4 ± 0.6% vs −2.4 ± 0.5%, P < 0.01). Bodyweight (−1.3 ± 0.4 kg vs −1.5 ± 0.3 kg, P = 0.69) or body fat mass/lean tissue mass; urinary albumin excretion (median −5.3 mg/g‐creatinine [interquartile range −60.6, 9.9 mg/g‐creatinine] vs −12.9 mg/g‐creatinine [interquartile range −70.8, −2.0 mg/g‐creatinine], P = 0.23); and frequency of hypoglycemia did not differ significantly between the groups over a period of 24 weeks. There were no cases of study discontinuation owing to adverse effects. Conclusions Liraglutide addition to ongoing insulin therapy more effectively reduced glycated hemoglobin and glycated albumin levels than empagliflozin in patients with inadequately controlled type 2 diabetes.
Liraglutide (Lira) and empagliflozin (Empa) have been reported to suppress cardiovascular events in large-scale clinical trials. However, reports of their long-term combined use with insulin therapy or direct comparisons of both drugs are limited. This open-label, parallel-group, randomized controlled trial aimed to compare the effects of Lira and Empa used in combination with insulin therapy in patients with type 2 diabetes (T2D). Adult outpatients with T2D undergoing stable insulin therapy with HbA1c level of 7.0%-9.5% were eligible for participation. Subjects received 0.9 mg/day Lira or 10 mg/day Empa for 24 weeks. The primary endpoint was the change in HbA1c levels from baseline to week 24. Body composition was assessed using the dual energy X-ray absorptiometry method (UMIN-CTR 000027614). Overall, 66 insulin-treated patients with T2D were randomized to receive Lira or Empa; 57 patients completed 24 weeks of weekly administration of Lira (n = 29) or Empa (n = 28). HbA1c and glycated albumin (GA) levels were lower in the Lira group than in the Empa group (HbA1c, Lira, −1.23 ± 0.85% vs. Empa, −0.32 ± 0.68%, p < 0.001; GA, Lira, −4.3 ± 3.1% vs. Empa, −2.2 ± 2.9%, p = 0.01). There was no difference between the two groups in terms of change in body weight (∆BW: Lira, −1.4 ± 1.9 kg vs. Empa, −1.4 ± 1.9 kg, p = 0.97) or in body fat mass/lean tissue mass. There was no difference between the groups in terms of change in urinary albumin excretion [∆UAE (median, IQR): Lira, −6.2 (−63.5, −10.1) mg/g-creatinine vs. Empa, −20.4 (−69.7, −2.0) mg/g-creatinine, p = 0.28]. There was no significant difference in the frequency of hypoglycemia between the groups over 24 weeks (p = 0.46). In conclusion, the addition of Lira to ongoing insulin therapy significantly reduced HbA1c and GA levels to a larger extent than the addition of Empa in patients with inadequately controlled T2D. Disclosure H. Nakaguchi: None. Y. Kondo: None. Y. Terauchi: Advisory Panel; Self; AstraZeneca, Daiichi Sankyo Company, Limited, Eli Lilly and Company, Merck Sharp & Dohme Corp., Mitsubishi Tanabe Pharma Corporation, Novo Nordisk A/S, Sanofi. Research Support; Self; Daiichi Sankyo Company, Limited, Eli Lilly and Company, Merck Sharp & Dohme Corp., Novartis Pharmaceuticals Corporation, Novo Nordisk A/S, Ono Pharmaceutical Co., Ltd., Sanofi, Shionogi & Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd. Speaker's Bureau; Self; Astellas Pharma Inc., AstraZeneca, Bayer Yakuhin, Ltd., Daiichi Sankyo Company, Limited, Eli Lilly and Company, Merck Sharp & Dohme Corp., Mitsubishi Tanabe Pharma Corporation, Novartis Pharmaceuticals Corporation, Novo Nordisk A/S, Ono Pharmaceutical Co., Ltd., Sanofi, Sanwa Kagaku Kenkyusho, Shionogi & Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd.
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