Low-intensity shockwave therapy (LiSWT) has emerged as a promising non-invasive treatment modality for erectile dysfunction (ED) yet the well-designed randomized clinical trials are still lacking to prove its claimed benefits. A randomized, prospective, double-blinded sham-controlled study was conducted to evaluate the effectiveness and safety profile of short course LiSWT on vasculogenic ED patients. The International Index of Erectile Function-5 (IIEF-5) and Erection Hardness Score (EHS) questionnaires were used for evaluation. Patients underwent weekly sessions for 4 weeks and were re-assessed at 1, 3 and 6 months post therapy. Fifty one patients were recruited and randomized into sham and treatment arms. The mean IIEF-5 scores were significantly improved in the treatment arm compared to worsening of scores in the sham arm after 1 month (14.1 vs. 9.3 p < 0.001), 3 months (14.9 vs. 8.6, p < 0.001) and 6 months (14.2 vs. 7.9, p < 0.001) post treatment. A significant improvement of EHS was demonstrated at 1 month (2.4 vs. 1.8, p = 0.001, 3 months 2.7 vs. 1.7, p < 0.001) and 6 months (2.7 vs. 1.6, p < 0.001) in the treatment arm compared to sham arm. The success rate based on IIEF score increment more than five points was 26% in treatment arm and 0% in sham arm. Improvement in EHS score ≥3 in the treatment versus sham arm was 63% and 4%, respectively.There was no adverse effect reported. This 4-week LiSWT protocol reflects better treatment compliance, and it prevents further deterioration of erectile function among this cohort of patients. This study proves that LiSWT is a well-tolerated treatment with modest improvements in erectile function and hardness, among patients with vasculogenic ED.

Background: Currently, comparison studies on glycaemic control by originator versus generic fixed-dose antidiabetic drugs are limited. Aim: This study assessed the efficacy, adherence and adverse effects between originator and generic fixed-dose glibenclamide/metformin after switching from gliclazide coadministered with metformin, and after interchanging the originator and generic fixed-dose tablets between the study groups. Methods: A prospective randomised cross-over study was conducted among type 2 diabetes mellitus patients treated with stable doses of at least 240 mg gliclazide plus 1000 mg metformin in the Out-Patient Clinic, Penang Hospital. Patients were randomised to receive either originator (Group A) or generic (Group B) glibenclamide/metformin 2.5/500 mg, two tablets twice daily for 12 weeks. After 12 weeks, Group A and Group B were switched to generic and originator, respectively, for another 12 weeks. HbA1c, pill count and hypoglycaemic episodes were measured at baseline and at 12 and 24 weeks. Results: The mean (AESD) age of the 84 patients in the study was 58.01 AE 7.87 years, and the median duration of diabetes was 10.00 years (interquartile range 7.00-16.75 years). Baseline characteristics were similar between the two groups. Mean HbA1c decreased significantly from 0 to 12 weeks in Groups A and B (À0.76% and À0.56%, respectively), but increased significantly from 12 to 24 weeks (+0.39% and +0.33%, respectively). There was no significant difference in the mean change in HbA1c between the two groups. Adherence improved significantly by 11% when patients were switched to fixed-dose glibenclamide/metformin regardless of whether it was originator or generic. There was no significant difference between originator and generic in the number of hypoglycaemic episodes (11 vs 32; p = 0.825) after switching to fixed-dose glibenclamide/metformin. Conclusion: Generic glibenclamide/metformin was therapeutically equivalent to its originator.

Background: Currently, there is limited documentation on adverse reactions associated with generic fixed-dose combination antidiabetic drugs. Aim: The aim of this study was to report the incidental finding of drowsiness associated with brand substitution of a fixed-dose glibenclamide/metformin combination tablet. Methods: A prospective cross-over study was conducted among 84 patients previously treated with a stable dose of 320 mg gliclazide coadministered with 2000 mg metformin. Patients were switched to two tablets twice daily of originator or generic fixeddose glibenclamide 2.5 mg/metformin 500 mg for 12 weeks. After 12 weeks, patients who received originator fixed-dose glibenclamide/metformin were switched to generic tablets, whereas patients who had received generic tablets were switched to originator tablets. Both groups were subsequently followed-up for another 12 weeks. Results: Six patients (7.14%) experienced drowsiness with generic fixed-dose glibenclamide/metformin but not with the originator tablets. The patients complained of being unable to perform normal activities unless they had a nap. Blood glucose levels during these symptoms in four of the patients were between 8.3 and 9.4 mmol/L. There were no significant changes in fasting plasma glucose (FPG) or HbA1c levels in any of the affected patients. One patient had a 9.3-mmol/L decrease in FPG, but the HbA1c was still within the normal range. Conclusion: The cases of drowsiness with generic fixed-dose glibenclamide/metformin were unlikely to be associated with hypoglycaemia.