Background: Recent patents reveal that Soluplus® has proved to be a promising excipient that modulates dissolution characteristics of many active pharmaceutical ingredients (WO2016161995A1, WO2016169534A1 and WO2016165676A1).
Objective: Current article investigates stable solid solution of furosemide with Soluplus® to enhance the dissolution properties of the drug.
Method: Drug to carrier ratios to prepare solid dispersion were selected based on the phase solubility study. Solid dispersions of furosemide with Soluplus® were prepared by solvent evaporation and fusion methods. Physicochemical parameters were characterized using Fourier transform infra-red spectrophotometer, thermo- gravimetric analyzer, differential thermal analyzer, and scanning electron microscopy. Drug release from the formulations was compared using USP type II (paddle type) dissolution apparatus containing 900 mL of phosphate buffer (pH - 6.8) maintained at 37±0.5°C at a paddle rotation speed of 50rpm.
Results: Fourier transform infra-red spectroscopy confirmed absence of any chemical interaction while thermo-gravimetry and differential thermal analysis showed evidences of formation of a solid solution of furosemide. No furosemide crystals were observed under scanning electron microscope in case of solid dispersion. Dissolution data indicated that furosemide dissolution was enhanced to a great extent and drug to carrier ratio of 1:10 was found to be most suitable.
Conclusion: Solid dispersions prepared by fusion method exhibited faster drug release compared to those prepared by solvent evaporation.
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http://dx.doi.org/10.2174/1872211311666171129120020 | DOI Listing |
Clin Kidney J
January 2025
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Background: Knowledge of which medications may lead to acute kidney injury (AKI) is limited, relying mostly on spontaneous reporting in pharmacovigilance systems. We here conducted an exploratory drug-wide association study (DWAS) to screen for associations between dispensed drugs and AKI risk.
Methods: Using two large Danish and Swedish data linkages, we identified AKI hospitalizations occurring between April 1997 and December 2021 in Denmark and between March 2007 and December 2021 in Sweden.
J Hypertens
December 2024
University/British Heart Foundation Centre for Cardiovascular Science, The University of Edinburgh, Edinburgh, Scotland, UK.
Introduction: Hypertension is the leading preventable cause of cardiovascular morbidity and mortality globally, with a disproportionate impact on low-income and middle-income countries like Sri Lanka. Effective blood pressure (BP) control improves outcomes in patients with hypertension. This study aimed to assess the prevalence of uncontrolled hypertension, and its correlates among Sri Lankan patients with hypertension in clinic settings.
View Article and Find Full Text PDFPLoS One
January 2025
Genome and Structural Bioinformatics Group, Faculty of Medicine, Health and Life Science, Swansea University, Swansea, Wales, United Kingdom.
Aquaporin 1 (AQP1) is a key channel for water transport in peritoneal dialysis. Inhibition of AQP1 could therefore impair water transport during peritoneal dialysis. It is not known whether inhibition of AQP1 occurs unintentionally due to off-target interactions of administered medications.
View Article and Find Full Text PDFCrit Care Resusc
December 2024
Paediatric Intensive Care Unit, Royal Children's Hospital, Melbourne, VIC, Australia.
Objective: Frusemide is a common diuretic administered to critically ill children intravenously, by either continuous infusion (CI) or intermittent bolus (IB). We aim to describe the characteristics of children who receive intravenous frusemide, patterns of use, and incidence of acute kidney injury (AKI), and to investigate factors associated with commencing CI.
Design: Retrospective observational study.
Clin Pediatr Endocrinol
January 2025
Department of Pediatrics, Tohoku University Graduate School of Medicine, Sendai, Japan.
Idiopathic infantile hypercalcemia (IIH) is characterized by hypercalcemia, nephrocalcinosis, vomiting, dehydration, and failure to thrive. It is caused by the presence of biallelic loss-of-function variants in the locus. Although hypercalcemia has been linked to the consumption of vitamin D-fortified milk, no reports have documented its role in triggering IIH in patients with variants.
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