98%
921
2 minutes
20
Aim: Some clinical trials have shown that sodium-glucose cotransporter-2 (SGLT2) inhibitors are associated with fracture risk. However, this notion remains controversial. This study aimed to evaluate hip fracture risk after the use of SGLT2 inhibitors while controlling for factors that may affect fracture risk. Furthermore, hip fracture risk is evaluated in relation to the SGLT2 inhibitors component and its concomitant use with other antidiabetic agents.
Methods: Using large-scale real-world data, this case-control study investigated hospitalized patients between January 2018 and December 2020. Patients were aged 65-89 years and had been prescribed with SGLT2 inhibitors at least twice. Patients with hip fracture (cases) and those without (controls) were identified via 1:3 matching according to sex, age (±3 years), hospital size classification, and number of concomitant antidiabetic agents. Exposure to SGLT2 inhibitors of the cases and controls was compared with the use of multivariate conditional logistic regression.
Results: After matching, 396 cases and 1081 controls were identified. The adjusted odds ratio for patients receiving treatment with SGLT2 inhibitors was 0.83 (95% confidence interval: 0.55-1.26), indicating no increase in hip fracture risk. Additionally, no increased risk was observed with respect to SGLT2 inhibitors by component or concomitant use with other antidiabetic agents.
Conclusion: Our study showed that SGLT2 inhibitors do not increase hip fractures in older patients. However, because the risk assessment of SGLT2 inhibitors by component and their concomitant use with other antidiabetic agents is based on a limited number of patients, it is important to interpret the results with caution. Geriatr Gerontol Int 2023; 23: 418-425.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1111/ggi.14591 | DOI Listing |
Int Immunopharmacol
September 2025
Clinical Pharmacy Department, School of Pharmacy, Newgiza University, Giza, Egypt. Electronic address:
Ulcerative colitis (UC) is a persistent inflammatory condition marked by the destruction of the intestinal mucosal barrier, infiltration of inflammatory cells, and ulceration. M1/M2 macrophage polarization plays an imperative function in the regulation of inflammation through the nuclear factor-kappa B (NFκB) signaling pathway and modulating microRNA-155 (miR-155). Recent studies have highlighted the anti-ulcerogenic and colo-protective properties of sodium-glucose co-transporter-2 (SGLT2) inhibitors.
View Article and Find Full Text PDFHeart Lung Circ
September 2025
Lifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, SA, Australia; Adelaide Medical School, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, SA, Australia; Department of Cardiology, Central Adelaide Local Health Network, Adelaide, SA,
Cardiovascular-kidney-metabolic (CKM) syndrome is a term that is increasingly used to describe interconnected conditions that lead to poor health outcomes, including cardiovascular disease, chronic kidney disease, type 2 diabetes, and obesity. Historically, there have been very few targeted pharmacotherapies available that have changed cardiovascular outcomes for people with CKM syndromes; however, over the past decade, new pharmacologic options have rapidly expanded, with strong evidence for cardiovascular and kidney protective benefits in CKM conditions. Of note, sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 receptor agonists have emerged as key therapeutic options and are now widely guideline-endorsed.
View Article and Find Full Text PDFCell Regen
September 2025
Institute of Physical Chemistry, Polish Academy of Sciences, Warsaw, Poland.
Diabetes mellitus is a common and serious metabolic disease globally, characterized by increased blood glucose levels. The major pathogenesis is the functional impairment of insulin-producing beta cells in the pancreas and the lack of insulin secretion. Although both type 1 and type 2 diabetes develop through distinct pathological mechanisms, they lead to the destruction and/or dysfunction of beta cells, resulting in inadequate beta cell mass to maintain normal blood glucose levels.
View Article and Find Full Text PDFHeart Lung Circ
September 2025
Centre of Excellence for Cardiometabolic Health, Fiona Stanley Hospital, Perth, WA, Australia; Department of Cardiology, Fiona Stanley Hospital, Perth, WA, Australia; Medical School, The University of Western Australia, Perth, WA, Australia; Harry Perkins Institute of Medical Research, Perth, WA, Au
Background: In patients with type 2 diabetes (T2D) and chronic kidney disease (CKD), sodium-glucose cotransporter 2 (SGLT2) inhibitors, semaglutide (glucagon-like peptide-1 [GLP-1] agonist), and finerenone (non-steroidal mineralocorticoid receptor antagonist) improve renal and cardiovascular outcomes. We assessed real-world prescribing of these drugs in patients with T2D and CKD.
Method: The ReDiCare project retrospectively identified patients with T2D and CKD admitted to an Australian hospital between January 2020 and September 2024 using International Statistical Classification of Diseases and Related Health Problems 10th Revision Australian Modification codes.
Diabetes Res Clin Pract
September 2025
Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy; Pollution and Cardiovascular Diseases Research Centre, University of Campania "Luigi Vanvitelli", Naples, Italy.
Background: Type-2-diabetes-mellitus (T2DM) impairs outcomes in patients undergoing cardiac-resynchronization-therapy-with-defibrillator (CRTd).While both sodium-glucose co-transporter 2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1RAs) have cardiovascular benefits, their combination impact in CRTd-treated T2DM patients remains unclear.
Methods: In this prospective multicenter observational study, 2,257 T2DM patients treated with CRTd were stratified into three groups: SGLT2i monotherapy (n 874), GLP-1RAs monotherapy (n 808), and combination therapy with GLP-1RAs/SGLT2i (n 575).