Characteristics of Patients with Type 2 Diabetes Mellitus with Sodium-Glucose Cotransporter Protein-2...

This study aimed to investigate the pathogen distribution and drug resistance of sodium-glucose cotransporter protein-2 (SGLT-2) inhibitors in patients with urinary tract infection (UTI) during the treatment of type 2 diabetes mellitus (T2DM).

A retrospective study was conducted to collect clinical data from patients with T2DM who developed UTI during treatment with SGLT-2 inhibitors. Patients were admitted to the West China Tianfu hospital, Sichuan University between December 2023 and February 2025. Urine samples were used to analyse the distribution of pathogenic bacteria and antibiotic resistance rates.

A total of 233 patients, including 71 males (30.47%) and 162 females (69.53%), who met the inclusion and exclusion criteria were admitted. Sixty-one strains (26.18%) of Gram-positive bacteria and 167 strains (71.67%) of Gram-negative bacteria were detected. Five cases (2.15%) of fungi (Candida albicans) were recorded. The top two Gram-positive bacteria were Enterococcus faecalis (E. faecalis) (34.43%) and Enterococcus faecium (E. faecium) (22.95%), and the top two Gram-negative bacteria were Escherichia coli (E. coli) (79.04%) and Klebsiella pneumoniae (K. pneumoniae) (11.38%). Different pathogens were resistant to different types of antibiotics. The resistance rates of E. faecium to penicillin, gentamicin, ciprofloxacin, clindamycin, erythromycin and cotrimoxazole were significantly different from those of E. faecalis (p < 0.05). The resistance rates of E. coli to piperacillin/tazobactam, ceftriaxone, nitrofurantoin and ciprofloxacin were significantly different from those of K. pneumoniae (p < 0.05).

The distribution of pathogenic bacteria complicated by UTI in patients with T2DM treated with SGLT-2 inhibitors was dominated by Gram-negative bacteria such as E. coli, some Gram-positive bacteria, and a small number of fungi. Antibiotics should be used appropriately in this population because of the pharmacological mechanism of SGLT-2 inhibitors.