Genital yeast infections are increased with this class of medication due to the increased urinary glucose excretion:

Rationale: A. DPP4 inhibitors, such as sitagliptin, work by increasing the concentrations of incretin hormones, which stimulate insulin release and decrease glucagon levels. They do not utilize the renal pathway for glucose clearance and do not alter the carbohydrate concentration of the urine. Consequently, they are not associated with an increased risk of mycotic infections in the genitourinary tract. B. GLP-1 receptor agonists are injectable incretin mimetics that delay gastric emptying and enhance glucose-dependent insulin secretion. Their primary mechanism of action is systemic and gastrointestinal rather than renal-specific. Since they do not promote the excretion of glucose through the kidneys, they do not create the sugary environment required for fungal overgrowth in the genital region. C. Sulfonylureas function by directly stimulating the beta cells of the pancreas to secrete more insulin into the bloodstream. While effective at lowering systemic blood glucose, they do not induce glycosuria as a primary therapeutic mechanism. Therefore, patients taking these medications do not experience the local perineal glucose elevations that predispose individuals to vulvovaginal or balanitis infections. D. SGLT 2 inhibitors, such as canagliflozin, selectively inhibit the sodium-glucose co-transporter in the proximal convoluted tubule to prevent glucose reabsorption. This mechanism results in significant glycosuria, where excess glucose is eliminated through the urine. The resulting high glucose concentration in the urogenital tract provides a nutrient-rich substrate for Candida albicans, significantly increasing the risk of genital yeast infections.