Molecular Pathophysiology and Potential Therapeutic Strategies of Ketamine-Related Cystitis

SIMPLE SUMMARY: Ketamine, an N-Methyl-D-aspartate receptor antagonist, acts as a quick-acting and general anesthetic for human and animal anesthesia. In recent years, ketamine has been widely abused among young people and commonly abused in combination with other drugs. Continued use of ketamine will damage mental status and cognitive function. Some abusers will suffer from ketamine-related cystitis (KC) and experienced severe lower urinary tract symptoms, such as frequent urination, hematuria, urinary incontinency, and bladder pain. The etiology of KC is still uncertain and therefore no definite treatment has been established. This review article focuses on current evidence of molecular pathophysiology and possible therapies for KC. ABSTRACT: Ketamine was first synthesized as a clinical medicine for anesthesia in 1970. It has been used as a recreational drug because of its low cost and hallucination effect in the past decade. Part of ketamine abusers may experience ketamine-related cystitis (KC) and suffer from lower urinary tract symptoms, including urinary frequency, urgency, and severe bladder pain. As the disease progression, a contracted bladder, petechial hemorrhage of the bladder mucosa, and ureteral stricture with hydronephrosis may occur. The pathophysiology of KC is still uncertain, although several hypotheses have been raised. Cessation of ketamine abuse is critical for the management of KC to prevent progressive disease, and effective treatment has not been established. Research has provided some theoretical bases for developing in vitro experiments, animal models, and clinical trials. This review summarized evidence of molecular mechanisms of KC and potential treatment strategies for KC. Further basic and clinical studies will help us better understand the mechanism and develop an effective treatment for KC.