Ketamine-Induced Cholangiopathy With Concomitant Hemorrhagic Cystitis: An Emerging and Underrecognized Cause of Cholestasis.
Kamran Nazir, Waqas Ahmed, Salman Rafi, Adeel Ahmad, Asim Khaleeq
Cureus December 1, 2025 DOI: 10.7759/cureus.99972 via PubMed
Summary
AI-generated from the abstractChronic ketamine use can damage both the liver and urinary tract. A 55-year-old woman with recurrent hemorrhagic cystitis and long-term recreational ketamine use had abnormal liver enzymes without symptoms. Imaging showed fatty liver and a beaded pattern of bile duct narrowing, while tests ruled out autoimmune or infectious causes. Bladder biopsy confirmed ketamine-induced cystitis. After stopping ketamine, her liver enzymes improved. This case illustrates that ketamine toxicity can cause cholangiopathy alongside cystitis, an emerging cause of cholestasis and urinary injury.
Study at a glance
| Characteristics | Case study Case report Peer reviewed |
|---|---|
| Sample size | 1 |
| Population | 55-year-old female with recurrent hemorrhagic cystitis and chronic ketamine use |
| Intervention | cessation of ketamine use |
| Keywords | Biliary stricture Hepatobiliary complication Ketamine-induced cholangiopathy Ketamine-induced cystitis Recurrent hemorrhagic cystitis |
| Key finding | Ketamine-induced cholangiopathy with biliary stricturing and concurrent hemorrhagic cystitis improved biochemically after cessation of ketamine use. |
Abstract
Ketamine-induced cholangiopathy (KIC) is a rare but increasingly recognized manifestation of chronic ketamine toxicity, often accompanied by urinary tract injury such as hemorrhagic cystitis. We report the case of a 55-year-old female with recurrent hemorrhagic cystitis and a long-standing history of intermittent recreational ketamine use who presented with asymptomatic cholestatic liver enzyme abnormalities. Hepatobiliary ultrasound revealed hepatic steatosis without ductal dilatation, and magnetic resonance cholangiopancreatography demonstrated multifocal biliary stricturing with a beaded appearance of the intrahepatic bile ducts. Serological testing for autoimmune and infectious etiologies was negative. Cystoscopy revealed inflammatory bladder changes, and histopathology confirmed ketamine-induced hemorrhagic cystitis. Following cessation of ketamine use, the patient demonstrated biochemical improvement. This case emphasizes the multisystem toxic potential of ketamine, highlighting the importance of recognizing KIC with concomitant hemorrhagic cystitis as an emerging cause of cholestasis and urinary tract injury.