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Korean J Pancreas Biliary Tract > Volume 29(1):2024 > Article
케타민 유발 담관병증의 국내 첫 증례보고


케타민은 진단을 위한 시술과 수술에 사용하는 마취제이다. 하지만 해리성 마취를 일으키고 환각을 유발할 수 있어 유희적인 목적으로 남용되는 경향이 있다. 만성적인 케타민 사용은 케타민 유발 담관병증, 궤양성 방광염 등 많은 부작용을 일으킬 수 있다. 케타민 유발 담관병증은 1980년대부터 보고되었으며 대부분의 증례는 서구 국가와 남아시아에서 보고되었다. 이에 저자들은 국내에서 케타민 유발 담관병증이 발생한 증례를 처음으로 보고하고자 한다. 국내에서 유희적인 목적의 약물 남용이 증가하고 있는 점을 감안하여 젊은 환자에서 원인을 알 수 없는 담관염이 발생한다면 케타민 유발 담관병증을 감별 진단으로 고려해야 한다.


Ketamine is an anesthetic agent for diagnostic and surgical procedures. However, it can produce dissociative anesthesia and induce hallucinations. Therefore, it tends to be abused as a recreational drug. Chronic ketamine use can cause numerous adverse effects including ketamine-induced chlangiopathy and ulcerative cystitis. Ketamineinduced cholangiopathy has been reported since the 1980s and most cases were found in Western countries and South Asia. Here, we report the first case of ketamineinduced cholangiopathy in Korea. Owing to increasing recreational drug use among Koreans, ketamine-induced cholangiopathy should be considered in the differential diagnosis in young patients with cholangitis of unknown etiology.


Ketamine is an anesthetic agent used in medical care. However, it is also currently illegally abused in Korea. Ketamine-induced liver injury, including ketamine-induced cholangiopathy, has been reported since 1982 [1]. Awareness of these adverse effects will help treat patients with cholangitis of unknown cause. Herein, we present the first case report of ketamine-induced cholangiopathy in Korea.


A 26-year-old woman with a four-month history of recurrent abdominal pain, dysuria, urinary frequency, and gross hematuria presented to the emergency department for evaluation of diffuse abdominal pain. Abdominal examination showed no evidence of peritonitis but revealed tenderness in the epigastric area and lower abdomen regions. Liver function tests (LFTs) showed serum aspartate aminotransferase, 74 U/L; alanine aminotransferase levels of 251 U/L; alkaline phosphatase, 242 U/L; gamma-glutamyl transpeptidase 368 U/L, total bilirubin 0.6 mg/dL; and direct bilirubin, 0.13 mg/dL. Autoimmune antibody tests, including anti-nuclear antibody, anti-neutrophil cytoplasmic antibody, anti-mitochondria antibody, and anti-smoot muscle antibody, were negative. Serum IgG, IgG4, and complement component 3 and 4 (C3 and C4) were within normal ranges. Urinalysis showed straw-colored urine with white blood cells (5-9/high-power field [HPF]) and red blood cells (>50/HPF). Abdominopelvic computed tomography revealed common bile duct (CBD) wall thickening and a small capacity of the urinary bladder with severe wall thickening (Fig. 1A, B). Abdominal ultrasonography confirmed significant CBD wall thickening; however, no gallstones were detected (Fig. 1D). Magnetic resonance cholangiopancreatography revealed extrahepatic bile duct dilatation with hilar and intrahepatic bile duct (IHD) strictures (Fig. 2B). Endoscopic retrograde cholangiopancreatography (ERCP) performed the day following admission revealed IHD strictures and extrahepatic bile duct dilatation with irregular contour (Fig. 2A). The patient’s abdominal pain gradually improved after ERCP; however, lower urinary tract symptoms persisted. On the seventh day of hospitalization, a plastic bag containing white powder was discovered among the patient’s belongings. The substance was identified as ketamine, and she was admitted to a psychiatric hospital for drug addiction treatment. At follow-up, the patient had not experienced significant recurrent abdominal pain or elevated LFT.


Ketamine, N-methyl-D-aspartate (NMDA) receptor antagonist, was introduced in 1962. Ketamine infusions, which are used for surgical and endoscopic procedures, induce rapid anesthesia and a unique cataleptic state with amnesia and unresponsiveness [2,3]. However, it can also produce dissociative anesthesia, which causes feelings of detachment from reality and induces hallucinations. Oral ingestion results in hallucinogenic effects that may last up to 1-2 hours. Therefore, it tends to be abused by young adults as a popular “club drug” [3].
Chronic ketamine use can produce numerous adverse effects including abdominal pain, LFT elevation, bile duct abnormalities, lower urinary dysfunction [2,4-6]. The cholangiopathy is a chronic liver diseases associated with cholangiocyte [7]. And ketamineinduced cholangiopathy is a clinical diagnosis, in which a chronic ketamine user develops LFT elevation along with bile duct abnormalities [1,2,8,9]. Yu et al. [9] reported a fusiform dilatation of CBD with smooth distal tapering as the most common feature of bile duct abnormality in ketamine-induced cholangiopathy. Another common finding is CBD wall thickening with contrast enhancement [10], as well as hilar and IHD strictures [1,8]. However, the exact pathophysiology of ketamine-induced cholangiopathy remains unknown. Most plausible explanation is that ketamine affects activity of NMDA ionotropic receptors located on smooth muscle in the biliary tract [1,3,11]. A previous study has shown that activation these receptors induces contraction of the human ureter [11]. Based on this finding, it can be hypothesized that ketamine (a NMDA antagonist), may affect motility of the urinary and biliary tracts and, in chronic cases, lead to inflammation, fibrosis and strictures [1,3]. Ketamine is metabolized by the cytochrome P450 system in the liver and excreted in bile and urine [8]. Therefore, direct toxic injury to the surface epithelium is another hypothesis [8]. Ketamine-induced GB dyskinesia has also been suggested as an explanation for the pathophysiology of ketamine-induced cholangiopathy [3].
Lower urinary tract symptoms and ulcerative cystitis are other common adverse effects of chronic ketamine use [5,10]. The pathophysiology of ketamine-induced urinary tract dysfunction is thought to be similar to that of ketamine-induced cholangiopathy [3,8,11]. Hydronephrosis and shrunken bladder with diffuse wall thickening, which were present in this patient, are common radiologic finings of ketamine-induced ulcerative cystitis [6]. Wong et al. [5] found that 9.8% of patients with ketamine-associated urinary tract dysfunction had LFT elevation with a cholestatic pattern. Therefore, If a young patient with an unknown cause of cholangitis has lower urinary tract symptoms, chronic ketamine use should be considered.
Previous studies have reported that ketamine cessation usually leads to complete resolution of LFT elevation [3,4]. Additionally, in most cases, slow reversal of biliary stricture is also occurs [2]. Therefore, ketamine cessation is the main treatment option for ketamine-induced cholangiopathy. However, in some case reports, biliary stenting was necessary to relieve the obstruction [2,8].
Ketamine-induced cholangiopathy is mostly been reported in Western countries and South Asia [1,3,4,10]. This is the first case of ketamine-induced cholangiopathy to be reported in Korea. Owing to increasing recreational drug use among Koreans, a greater number of ketamine-induced adverse effects are expected to be reported in the future. Ketamine-induced cholangiopathy should be considered in the differential diagnosis in young patients with cholangitis of unknown etiology.


Conflict of Interest
The authors have no conflicts to disclose.


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Fig. 1.
(A) Coronal plane of abdominopelvic computed tomography showing common bile duct wall thickening (black arrow) and small capacity of urinary bladder with severe wall thickening (white arrow). (B) Axial plane of abdominopelvic computed tomography showing common bile duct wall thickening (black arrow). (C) Coronal plane of prior abdominopelvic computed tomography, which was taken 10 days ago, showing small capacity of urinary bladder with severe wall thickening (white arrow). (D) Abdominal ultrasonography showing marked wall thickening of common bile duct.
Fig. 2.
(A) Cholangiography demonstrating intrahepatic bile duct strictures and extrahepatic bile duct dilatation with irregular contour. (B) Magnetic resonance cholangiopancreatography showing extrahepatic bile duct dilatation with hilar and intrahepatic bile duct strictures.
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