Published online Oct 27, 2019. doi: 10.4254/wjh.v11.i10.719
Peer-review started: July 24, 2019
First decision: August 7, 2019
Revised: August 20, 2019
Accepted: October 2, 2019
Article in press: October 2, 2019
Published online: October 27, 2019
Processing time: 94 Days and 19.7 Hours
Depression is a growing public health problem that affects over 350 million people globally and accounts for approximately 7.5% of healthy years lost due to disability. Escitalopram, one of the first-line medications for the treatment of depression, is a selective serotonin reuptake inhibitor and one of the most commonly prescribed antidepressant medications worldwide. Although thought to be generally safe and with minimal drug-drug interactions, we herein present an unusual case of cholestatic liver injury, likely secondary to escitalopram initiation.
A 56-year-old Chinese lady presented with fever and cholestatic liver injury two weeks after initiation of escitalopram for the treatment of psychotic depression. Physical examination was unremarkable. Further investigations, including a computed tomography scan of the abdomen and pelvis and tests for hepatitis A, B and C and for autoimmune liver disease were unyielding. Hence, a diagnosis of escitalopram-induced liver injury was made. Upon stopping escitalopram, repeat liver function tests showed downtrending liver enzymes with eventual normalization of serum aspartate aminotransferase and alanine aminotransferase one-week post-discharge.
Clinicians should be aware of the possibility of escitalopram-induced liver injury when initiating depressed patients on antidepressant treatment. This requires extra vigilance as most patients may remain asymptomatic. Measurement of liver function tests could be considered after initiation of antidepressant treatment, especially in patients with pre-existing liver disease.
Core tip: We herein report a probable case of escitalopram-induced liver injury. A 56-year-old Chinese lady presented with fever and cholestatic liver injury two weeks after initiation of escitalopram for the treatment of psychotic depression. Physical examination and investigations for stones, viral hepatitis and autoimmune liver disease were unyielding. Upon stopping escitalopram, repeat liver function tests showed downtrending liver enzymes with eventual normalization of serum aminotransferase levels. Clinicians should be aware of the possibility of drug-induced liver injury associated with escitalopram use, when initiating depressed patients on antidepressant treatment. This requires extra vigilance as most patients may remain asymptomatic.