Qian JD, Hou FQ, Wang TL, Shao C, Wang GQ. Gilbert syndrome combined with prolonged jaundice caused by contrast agent: Case report. World J Gastroenterol 2018; 24(13): 1486-1490 [PMID: 29632429 DOI: 10.3748/wjg.v24.i13.1486]
Corresponding Author of This Article
Gui-Qiang Wang, MD, PhD, Professor, Department of Infectious Diseases and the Center for Liver Diseases, Peking University First Hospital, 8 Xishiku Dajie, Xicheng District, Beijing 100034, China. 04486@pkufh.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Case Report
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Apr 7, 2018; 24(13): 1486-1490 Published online Apr 7, 2018. doi: 10.3748/wjg.v24.i13.1486
Gilbert syndrome combined with prolonged jaundice caused by contrast agent: Case report
Jian-Dan Qian, Feng-Qin Hou, Tai-Ling Wang, Chen Shao, Gui-Qiang Wang
Jian-Dan Qian, Feng-Qin Hou, Gui-Qiang Wang, Department of Infectious Diseases and the Center for Liver Diseases, Peking University First Hospital, Beijing 100034, China
Tai-Ling Wang, Department of Pathology, China-Japan Friendship Hospital, Beijing 100029, China
Chen Shao, Department of Pathology, Beijing YouAn Hospital Capital Medical University, Beijing 100069, China
Gui-Qiang Wang, The Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, Hangzhou 310003, Zhejiang Province, China
Gui-Qiang Wang, Peking University International Hospital, Beijing 102206, China
Author contributions: Qian JD designed and wrote the report; Hou FQ reviewed the manuscript for its intellectual content and revised the entire work; Wang TL and Shao C performed the histological assessments and evaluations; Wang GQ reviewed the manuscript for its intellectual content.
Supported by National Natural Science Foundation of China, No. 81470849.
Informed consent statement: The patient involved in this study gave written informed consent authorizing the use and disclosure of his protected health information.
Conflict-of-interest statement: The authors of this manuscript have no conflicts of interest to disclose.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Gui-Qiang Wang, MD, PhD, Professor, Department of Infectious Diseases and the Center for Liver Diseases, Peking University First Hospital, 8 Xishiku Dajie, Xicheng District, Beijing 100034, China. 04486@pkufh.com
Received: January 19, 2018 Peer-review started: January 20, 2018 First decision: February 3, 2018 Revised: February 7, 2018 Accepted: February 26, 2018 Article in press: February 26, 2018 Published online: April 7, 2018 Processing time: 75 Days and 0.4 Hours
Abstract
This case highlights a patient with Gilbert syndrome who underwent endoscopic retrograde cholangiopancreatography (ERCP) with removal of bile duct stones, who then experienced an unexplained increase in bilirubin, with total bilirubin (TBIL) levels increasing from 159.5 μmol/L to 396.2 μmol/L and to a maximum of 502.8 μmol/L after 9 d. Following the decrease in the TBIL level, enhanced magnetic resonance cholangiopancreatography (MRCP) was performed to exclude any possible remaining choledocholithiasis. Nevertheless, the serum bilirubin level increased again, with TBIL levels rising from 455.7 μmol/L to 594.8 μmol/L and a maximum level of 660.3 μmol/L with no remaining bile duct stones. A liver biopsy showed severe bile duct cholestasis with no inflammation. Based on the exclusion of other potential causes of hyperbilirubinemia and the fact that both instances of increased bilirubin occurred after ERCP and MRCP, the contrast agents iopromide and gadoterate meglumine were suspected to be the causes of the hyperbilirubinemia. As of the writing of this report, the patient’s bilirubin levels have spontaneously returned to baseline levels. In summary, ERCP and MRCP utilizing the contrast agents iopromide and gadoterate meglumine may possibly induce prolonged hyperbilirubinemia.
Core tip: Over the past years, only few cases of prolonged postendoscopic retrograde cholangiopancreatography jaundice caused by toxicity of the contrast agent iobitridol have been reported in the world. Up to now, no case of postenhanced magnetic resonance cholangiopancreatography-related jaundice has been reported. Persistent jaundice affects the patient’s quality of life, even seriously to life-threatening. Because of the high rarity, treatment experience is not sufficient and more cases need to be accumulated for further analysis.
