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Clinical analysis of Wernicke encephalopathy after liver transplantation |
Li-Min Ding a , b , c , d , # , Li-Shan Deng e , # , Jun-Jie Qian a , b , c , d , Gang Liu f , Lin Zhou b , c , d , g , Shu-Sen Zheng a , b , c , d , g , ∗ |
a Division of Hepatobiliary Pancreatic Surgery, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
b NHFPC Key Laboratory of Combined Multi-organ Transplantation, Hangzhou 310003, China
c Key Laboratory of the Diagnosis and Treatment of Organ Transplantation, Chinese Academy of Medical Sciences, Hangzhou 310003, China
d Key Laboratory of Organ Transplantation, Research Center for Diagnosis and Treatment of Hepatobiliary Diseases, Hangzhou 310003, China
e Culture and Sports Center for the Disabled of Jiangxi Province, Nanchang 330000, China
f Department of Transplantation, Jiangxi Provincial People’s Hospital, Nanchang 330000, China
g Collaborative Innovation Center for Diagnosis Treatment of Infectious Diseases, Hangzhou 310003, China
∗Corresponding author at: Division of Hepatobiliary Pancreatic Surgery, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
E-mail address: shusenzheng@zju.edu.cn (S.-S. Zheng).
# Contributed equally. |
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Abstract Background: Wernicke encephalopathy (WE) is an acute neurological disease resulting from vitamin B1 deficiency, and there are only very few case reports of WE after liver transplantation. The present study aimed to investigate the clinical characteristics, etiology, magnetic resonance imaging (MRI) features, treatment and prognosis of patients with WE after liver transplantation.
Methods: Twenty-three patients with WE after liver transplantation from the First Affiliated Hospital, Zhejiang University School of Medicine and Jiangxi Provincial People’s Hospital between January 2011 and December 2021 were retrospectively analyzed.
Results: Among the 23 patients diagnosed with WE after liver transplantation, 6 (26%) had a classic triad of impaired consciousness, oculomotor palsy and ataxia, and 17 (74%) had two features. The misdiagno- sis rate was 65%. After treatment with high-dose vitamin B1, 19 (83%) patients showed improvement, whereas 4 (17%) showed no improvement, including 3 with residual short-term memory impairments and 1 with residual spatial and temporal disorientation and ataxia.
Conclusions: The misdiagnosis rate is high in the early stage of WE, and the prognosis is closely associated with whether WE is diagnosed early and treated timely. High-dose glucose or glucocorticoids can trigger WE and cannot be administered before vitamin B1 treatment. Vitamin B1 is suggested to be used as a prophylactic treatment for patients with WE after liver transplantation.
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