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 investi...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 asso-ciated 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.展开更多
Background:Wernicke encephalopathy is caused by thiamine(vitamin B1)defi ciency.It is generally considered to be a disease of adult alcoholics.However,it is known to occur in the pediatric population and in non-alcoho...Background:Wernicke encephalopathy is caused by thiamine(vitamin B1)defi ciency.It is generally considered to be a disease of adult alcoholics.However,it is known to occur in the pediatric population and in non-alcoholic conditions.Data sources:We searched PubMed with the key words Wernicke,thiamine,pediatric,children and adolescents and selected publications that were deemed appropriate.Results:The global prevalence rates of hunger,poverty and resultant nutrient deprivation have decreased in the 21st century.However,several scenarios which may predispose to Wernicke encephalopathy may be increasingly prevalent in children and adolescents such as malignancies,intensive care unit stays and surgical procedures for the treatment of obesity.Other predisposing conditions include magnesium defi ciency and defects in the SLC19A3 gene causing thiamine transporter-2 deficiency.The classic triad consists of encephalopathy,oculomotor dysfunction and gait ataxia but is not seen in a majority of patients.Treatment should be instituted immediately when the diagnosis is suspected clinically without waiting for laboratory confi rmation.Common magnetic resonance findings include symmetric T2 hyperintensities in dorsal medial thalamus,mammillary bodies,periaqueductal gray matter,and tectal plate.Conclusions:Wernicke encephalopathy is a medical emergency.Delay in its recognition and treatment may lead to significant morbidity,irreversible neurological damage or even death.This article aims to raise the awareness of this condition among pediatricians.展开更多
基金approved by Jiangxi Provincial People’s Hospital and First Affiliated Hospital,Zhejiang University School of Medicine(2022068 and 2022370).Written informed consent was obtained from all participants.
文摘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 asso-ciated 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.
基金Funding:The authors report receipt of no financial support for the research and/or authorship of this article
文摘Background:Wernicke encephalopathy is caused by thiamine(vitamin B1)defi ciency.It is generally considered to be a disease of adult alcoholics.However,it is known to occur in the pediatric population and in non-alcoholic conditions.Data sources:We searched PubMed with the key words Wernicke,thiamine,pediatric,children and adolescents and selected publications that were deemed appropriate.Results:The global prevalence rates of hunger,poverty and resultant nutrient deprivation have decreased in the 21st century.However,several scenarios which may predispose to Wernicke encephalopathy may be increasingly prevalent in children and adolescents such as malignancies,intensive care unit stays and surgical procedures for the treatment of obesity.Other predisposing conditions include magnesium defi ciency and defects in the SLC19A3 gene causing thiamine transporter-2 deficiency.The classic triad consists of encephalopathy,oculomotor dysfunction and gait ataxia but is not seen in a majority of patients.Treatment should be instituted immediately when the diagnosis is suspected clinically without waiting for laboratory confi rmation.Common magnetic resonance findings include symmetric T2 hyperintensities in dorsal medial thalamus,mammillary bodies,periaqueductal gray matter,and tectal plate.Conclusions:Wernicke encephalopathy is a medical emergency.Delay in its recognition and treatment may lead to significant morbidity,irreversible neurological damage or even death.This article aims to raise the awareness of this condition among pediatricians.
