Therapeutic dilemma: alcohol withdrawal syndrome and concurrent hepatic encephalopathy. A case report

Lopez, Alejandra E; Chavarría, Roberto; Oviedo, Gabriel

doi:10.1016/j.rcpeng.2019.10.002

Cited by 3 publications

(1 citation statement)

References 11 publications

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“…Administration of haloperidol sufficiently controls delirium, agitation, and epileptic seizures in patients with HE. 105 The protective effect of clozapine on HE is still debated. Previous studies have reported hepatotoxic effects for clozapine.…”

Section: Discussionmentioning

confidence: 99%

New Insight Into Mechanisms of Hepatic Encephalopathy: An Integrative Analysis Approach to Identify Molecular Markers and Therapeutic Targets

Sepehrinezhad

Shahbazi

Negah

et al. 2023

Bioinform Biol Insights

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Hepatic encephalopathy (HE) is a set of complex neurological complications that arise from advanced liver disease. The precise molecular and cellular mechanism of HE is not fully understood. Differentially expressed genes (DEGs) from microarray technologies are powerful approaches to obtain new insight into the pathophysiology of HE. We analyzed microarray data sets of cirrhotic patients with HE from Gene Expression Omnibus to identify DEGs in postmortem cerebral tissues. Consequently, we uploaded significant DEGs into the STRING to specify protein-protein interactions. Cytoscape was used to reconstruct the genetic network and identify hub genes. Target genes were uploaded to different databases to perform comprehensive enrichment analysis and repurpose new therapeutic options for HE. A total of 457 DEGs were identified in 2 data sets totally from 12 cirrhotic patients with HE compared with 12 healthy subjects. We found that 274 genes were upregulated and 183 genes were downregulated. Network analyses on significant DEGs indicated 12 hub genes associated with HE. Enrichment analysis identified fatty acid beta-oxidation, cerebral organic acidurias, and regulation of actin cytoskeleton as main involved pathways associated with upregulated genes; serotonin receptor 2 and ELK-SRF/GATA4 signaling, GPCRs, class A rhodopsin-like, and p38 MAPK signaling pathway were related to downregulated genes. Finally, we predicted 39 probable effective drugs/agents for HE. This study not only confirms main important involved mechanisms of HE but also reveals some yet unknown activated molecular and cellular pathways in human HE. In addition, new targets were identified that could be of value in the future study of HE.

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Section: Discussionmentioning

confidence: 99%

New Insight Into Mechanisms of Hepatic Encephalopathy: An Integrative Analysis Approach to Identify Molecular Markers and Therapeutic Targets

Sepehrinezhad

Shahbazi

Negah

et al. 2023

Bioinform Biol Insights

View full text Add to dashboard Cite

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Lorazepam

2021

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Hyperammonaemia and aggravation of underlying hepatic encephalopathy: case reportA 72-year-old man developed hyperammonaemia and aggravation of underlying hepatic encephalopathy during treatment with lorazepam for alcohol withdrawal syndrome.The man had liver cirrhosis, recurrent hepatic encephalopathy, oesophageal varicose veins, small fungal varicose veins, diastolic dysfunction type I and mild mitral insufficiency. He was receiving spironolactone [spirinolactone], lactulose and thiamine. He had a pattern of chronic alcohol consumption. He was hospitalised. Upon admission, he was diagnosed with Grade III hepatic encephalopathy. Alcohol withdrawal syndrome was suspected. He was found to have hyponatraemia that increased the degree of drowsiness. He was treated with lactulose and rifaximin [rhyphaximine]. Following diagnosis of alcohol withdrawal syndrome, he started receiving oral lorazepam 1mg every 12 hours. However, on day 4, he demonstrated inattention, marked fluctuations in consciousness state, multisensory hallucinations, reversal of the wakefulness-sleep pattern along with neurovegetative instability. He was diagnosed with acute confusion syndrome. After 6 days of lorazepam treatment, he demonstrated predominantly psychomotor inhibition and lethargy. Signs such as slapping were observed on the physical exam (flapping). Laboratory investigation revealed elevated serum ammonia level and aggravation of liver function tests. He also developed health careassociated pneumonia, which was treated with piperacillin/tazobactam. EEG showed a slow wave pattern, with predominant beta rhythm and few delta and theta waves. Based on clinical presentation and investigational findings, he was diagnosed with hyperammonaemia and aggravation of underlying hepatic encephalopathy secondary to lorazepam [not all time to reaction onsets clearly stated].Lorazepam dose was reduced to 0.5mg every 12 hours. The man was treated with thiamine. Six days later, marked drowsiness and little alertness was observed. Lorazepam was switched to haloperidol. The replacement led to an improvement in his confusional picture. His mental state progressively improved. However, he developed various unspecified complications due to pneumonia, as well as liver failure which caused his death [not all outcomes stated].

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Management of Alcohol Withdrawal Syndrome in Patients with Alcoholic Liver Disease

Chand

Panda

Mahadevan

et al. 2022

Journal of Clinical and Experimental Hepatology

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Therapeutic dilemma: alcohol withdrawal syndrome and concurrent hepatic encephalopathy. A case report

Cited by 3 publications

References 11 publications

New Insight Into Mechanisms of Hepatic Encephalopathy: An Integrative Analysis Approach to Identify Molecular Markers and Therapeutic Targets

New Insight Into Mechanisms of Hepatic Encephalopathy: An Integrative Analysis Approach to Identify Molecular Markers and Therapeutic Targets

Lorazepam

Management of Alcohol Withdrawal Syndrome in Patients with Alcoholic Liver Disease

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