Assessment of low-grade hepatic encephalopathy: A critical analysis

Kircheis, G.; Fleig, Wolfgang E.; Görtelmeyer, Roman; Grafe, Susanne; Häussinger, Dieter

doi:10.1016/j.jhep.2007.05.019

Cited by 61 publications

(41 citation statements)

References 33 publications

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“…This condition has been termed minimal HE (mHE);2 16 however, so far, no standardisation for the diagnosis of mHE has been achieved. Routinely used paper–pencil test batteries suffer from training and education effects and may exhibit low sensitivity 5 17 18. The problems in assessing the severity of mild HE also became apparent in a recent re-evaluation of a clinical trial,18 which showed that about 30% of paper–pencil tests were performed invalidly and that clinical assessment of patients with HE 0–II yielded 30–50% misgradations.…”

Section: Assessment Of the Severity Of Hepatic Encephalopathymentioning

confidence: 99%

“…Routinely used paper–pencil test batteries suffer from training and education effects and may exhibit low sensitivity 5 17 18. The problems in assessing the severity of mild HE also became apparent in a recent re-evaluation of a clinical trial,18 which showed that about 30% of paper–pencil tests were performed invalidly and that clinical assessment of patients with HE 0–II yielded 30–50% misgradations. In view of this, a new description for the severity of HE in patients with cirrhosis has been proposed recently, which discriminates “low-grade HE” from “high-grade HE” only.…”

Section: Assessment Of the Severity Of Hepatic Encephalopathymentioning

confidence: 99%

“…Single paper–pencil test are insufficient to detect or rule out mHE; test batteries such as the psychometric hepatic encephalopathy score (PHES) test are preferred18…”

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confidence: 99%

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Pathogenetic mechanisms of hepatic encephalopathy

Häussinger

Schliess

2008

Gut

335

229

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Hepatic encephalopathy (HE) in liver cirrhosis is a clinical manifestation of a low-grade cerebral oedema, which is exacerbated in response to ammonia and other precipitating factors. This low-grade cerebral oedema is accompanied by an increased production of reactive oxygen and nitrogen oxide species (ROS/RNOS), which trigger multiple protein and RNA modifications, thereby affecting brain function. The action of ammonia, inflammatory cytokines, benzodiazepines and hyponatraemia integrates at the level of astrocyte swelling and oxidative stress. This explains why heterogenous clinical conditions can precipitate HE episodes. Oxidised RNA species, which are formed in response to oxidative stress, also participate in local postsynaptic protein synthesis in neurons, which is required for memory formation. Although the functional consequences of RNA oxidation in this context remain to be established, these findings bear a potential biochemical explanation for the multiple alterations of neurotransmitter receptor systems and of synaptic plasticity. Such changes may in part also underlie the pathologically altered oscillatory networks in the brain of HE patients in vivo, as detected by magnetencephalography. These disturbances of oscillatory networks, which in part are triggered by hypothalamic structures, can explain the motor and cognitive deficits in patients with HE. Current therapeutic strategies aim at the elimination of precipitating factors. The potential of therapies targeting downstream pathophysiological events in HE has not yet been explored, but offers novel potential sites of therapeutic intervention.

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Section: Assessment Of the Severity Of Hepatic Encephalopathymentioning

confidence: 99%

Section: Assessment Of the Severity Of Hepatic Encephalopathymentioning

confidence: 99%

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Pathogenetic mechanisms of hepatic encephalopathy

Häussinger

Schliess

2008

Gut

335

229

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“…According to the 2014 joint AASLD/EASL guidelines, HE is defined as a brain dysfunction caused by liver insufficiency and/or portosystemic shunt and manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subclinical alterations (occult or minimal HE) to coma. The West Haven Criteria are applied for clinical grading, but this approach is hampered by a broad interobserver variability [1][2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Long-Term Effect of Rifaximin with and without Lactulose on the Active Bacterial Assemblages in the Proximal Small Bowel and Faeces in Patients with Minimal Hepatic Encephalopathy

Schulz

Schütte

Vílchez-Vargas

et al. 2018

Dig Dis

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Background: Gut microbiota play an essential role in the pathogenesis of hepatic encephalopathy (HE). Treatment strategies are directed to modulate intestinal microbiota profiles and their function by the administration of the non-absorbable disaccharide lactulose and the non-absorbable antibiotic rifaximin, which are required for long terms, but little is known on their long-term effect on gut microbiota composition and function. Aim: To characterize the active bacterial assemblages in duodenum and faeces in patients with minimal HE (MHE) before, during and after long-term therapy with rifaximin. Methods: We analysed the microbiota composition in 5 patients with liver cirrhosis and MHE treated either with rifaximin 550 mg bid alone continuously for a period of 3 months or combined with lactulose 30–60 mL daily for 3 months. In addition to clinical assessments of HE, biopsies from duodenum and stool samples were analysed for their specific bacterial community applying NGS after RNA isolation before treatment, after 3 months of treatment and 3 months after the end of treatment. Results: All 5 patients had a significant improvement of their MHE. Bacterial communities were different and distinct in duodenal samples and faeces. No statistically significant changes were found in the bacterial community profile at the different time points. Conclusion: Rifaximin therapy with and without lactulose over a period of 3 months does not affect the bacterial community composition. The improvement of HE with rifaximin is lasting also after the end of treatment and therefore a prolonged effect on microbiota metabolic function is suggested.

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“…Kircheis et al performed a placebo-controlled, clinical multicenter trial with 217 cirrhosis patients, to study the discrepancy in the expected and observed severity of HE. 12 The study revealed that up to 50% of the patients were wrongly allocated with regard to HE severity because of the difficulty in differentiating mild OHE from mHE. Moreover, mistakes were made in analyzing and scoring the results of PHES.…”

Section: Introductionmentioning

confidence: 99%