Tools and tactics for improving the diagnosis of hepatic encephalopathy

Olesen, Søren Schou; Jackson, Clive; Morgan, Marsha Y.

doi:10.1016/j.jhep.2017.01.034

Cited by 3 publications

(2 citation statements)

References 5 publications

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“…The presence of MHE can be detected using a range of neuro-psychometric and neurophysiological tools. The latter has been thoroughly testes and validated in numerous countries (5)(6)(7)(8). Several precipitating factors of HE have been identified, in particular infection and dehydration (9).…”

Section: Introductionmentioning

confidence: 99%

The Psychometric Hepatic Encephalopathy Syndrome score does not correlate with blood ammonia, endotoxins or markers of inflammation in patients with cirrhosis

Kimer¹,

Gluud²,

Pedersen³

et al. 2021

Transl Gastroenterol Hepatol

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Background: The pathogenesis of hepatic encephalopathy (HE) remains unclear but impaired clearance of gut-derived neurotoxins and increased systemic inflammation are thought to play key roles. The diagnosis is based on detection of neurophysiological and neuropsychometric abnormalities. The Psychometric Hepatic Encephalopathy Score (PHES) have been found to correlate with markers of systematic inflammation including interleukin 6, C-reactive protein (CRP) and tumor necrosis factor-α (TNF-α). This study explores the associations between the PHES score and systemic inflammation, endotoxins and disease severity using baseline data from a trial involving patients with cirrhosis and minimal or no HE (NCT01769040).Methods: Arterial blood was obtained during hepatic vein catheterization, from 54 patients [median age 55 (range, 33-70) years; 83% men] with decompensated but stable cirrhosis. None had clinical evidence of HE but 34 (55.6%) had an abnormal PHES score indicating the presence of minimal HE. Relationships were sought between the PHES score and markers of systemic inflammation, high sensitivity-CRP, cytokines (SDF-1α, TGF-b1, IP-10, IL-6, 10 and 18, and TNF-α; lipopolysaccharide (LPS), the lipopolysaccharide binding protein (LBP) and soluble CD14 (sCD14); and the blood ammonia.Results: No significant relationships were found between the PHES score and any of the variables tested with the single exception of the correlation with serum IL-6 (r=−0.29, 95% confidence interval, −0.53 to −0.02, P=0.031). No independent predictors of the PHES score were identified in regression analyses. Conclusions:No predictive associations were identified between the PHES scores and circulating blood ammonia, endotoxins, or markers of systemic inflammation in this patient population.

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Section: Introductionmentioning

confidence: 99%

The Psychometric Hepatic Encephalopathy Syndrome score does not correlate with blood ammonia, endotoxins or markers of inflammation in patients with cirrhosis

Kimer¹,

Gluud²,

Pedersen³

et al. 2021

Transl Gastroenterol Hepatol

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“…The diagnosis of hepatic encephalopathy is dependent on the admitting physician's completeness of documentation. Subclinical or minimal hepatic encephalopathy is a challenging diagnosis to capture from the electronic medical record alone 40 . Without neuropsychiatric testing or electroencephalography (EEG), encephalopathy may not be captured precisely in the medical record, thus post‐TIPS HE admissions likely represent a definitive, overt change in mental status 3 .…”

Section: Discussionmentioning

confidence: 99%

Case–control study: Proton pump inhibitor use is a major risk factor for hepatic encephalopathy after TIPS

2021

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Summary Background In cirrhotic patients, hepatic encephalopathy after transjugular intrahepatic portosystemic shunt (post‐TIPS HE) is common. Measures that reduce the severity of post‐TIPS HE are limited. Though recent data suggest an association between PPI use and HE, the risk in post‐TIPS HE is not well understood. Aims Examine the risk of post‐TIPS HE associated with differing classes of medications, including proton pump inhibitors (PPI). Methods Between 2012 and 2019, we collected data on known risk factors for post‐TIPS HE as well as medications used. Subjects were classified according to the development of overt hepatic encephalopathy requiring admission. Results In our cohort, admission after TIPS was common, with an average of 7.84 admissions in the post‐TIPS HE group versus 3.76 in the no HE group (P = 0.028). Consistent with previous studies, we found that MELD, grade of encephalopathy, and lower portosystemic gradient were associated with the development of post‐TIPS HE. PPI use prior to TIPS was highly associated with post‐TIPS HE (RR: 4.89, 95% CI: 1.91‐12.50). The risk of post‐TIPS HE was highest 1‐4 weeks post‐procedure but persisted for up to one year after TIPS. Other classes of acid‐suppressive medications, such as histamine receptor blockers (RR: 0.357, 0.154‐0.824) and sucralfate (RR: 0.123, 0.016‐0.924) did not demonstrate this association. Conclusions PPI use is a strong risk factor for the development of post‐TIPS HE. Clinicians should consider the risks and benefits of PPIs in cirrhotic patients undergoing TIPS. Further studies are needed to demonstrate the benefit of discontinuation of PPI, or switching to alternatives.

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