Lactulose vs Polyethylene Glycol 3350-Electrolyte Solution for Treatment of Overt Hepatic Encephalopathy

Rahimi, Robert S.; Singal, Amit G.; Cuthbert, Jennifer A.; Rockey, Don C.

doi:10.1001/jamainternmed.2014.4746

Cited by 170 publications

(164 citation statements)

References 27 publications

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“…In early stages of encephalopathy, ammonia levels should be followed and lactulose, polyethylene glycol, or rifaximin used for treatment. 138,139 Volume depletion should be monitored and addressed by fluid replacement. Fluidrefractory hypotension may warrant the use of vasopressor agents.…”

Section: Treatment Of Post-hepatectomy Liver Failurementioning

confidence: 99%

Defining Post Hepatectomy Liver Insufficiency: Where do We stand?

Lafaro

Buettner

Maqsood

et al. 2015

Journal of Gastrointestinal Surgery

101

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Section: Treatment Of Post-hepatectomy Liver Failurementioning

confidence: 99%

Defining Post Hepatectomy Liver Insufficiency: Where do We stand?

Lafaro

Buettner

Maqsood

et al. 2015

Journal of Gastrointestinal Surgery

101

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“…In a randomized controlled trial, PEG was compared headtohead with lactulose among inpatients with HE. Among patients who were randomly assigned to four liters of PEG over four hours, there was greater improvement in HE after 24 h compared to those who were given three or more doses of lactulose, each 20 to 30 g, over 24 h. Furthermore, median time to resolution of HE was shorter in the PEG cohort [48] . The study was limited by its singlecenter design and lack of blinding.…”

Section: Acute Ohementioning

confidence: 91%

Advances in cirrhosis: Optimizing the management of hepatic encephalopathy

Liu

Perumpail

Kumari

et al. 2015

WJH

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Hepatic encephalopathy (HE) is a major complication of cirrhosis resulting in significant socioeconomic burden, morbidity, and mortality. HE can be further subdivided into covert HE (CHE) and overt HE (OHE). CHE is a subclinical, less severe manifestation of HE and requires psychometric testing for diagnosis. Due to the time consuming screening process and lack of standardized diagnostic criteria, CHE is frequently underdiagnosed despite its recognized role as a precursor to OHE. Screening for CHE with the availability of the Stroop test has provided a pragmatic method to promptly diagnose CHE. Management of acute OHE involves institution of lactulose, the preferred first-line therapy. In addition, prompt recognition and treatment of precipitating factors is critical as it may result in complete resolution of acute episodes of OHE. Treatment goals include improvement of daily functioning, evaluation for liver transplantation, and prevention of OHE recurrence. For secondary prophylaxis, intolerance to indefinite lactulose therapy may lead to non-adherence and has been identified as a precipitating factor for recurrent OHE. Rifaximin is an effective add-on therapy to lactulose for treatment and prevention of recurrent OHE. Recent studies have demonstrated comparable efficacy of probiotic therapy to lactulose use in both primary prophylaxis and secondary prophylaxis.

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“…Although the utility of lactulose as first line in the treatment of acute HE has been hotly debated (Als-Nielsen et al 2004; in the absence of any large multicentre randomized controlled trial ever being performed, there are robust data to support its use in the secondary prophylaxis of recurrence of overt HE (Sharma et al 2009) and in the treatment of covert HE (Prasad et al 2007). Recently, the hepatic encephalopathy: lactulose vs polyethylene glycol (HELP) trial recently showed statistically significant reduction in both HE grade and resolution of symptoms when polyethylene glycol (PEG) solution was used instead of lactulose (Rahimi et al 2014). The increase in renal ammonia excretion as a consequence of administering 4 l of PEG solution could however explain its non-inferiority compared to lactulose in this trial.…”

Section: Therapeutic Strategies Targeting the Gut-liver-brain Axismentioning

confidence: 99%

Clinical science workshop: targeting the gut-liver-brain axis

et al. 2015

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A clinical science workshop was held at the ISHEN meeting in London on Friday 11th September 2014 with the aim of thrashing out how we might translate what we know about the central role of the gut-liver-brain axis into targets which we can use in the treatment of hepatic encephalopathy (HE). This review summarises the integral role that interorgan ammonia metabolism plays in the pathogenesis of HE with specific discussion of the roles that the small and large intestine, liver, brain, kidney and muscle assume in ammonia and glutamine metabolism. Most recently, the salivary and gut microbiome have been shown to underpin the pathophysiological changes which culminate in HE and patients with advanced cirrhosis present with enteric dysbiosis with small bowel bacterial overgrowth and translocation of bacteria and their products across a leaky gut epithelial barrier. Resident macrophages within the liver are able to sense bacterial degradation products initiating a pro-inflammatory response within the hepatic parenchyma and release of cytokines such as tumour necrosis factor alpha (TNF-α) and interleukin-8 into the systemic circulation. The endotoxemia and systemic inflammatory response that are generated predispose both to the development of infection as well as the manifestation of covert and overt HE. Co-morbidities such as diabetes and insulin resistance, which commonly accompany cirrhosis, may promote slow gut transit, promote bacterial overgrowth and increase glutaminase activity and may need to be acknowledged in HE risk stratification assessments and therapeutic regimens. Therapies are discussed which target ammonia production, utilisation or excretion at an individual organ level, or which reduce systemic inflammation and endotoxemia which are known to exacerbate the cerebral effects of ammonia in HE. The ideal therapeutic strategy would be to use an agent that can reduce hyperammonemia and reduce systemic inflammation or perhaps to adopt a combination of therapies that can address both.

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Lactulose vs Polyethylene Glycol 3350-Electrolyte Solution for Treatment of Overt Hepatic Encephalopathy

Cited by 170 publications

References 27 publications

Defining Post Hepatectomy Liver Insufficiency: Where do We stand?

Defining Post Hepatectomy Liver Insufficiency: Where do We stand?

Advances in cirrhosis: Optimizing the management of hepatic encephalopathy

Clinical science workshop: targeting the gut-liver-brain axis

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