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Glycerol phenylbutyrate reduces hepatic encephalopathy events in cirrhosis

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HE treatments are difficult to study

The publication by Dr. Rockey and his colleagues describes the findings of a randomized, double-blind controlled trial using glycerol phenylbutyrate to treat hepatic encephalopathy. The study design essentially enrolled patients who had at least two "bouts of HE in the previous 6 months." This drug is given orally and promotes excretion of waste nitrogen through the kidneys in the form of urinary phenylacetylglutamine. It has been approved and used for the treatment of hyperammonemia in patients with urea cycle defects.

Dr. Kevin D. Mullen
The primary end point of the study was the proportion of patients with a bout of documented HE while taking the placebo or GPB during the 16 weeks of the study. Of those randomized to GPB, 21% developed HE versus 36% of the placebo arm (P = .02). The number of patients enrolled did not quite meet the number adequate to power the study (178 vs. 186). However, it is always very difficult to enroll cirrhotic patients into clinical trials for the treatment of HE. The multiple precipitating factors for bouts of HE typically occur in patients experiencing bouts of recurrent HE. Withholding therapy for these patients with recognized precipitating factors is not ethical, so clinical trials tend to try and avoid them and make the precipitating factors exclusionary criteria. In theory that might enrich the enrolled population with so-called spontaneous and recurrent HE. In any event, designing HE treatment trials is a very challenging process. Indeed, one should note the striking similarity of the study design in this trial to that of the original rifaximin trial (N. Engl. J. Med. 2010;362:1071-81). Since the approval of rifaximin in the United States, all investigators running HE trials have to factor in the impact of adding or continuing rifaximin in HE patients, which further complicates the process of HE study design.

In light of all the issues involved, the authors appear to have conducted the study in a satisfactory fashion. The 50% of enrollees coming from Russia and the Ukraine reflects the difficulty in enrolling patients in the United States. This must have posed some difficulties in running the study such as standardization of the ammonia assays. Nonetheless, this is an important study demonstrating that this agent has a measurable degree of efficacy in the control of HE. Further studies are needed to verify the findings with more and larger randomized controlled trials.

Dr. Kevin D. Mullen, professor of medicine, Case Western Reserve University, Metrohealth Medical Center, Cleveland. He has consulted for Salix and Abbott.


 

Glycerol phenylbutyrate significantly reduced the number of cirrhosis patients experiencing hepatic encephalopathy and the time to first event, a phase II trial has shown.

The randomized, double-blind placebo-controlled trial in 178 patients with cirrhosis found that only 21% of patients treated with glycerol phenylbutyrate (GPB) had a hepatic encephalopathy (HE) event compared with 36% of the placebo group (P =.02).

Treatment with 6 mL of oral GPB twice daily also significantly reduced the time to a first HE event (HR 0.56, 95% CI 0.32-0.99, P less than .05), in particular, more severe West Haven grade 2 events, according to a study published in the March issue of Hepatology.

The HE group also had significantly fewer total events (35 vs. 57, P less than .05), and treatment was associated with a nonsignificant reduction in HE hospitalizations (13 vs. 25; P = .06)

The treatment effect was more pronounced in the 119 patients not taking the antibiotic rifaximin at entry; among patients taking rifaximin there were no differences between the treatment arms in the number of patients experiencing an HE event, time to event, or total number of events (Hepatology 2014;59:1073-83).

Glycerol phenylbutyrate is currently approved for the treatment of urea cycle disorders and other inherited disorders characterized by an excess of ammonia in the blood.

This study followed a previous 4-week, open-label study that suggested this dose of GPB was well tolerated and lowered ammonia levels in patients with cirrhosis and HE.

"Though elevated blood ammonia has long been suspected as important, the evidence is largely correlative, other factors have been postulated, and evidence against ammonia has been reported," wrote Dr. Don C. Rockey of the Medical University of South Carolina, Charleston, and his colleagues.

In the current study, "GPB significantly lowered plasma ammonia and correlated strongly with HE events when assessed either at baseline or during the study."

Baseline ammonia levels were also higher among patients who subsequently experienced an HE event compared with those who did not, prompting the authors to suggest that elevated blood ammonia level does in fact play an important role in the pathogenesis of recurrent, overt HE.

Researchers reported similar types of adverse events in the two treatment arms and a similar frequency of these events, although serious adverse events and study drug discontinuations associated with adverse events occurred slightly more often in the GPB group.

"There were no treatment-related effects on liver biochemical tests, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), bilirubin, international normalized ratio (INR), or MELD [score]," the investigators wrote.

They concluced that "that GPB reduced the likelihood of HE events in patients with preexisting HE, and ... that it deserves further study as a potential therapeutic for these patients."

The study was funded by Hyperion Therapeutics. There were no other conflicts of interest declared.

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