About HE

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Risk of overt hepatic encephalopathy (OHE)

Chronic liver disease (CLD) is a growing problem, often goes unrecognized, and is a leading cause of death in the US1,2

Cirrhosis puts patients at higher risk for complications3,4

Cirrhosis is typically categorized as compensated or decompensated. The compensated stage is the most prolonged phase of the disease and typically remains clinically silent.4

Decompensation can4:

  • Happen at any time
  • Occur with complications of cirrhosis, such as the development of hepatic encephalopathy (HE), ascites, or gastrointestinal bleeding due to portal hypertension

HE is one of the most common complications of cirrhosis4

HE is a brain dysfunction caused by advanced liver disease3,5-8

Buildup of toxins over time may precipitate cognitive episodes that present as alterations in consciousness and behavior changes that range from minimal to severe.

Varices

Screening for potential symptoms is critical for management according to guideline-based care4,5

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AASLD Guidelines for cirrhosis and portal hypertension include management of HE, ascites, and varices3,5,9

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Dr. Modi discuss development and risks of Hepatic Encephalopathy

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Recognize the impact of OHE

OHE is a significant burden on patients and healthcare resources and impacts patient survival10,11

The risk of OHE is high5

Multiple OHE episodes can8,11,12:

  • Carry significant risk of cognitive impairment
  • Signify potential underlying damage, such as neuroinflammation
  • Result in death

65%

Of new HE diagnoses are made in an inpatient setting13,*

31%

Average hospital readmission rate for HE in 202010,†

5.2

days

Average inpatient stay for patients hospitalized for HE in 202010,†

*Based on an IQVIA analysis of 2013-2018 health insurance claims data of patients diagnosed in the inpatient setting, which trended toward being more medically complex.13

†In Medicare patients with diagnosis from HE code group.

Patients with HE have significantly decreased survival when compared with other cirrhosis complications11,‡

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‡Data from 3 Danish healthcare registries of patients with cirrhosis due to alcohol use disorder and not previously examined for suspected cirrhosis (N=466) diagnosed between January 1, 1993, and August 31, 2005. The diagnosis of HE was based on the patient’s clinical presentation, usually supported by the blood ammonia level and/or a continuous reaction time. Minimal HE was excluded. Values represent survival probabilities after diagnosis of the complication, with or without development of additional complications.11

Recognize OHE symptoms before hospitalization.

DON’T WAIT

See what to look for:
Use these criteria to
screen for HE
WEST HAVEN CRITERIA FOR HE

Align with the guidelines
for patients at risk
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INDICATIONS

XIFAXAN® (rifaximin) 550 mg tablets are indicated for the reduction in risk of overt hepatic encephalopathy (HE) recurrence in adults and for the treatment of irritable bowel syndrome with diarrhea (IBS-D) in adults.

XIFAXAN® (rifaximin) 550 mg tablets are indicated for the reduction in risk of overt hepatic encephalopathy (HE) recurrence in adults.

IMPORTANT SAFETY INFORMATION

  • XIFAXAN is contraindicated in patients with a hypersensitivity to rifaximin, rifamycin antimicrobial agents, or any of the components in XIFAXAN. Hypersensitivity reactions have included exfoliative dermatitis, angioneurotic edema, and anaphylaxis.
  • Clostridium difficile-associated diarrhea (CDAD) has been reported with use of nearly all antibacterial agents, including XIFAXAN, and may range in severity from mild diarrhea to fatal colitis. If CDAD is suspected or confirmed, ongoing antibiotic use not directed against C. difficile may need to be discontinued.
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INDICATIONS

XIFAXAN® (rifaximin) 550 mg tablets are indicated for the reduction in risk of overt hepatic encephalopathy (HE) recurrence in adults and for the treatment of irritable bowel syndrome with diarrhea (IBS-D) in adults.

IMPORTANT SAFETY INFORMATION

  • XIFAXAN is contraindicated in patients with a hypersensitivity to rifaximin, rifamycin antimicrobial agents, or any of the components in XIFAXAN. Hypersensitivity reactions have included exfoliative dermatitis, angioneurotic edema, and anaphylaxis.
  • Clostridium difficile-associated diarrhea (CDAD) has been reported with use of nearly all antibacterial agents, including XIFAXAN, and may range in severity from mild diarrhea to fatal colitis. If CDAD is suspected or confirmed, ongoing antibiotic use not directed against C. difficile may need to be discontinued.
  • There is an increased systemic exposure in patients with severe (Child-Pugh Class C) hepatic impairment. Caution should be exercised when administering XIFAXAN to these patients.
  • Caution should be exercised when concomitant use of XIFAXAN and P-glycoprotein (P-gp) and/or OATPs inhibitors is needed. Concomitant administration of cyclosporine, an inhibitor of P-gp and OATPs, significantly increased the systemic exposure of rifaximin. In patients with hepatic impairment, a potential additive effect of reduced metabolism and concomitant P-gp inhibitors may further increase the systemic exposure to rifaximin.
  • In clinical studies, the most common adverse reactions for XIFAXAN (alone or in combination with lactulose) were:
    – HE (≥10%): Peripheral edema (17%), constipation (16%), nausea (15%), fatigue (14%), insomnia (14%), ascites (13%), dizziness (13%), urinary tract infection (12%), anemia (10%), and pruritus (10%)
    – IBS-D (≥2%): Nausea (3%), ALT increased (2%)
  • INR changes have been reported in patients receiving rifaximin and warfarin concomitantly. Monitor INR and prothrombin time. Dose adjustment of warfarin may be required.
  • XIFAXAN may cause fetal harm. Advise pregnant women of the potential risk to a fetus.

To report SUSPECTED ADVERSE REACTIONS, contact Salix Pharmaceuticals at 1-800-321-4576 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

To report SUSPECTED ADVERSE REACTIONS, contact Salix Pharmaceuticals at 1-800-321-4576 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

Please click here for full Prescribing Information.

References: 1. Cusi K, Isaacs S, Barb D, et al. American Association of Clinical Endocrinology Clinical Practice Guideline for the diagnosis and management of nonalcoholic fatty liver disease in primary care and endocrinology clinical settings: co-sponsored by the American Association for the Study of Liver Diseases (AASLD). Endocr Pract. 2022;28(5):528-562. doi:10.1016/j.eprac.2022.03.010 2. Chronic liver disease and cirrhosis. Centers for Disease Control and Prevention. Updated January 15, 2025. Accessed September 19, 2025. https://www.cdc.gov/nchs/fastats/liverdisease.htm 3. Kaplan DE, Ripoll C, Thiele M, et al. AASLD Practice Guidance on risk stratification and management of portal hypertension and varices in cirrhosis. Hepatology. 2024;79(5):1180-1211. doi:10.1097/HEP.0000000000000647 4. Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch J. Portal hypertensive bleeding in cirrhosis: risk stratification, diagnosis, and management: 2016 practice guidance by the American Association for the Study of Liver Diseases. Hepatology. 2017;65(1):310-335. doi:10.1002/hep.28906 5. Vilstrup H, Amodio P, Bajaj J, et al. Hepatic encephalopathy in chronic liver disease: 2014 practice guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology. 2014;60(2):715-735. doi:10.1002/hep.27210 6. Vince AJ, Burridge SM. Ammonia production by intestinal bacteria: the effects of lactose, lactulose and glucose. J Med Microbiol. 1980;13(2):177-191. doi:10.1099/00222615-13-2-177 7. Khan A, Ayub M, Khan WM. Hyperammonemia is associated with increasing severity of both liver cirrhosis and hepatic encephalopathy. Int J Hepatol. 2016;2016:6741754. doi:10.1155/2016/6741754 8. Bajaj JS, Schubert CM, Heuman DM, et al. Persistence of cognitive impairment after resolution of overt hepatic encephalopathy. Gastroenterology. 2010;138(7):2332-2340. doi:10.1053/j.gastro.2010.02.015 9. Biggins SW, Angeli P, Garcia-Tsao G, et al. Diagnosis, evaluation, and management of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: 2021 Practice Guidance by the American Association for the Study of Liver Diseases. Hepatology. 2021;74(2):1014-1048. doi:10.1002/hep.31884 10. Data on file. Definitive Healthcare 2022. Framingham, MA. 11. Jepsen P, Ott P, Andersen PK, Sørensen HT, Vilstrup H. Clinical course of alcoholic liver cirrhosis: a Danish population-based cohort study. Hepatology. 2010;51(5):1675-1682. doi:10.1002/hep.23500 12. de Wit K, van Doorn DJ, Mol B, et al. Neurofilament light chain but not glial fibrillary acidic protein is a potential biomarker of overt hepatic encephalopathy in patients with cirrhosis. Ann Hepatol. 2024;29(3):101496. doi:10.1016/j.aohep.2024.101496 13. Data on file. XIFAXAN HE: quantified patient journey insights. Bausch Health, Bridgewater, NJ.

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