Sodium Benzoate for Treatment of Hepatic Encephalopathy.

Hepatic encephalopathy (HE) is a serious but usually reversible neuropsychiatric complication of cirrhosis, inborn errors of metabolism involving disorders of the urea cycle, and non-cirrhotic portosystemic shunting that most commonly arises from a transjugular intrahepatic portosystemic shunting pr...

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Publicado en:Gastroenterology & Hepatology Vol. 9; no. 4; pp. 219 - 228
Autores principales: Misel, Michael L., Gish, Robert G., Patton, Heather, Mendler, Michel
Formato: review Journal Article
Publicado: Gastro-Hep Communications, Inc Apr2013
Acceso en línea:Ver este registro en EBSCOhost
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      pub: Gastro-Hep Communications, Inc
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        atl: Sodium Benzoate for Treatment of Hepatic Encephalopathy.
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        au:
          Misel, Michael L.
          Gish, Robert G.
          Patton, Heather
          Mendler, Michel
        affil: Pharmacist Specialist for Liver/Kidney Transplant & Hepatology, Center for Abdominal Transplantation/ Department of Pharmacy Services, University of California San Diego Health System, San Diego, CA
      sug:
        subj:
          Hepatic Encephalopathy Drug Therapy
          Benzoic Acids Administration and Dosage
          Hepatic Encephalopathy Physiopathology
          Hepatic Encephalopathy Classification
          Severity of Illness
          Benzoic Acids Pharmacodynamics
          Treatment Outcomes
          Safety
      ab: Hepatic encephalopathy (HE) is a serious but usually reversible neuropsychiatric complication of cirrhosis, inborn errors of metabolism involving disorders of the urea cycle, and non-cirrhotic portosystemic shunting that most commonly arises from a transjugular intrahepatic portosystemic shunting procedure. Symptoms can include alterations in cognitive function, neuromuscular activity, and consciousness, as well as sleep disorders and mood changes. HE is associated with significant morbidity and mortality and, if not properly treated, will lead to increased hospital admissions and healthcare costs. Although the standard therapies of lactulose and rifaximin (Xifaxan, Salix) are effective for most patients, these drugs may be associated with significant adverse effects and expense and, in some patients, inadequate therapeutic response. A need for adjunctive therapies exists. Drugs that target serum and tissue ammonia metabolism and elimination may be important adjuncts to drugs that reduce ammonia production and absorption from the gastrointestinal tract for patients with severe or persistent overt symptoms of HE. Sodium benzoate is an inexpensive adjunctive agent that can be used in addition to lactulose and rifaximin and may provide an option for some select patients with refractory HE who have failed to respond to standard therapies or who cannot afford them. Although sodium benzoate does not share the same adverse effect profiles of standard therapies for HE, its efficacy has not been well established. Given the significant dose-dependent sodium content of this therapy, it may not be appropriate for patients with significant fluid retention or kidney dysfunction.
      pubtype: Academic Journal
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        review
        Journal Article
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    language: English
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