Experimental models for hepatic encephalopathy

Abstract

INTRODUCTIONAlthough there are many models for animal testing, the ideal model for chronic liver disease involving hepatic encephalopathy has not been described yet. Different problems associated with the models have led researchers to develop their own, sometimes unique experimental models, which makes difficult the comparison between the results of the conducted studies (1). Hepatic encephalopathy (HE) definition, nomenclature, diagnosis and quantification consensus were published in 2002 (2) where three types of HE were considered: type A, associated with acute liver failure, type B, associated with the existence of porto-systemic communication (by-pass) without intrinsic liver disease and type C, associated to liver cirrhosis. HE type C, in turn, is classified according to their form of presentation as spontaneous or episodic HE, in relation to precipitating factors, persistent HE is subdivided into mild (HE grade I), severe (HE II-IV) or treatment-dependent (early developed after abolition of treatment) and finally, the minimal HE, as the first manifestation of HE. HE type C is the most common form and from a clinical point of view, the episodic HE type because of liver cirrhosis decompensation is the most typical and relevant.

Successful Surgical Rescue of Hepatic Encephalopathy due to Anal Fissure in the Case of Acute Myeloid Leukemia

“…Hepatic encephalopathy (also known as portosystemic encephalopathy) presents with confusion, altered level of consciousness and coma, usually as a result of liver failure, which may ultimately result in death. Far less commonly, perirectal cellulitis may also cause hepatic encephalopathy as a result of NH3 drainage from the rectal venous plexus to systemic circulation [6][7]. To our knowledge, however, there has been no report of hepatic encephalopathy caused by an anal fissure in an immunocompromised patient with AML.…”

“…The treatment of hepatic encephalopathy depends on the suspected underlying cause (types A, B or C). Generally, hepatic encephalopathy type B may arise in those who have undergone a transjugular intrahepatic portosystemic shunt (TIPS) procedure or have suffered from various venoocclusive disorders [6][7][8]. In most cases, this resolves either spontaneously or with the medical treatments discussed below, but in a small proportion, about 5%, occlusion of the shunt is required to address the symptoms [9][10].…”

Hepatocyte Transplants Improve Liver Function and Encephalopathy in Portacaval Shunted Rats

“…All substrates absorbed in the gastrointestinal tract, among them noxious ones, appear in systemic circulation. In humans, a consequence of PCS operation is the development of neuropsychiatric disturbances, termed hepatic encephalopathy (HE) . HE also develops as a result of hepatic dysfunction; liver cirrhosis is the most common cause of HE .…”

A modified microsurgical model for end-to-side selective portacaval shunt in the rat: intraoperative microcirculatory investigations

“…Additionally, laboratory rats proved to be excellent models to study liver cirrhosis 11 , as well as hepatic encephalopathy [31][32][33] . In those experiments the liver atrophy and regeneration 34 , microvascular structural changes 35 , as well as remote effects were studied.…”