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Hepatic Encephalopathy: from Pathophysiology to Therapeutic Management Michael Bismutha, Natalie Funakoshia, Jean-Franc¸Ois Cadranelb and Pierre Blanca

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Hepatic Encephalopathy: from Pathophysiology to Therapeutic Management Michael Bismutha, Natalie Funakoshia, Jean-Franc¸Ois Cadranelb and Pierre Blanca 8 Review article Hepatic encephalopathy: from pathophysiology to therapeutic management Michael Bismutha, Natalie Funakoshia, Jean-Franc¸ois Cadranelb and Pierre Blanca Hepatic encephalopathy is a complex and potentially 23:8–22 c 2010 Wolters Kluwer Health | Lippincott reversible neuropsychiatric syndrome complicating acute Williams & Wilkins. or chronic liver disease. Clinical manifestations are multiple European Journal of Gastroenterology & Hepatology 2011, 23:8–22 and varied, ranging from minimal neurological changes to coma. Ammonia is the main toxic substance involved in the Keywords: cirrhosis, hepatic encephalopathy, portal hypertension portosystemic shunt pathogenesis of hepatic encephalopathy, although other a b mechanisms, such as modifications of the blood–brain He´pato-gastroente´rologie B, Hoˆ pital Saint Eloi, Montpellier Cedex and Service d’He´pato-Gastroente´rologie et de Nutrition, CHG Lae¨nnec, Boulevard Lae¨nnec, barrier, disruptions in neurotransmission and abnormalities Creil, France in GABAergic and benzodiazepine pathways may also play Correspondence to Pierre Blanc, MD, PhD, He´pato-gastroente´rologie B, Hoˆpital a role. The identification and treatment of precipitating Saint Eloi, CHU Montpellier, 80 Avenue Augustin Fliche, Montpellier 34295 Cedex 5, France factors is crucial in the management of patients with Tel: + 33 467337063; fax: + 33 467337575; e-mail: [email protected] hepatic encephalopathy. Current treatments are based Michael Bismuth and Natalie Funakoshi contributed equally to the writing of this on reducing intestinal ammonia load by agents such as article antibiotics or disaccharides, although their efficacy is yet Received 25 May 2010 Accepted 12 October 2010 to be clearly established. Eur J Gastroenterol Hepatol Introduction Ammonia, which is produced in the colon by intestinal Hepatic encephalopathy (HE) is a complex and poten- bacteria, is the principal toxic substance involved in the tially reversible neuropsychiatric syndrome characterized pathogenesis of HE. Enteric flora generates the pro- by symptoms such as somnolence, confusion, asterixis, duction of additional neurotoxic molecules, such as extrapyramidal hypertonia, convulsions and coma. HE, phenols, mercaptans, and short-chain fatty acids, which which can be either acute or chronic, may complicate one potentialize the toxic effects of ammonia. Additional of three major clinical situations: severe acute liver failure mechanisms involved in HE include modifications of the in the absence of pre-existing liver disease (e.g. fulminant blood–brain barrier, disruptions in neurotransmission hepatitis), portocaval anastomosis in a patient without and abnormalities in GABAergic and benzodiazepine pre-existing chronic liver disease and finally cirrhosis with pathways. Normal brain function requires anatomical or without portocaval anastomosis. neuron integrity, production of sufficient energy and efficient synapse neurotransmission, all of which can be HE involves the coexistence of two predisposing factors: affected in HE. liver dysfunction and portocaval anastomoses. Liver dysfunction plays an essential role in HE triggered by fulminant hepatitis or portocaval shunts in cirrhotics. Clinical manifestations of HE are multiple and varied, Anatomical lesions ranging from discreet neuropsychiatric symptoms to Anatomical lesions of the central nervous system cannot coma. Common manifestations include an altered state be held responsible for the clinical manifestations of HE of consciousness and neuromuscular abnormalities [1]. [11]. However, microscopic structural abnormalities have been found in glial cells of patients with HE, namely The occurrence of the first episode of HE in a cirrhotic astrocytes. Astrocytes are the only cells in the human patient is a pejorative prognostic factor, and constitutes a brain equipped with the enzymes necessary for ammoniac turning point in the evolution of liver disease. Estimated metabolism (glutamine synthase). These cells undergo survival rates are 42% at 1 year, and 23% at 3 years [2]. In functional and structural alterations in patients with HE, subfulminant or fulminant hepatitis, HE plays a pre- increasing in size and number [12]. These morphological dominant role in deciding whether the patient is a modifications predominate in the cortex, the cerebellum candidate for superurgent liver transplantation. and in the brainstem nuclei, and are the equivalent of type II Alzheimer astrocytosis. The most serious anato- Pathophysiological concepts mical lesion is brain oedema [13], which is mainly Pathophysiology of HE is complex and probably involves observed in fulminant hepatitis, and is a major progno- the association of several different factors [3–10]. stic factor [11]. Nevertheless, anatomical lesions in 0954-691X c 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins DOI: 10.1097/MEG.0b013e3283417567 Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Hepatic encephalopathy Bismuth et al. 9 HE are generally mild, thus allowing for complete and Both exogenous and endogenous ammonia is detoxified frequent reversibility of clinical symptoms in the majority by the liver into urea through the Krebs–Henseleit urea of cases. cycle. In cirrhotics, the elevation of portal venous pressure and the presence of collateral circulation lead Imaging techniques, such as magnetic resonance imaging to diversion of portal blood flow directly into systemic (MRI) allow for the detection of minimal cerebral circulation. In addition, decreased liver function leads to oedema in cirrhotics with mild HE, with oedema decreased ammonia detoxification. In the event of becoming more pronounced in severe HE [14]. These decreased liver function or portosystemic shunt, non- MRI abnormalities have been shown to regress after liver detoxified ammonia enters the systemic circulation and transplantation [14] or after medical treatment of HE crosses the blood–brain barrier, and thus may induce HE. [15]. In addition to MRI, other noninvasive techniques, such as magnetic resonance spectroscopy and positron Ammonia toxicity can be explained by three underlying emission tomography have recently been used to study mechanisms, as shown in Fig. 1 [3,21]: the effect of chronic liver disease on the central nervous (1) Depletion of cerebral alphaketoglutaric acid levels. system [16]. A detailed description of these techniques This acid is consumed to produce glutamine and and their findings is found in the review of Butterworth detoxify ammonia by two chemical reactions: [17]. These techniques have provided valuable insight on (a) alphaketoglutaric acid + NH -glutamic acid; and the modifications in brain chemistry and metabolism 3 (b) glutamic acid + NH -glutamine. Reduced levels of induced by liver disease. However, they are not currently 3 alphaketoglutaric acid in the brain are impossible to used in clinical practice because of debate over scientific compensate, as both this molecule and its precursor, results and lack of consensus over the correct methods oxaloacetate, are incapable of crossing the blood– and implementation of these techniques. Additional brain barrier. The consumption of glutamic acid multicentre studies with a high degree of consensus are further depletes reserves of alphaketoglutaric acid, needed to define the role of MRI and magnetic resonance which is a substrate of the Krebs cycle. spectroscopy in the diagnosis and monitoring of HE (2) Impairment of oxidative decarboxylation of pyruvic [18,19]. acid, which is a crucial step of the Krebs cycle. Impairment of cerebral energy metabolism Impairment of cerebral energy metabolism has been Fig. 1 suggested as one of the underlying mechanisms of HE. Studies evaluating glucose and oxygen consumption in Proteins Carbohydrates Lipids HE have shown a marked reduction in cerebral energy metabolism [20]. This metabolic disturbance may be because of excess quantities of neurotoxic substances, such as ammonia, short-chain fatty acids and mercaptans. Pyruvic acid The presence of abnormally high levels of ammonia is the NAD oldest theory used to explain the pathogenesis of HE NADH [3,8]. Ammonia is a product of protein catabolism and has two origins: Acetyl coenzyme A (1) Exogenous ammonia is produced in the intestine from alimentary proteins, and in blood from the Isocritic oxidative deamination of amino acids, which arises Oxaloacetic acid Cycle Citric acid from putrefying bacteria in the caecum. Ammonia is of also produced through hydrolysis of urea by ureases Krebs found in intestinal bacteria. Constipation and Oxalosuccinic Succinic acid haemorrhage within the digestive tract thus increase acid ammonia production. Ammonia from the colon enters the portal venous circulation by passive Alphaketoglutaric acid diffusion, which is influenced by faecal pH levels. I. Depletion of alphaketoglutaric acid - 6 ATP NH3 Hepatic venous inflow is therefore rich in ammonia, II. Insufficient decarboxylation of Glutamic acid with levels 2–8 times higher in the portal vein pyruvic acid III. Consumption of ATP for - 2 ATP compared with systemic venous circulation. glutamine synthesis (2) Endogenous ammonia is produced in muscle, brain Glutamine and renal tissue and results from transamination and deamination of amino acids (mainly glutamine, and Mechanisms of ammonia toxicity according to Blanc et al. [3]. asparagine, alanine and histidine). Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
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