Mechanistic insight, diagnosis, and treatment of ammonia‐induced hepatic encephalopathy

Abstract

Hepatic encephalopathy is a neuropsychological syndrome due to biochemical disturbance of brain function in advanced liver disease patients. Diagnosis and treatment of the condition is very demanding and has negative toll on finances with increased healthcare utilization. The pathophysiology is not completely understood; however, there is evidence that ammonia plays an important role in the etiology. Conventional methods of solely relying on blood ammonia level to diagnose hepatic encephalopathy did not help much; likewise, the use of lactulose alone in treating hepatic encephalopathy has also been discouraged. This paper analyzed the current knowledge regarding the mechanism of how ammonia disrupts the normal brain function as well as the use of latest diagnosing tools including those under development to evaluate the neuropsychiatric state of patients and their quality of life. The efficacies of lactulose and rifaximin combination for short-term and long-term treatment in addition to nutritional interventions and other drugs undergoing clinical trials were also reviewed.

Targeted puncture of left branch of intrahepatic portal vein in transjugular intrahepatic portosystemic shunt to reduce hepatic encephalopathy

“…HE is mainly due to absorption of toxic substances from the intestinal portal vein system, through the shunt without the liver first pass effect into the systemic circulation, caused by dysfunction of the central nervous system; a syndrome with mental and nervous symptoms[14]. One of the toxic substances that causes HE is blood ammonia[15]. There are two aspects of the source of blood ammonia in the body, endogenous ammonia is produced by catabolism in vivo , and exogenous ammonia is produced by catabolism of nitrogenous substances in the intestine[16].…”

“…The previous literature[15] only compared the overall incidence of HE in 3 years, and showed that HE occurred one year after TIPS[32]. Therefore, we compared the occurrence of HE after 1, 3, 6, 9 and 12 mo, and the total incidence of HE after 5 years.…”

Reduced Serum Cholinesterase Activity Distinguishes Hepatic Encephalopathy From 48 Types of Human Diseases

“…Increased blood ammonia levels have been considered as the main pathophysiological mechanism of HE [41,42] by causing swelling astrocytes, activation of microglia and neuroin ammation [43][44][45][46][47][48][49][50]. Microglia activation can promote the proliferation and release of pro-in ammatory cytokines [50], and the in ammation state can eventually lead to neuronal death [51].…”

The association between hepatic encephalopathy/minimal hepatic encephalopathy and depressive and anxiety disorders: a systematic review

“…HE is a neuropsychological syndrome caused by biochemical disturbance of brain function in advanced liver disease patients. 22 Like other neuropsychological syndromes, an increased rate of mood and anxiety disorders would not be surprising; however, the relationship between HE and depression is very complex, which can explain why different studies have reached different conclusions. Patients with cirrhosis may be under various psychosocial stresses, including relationship, occupational, and financial stress.…”