Hepatic encephalopathy is a common complication of
hepatic cirrhosis. The clinical diagnosis is based on two concurrent types of symptoms: impaired mental status and impaired neuromotor function. Impaired mental status is characterized by deterioration in mental status with psychomotor dysfunction, impaired memory, and increased reaction time, sensory abnormalities, poor concentration, disorientation and
coma. Impaired neuromotor function include
hyperreflexia, rigidity,
myoclonus and
asterixis. The pathogenesis of
hepatic encephalopathy has not been clearly defined. The general consensus is that elevated levels of
ammonia and an inflammatory response work in synergy to cause astrocyte to swell and fluid to accumulate in the brain which is thought to explain the symptoms of
hepatic encephalopathy.
Acetyl-L-carnitine, the short-chain
ester of
carnitine is endogenously produced within mitochondria and peroxisomes and is involved in the transport of acetyl-moieties across the membranes of these organelles.
Acetyl-L-carnitine administration has shown the recovery of neuropsychological activities related to attention/concentration, visual scanning and tracking, psychomotor speed and mental flexibility, language short-term memory, attention, and computing ability. In fact,
Acetyl-L-carnitine induces ureagenesis leading to decreased blood and brain
ammonia levels.
Acetyl-L-carnitine treatment decreases the severity of mental and physical
fatigue, depression
cognitive impairment and improves health-related quality of life. The aim of this review was to provide an explanation on the possible toxic effects of
ammonia in HE and evaluate the potential clinical benefits of ALC.