Rifaximin versus Nonabsorbable Disaccharides for the Treatment of Hepatic Encephalopathy: A Meta-Analysis
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Rifaximin versus Nonabsorbable Disaccharides for the
Treatment of Hepatic Encephalopathy: A Meta-Analysis
introduction
Hepatic encephalopathy (HE) is a complex and reversible neuropsychiatric syndrome that results from acute or chronic liver diseases, such as hepatic cirrhosis, alcoholic liver disease [1]. HE is an important complication of hepatic cirrhosis and is an independent predictor of mortality in patients with cirrhosis [2]. HE occurs in the presence of insufficient hepatic clearance of toxins absorbed from the intestine resulting in neurochemical abnormalities across the blood brain barrier [3]. The symptoms of HE, manifested on a continuum, are deterioration in mental status, with psychomotor dys- function, impaired memory, increased reaction time, sen- sory abnormalities, poor concentration, disorientation, even coma, and death [4, 5]. Overt HE means high mortality and poor prognosis. 1-year mortality for patients with severe HE in ICU is 54% [6]. Episodes of overt HE result in fre- quent hospitalizations and pose a formidable burden on the healthcare system, especially in China, a developing country with 100000000 hepatitis B carriers [7].
Diagnosis of overt hepatic encephalopathy should be made after the exclusion of other brain disorders [8]and based on two types of symptoms.Impaired mental status, as defined by the Conn score, with higher scores indicating more severe impairment, and impaired neuromotor func- tion includes hyperreflexia, rigidity, myoclonus, and asterixi [9, 10]. Minimal hepatic encephalopathy (MHE) that may has no clinical manifestations could be detected only by neuropsychological methods include portosystemic ence- phalopathy (PSE) syndrome test, Psychometric-Hepatic- Encephalopathy-Sum- (PHES-) Score [11]. Elevated serum ammonia level is an effective index of HE and is detected in 60%–80% of affected patients, but a single ammonia levelin the diagnosis of HE is uncertain given the substantial overlap of ammonia levels in both patients with and without encephalopathy [12]. Current treatment strategies include measures aimed at reducing the serum level of ammonia, pro- viding specialized nursing care as well as correcting precipi- tating factors such as gastrointestinal hemorrhage, infection, constipation, and electrolyte disturbances [5].
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