Abstract
Objective:To compare efficacy of high vs low dose rifaximin for primary prophylaxis of portosystemic encephalopathy (PSE) in decompensated liver cirrhosis.Methods:In a quasi-experimental double blind randomized study at Services Institute of Medical Sciences (SIMS), Lahore from August 2017 to August 2018, patients of decompensated cirrhosis with no previous PSE were randomized to receive twice daily rifaximin 200mg in Group-A and 550mg in Group-B. Patients were followed for 6 months for development of PSE.Results:In 75 included patients, mean age was 53.8(±10.7) years and male/female ratio was 0.97/1(37/38). After randomization, 34 (45.3%) patients were included in Group-A and 41 (54.7%) patients in Group-B. During 6 month follow up 24 (32%) patients developed PSE, 12 (35.2%) in Group-A and 12 (29.2%) in Group-B, difference was not significant (p value 0.57). In 6 months, 13 (17.3%) patient died, 6 (17.6%) in Group-A and 7 (17.07%) patients in Group-B, difference not significant (p value 0.94). Patients who died had higher bilirubin (p < 0.00), higher serum creatinine (p 0.05), high CTP score (p 0.04) and worse MELD score (p 0.004).Conclusion:Rifaximin is not effective for primary prophylaxis of overt hepatic encephalopathy in decompensated cirrhosis patients.
Highlights
Hepatic encephalopathy is a neuropsychiatric disorder seen in patients with liver cirrhosis.[1]
Development of encephalopathy in a cirrhosis patient is associated with high mortality and bad prognosis.[2]
It has shown to be effective in treating as well as reducing recurrence of hepatic encephalopathy in liver cirrhosis and is presently recommended as add-on therapy with lactulose for secondary prophylaxis of overt hepatic encephalopathy.[1]
Summary
Hepatic encephalopathy is a neuropsychiatric disorder seen in patients with liver cirrhosis.[1]. Hepatic encephalopathy is the consequence of failure of liver to detoxify various toxins circulating in body due to impaired liver functions.[3] Accumulation of these toxins mainly ammonia results in passage of these harmful substances across blood brain barrier. Ammonia is converted in to glutamate in astrocytes resulting in cerebral edema and altered sensorium.[4]. Majority of these toxins including ammonia are produced in intestine by bacterial fermentation of dietary protein. Pak J Med Sci September - October 2019 Vol 35 No 5 www.pjms.org.pk 1446 these toxins are free to produce complications like hepatic encephalopathy due to insufficiency of hepatic metabolism.[5]
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