Is Lactulose Plus Rifaximin Better Than Lactulose Alone In The Management Of Hepatic Encephalopathy?

Butt, Nauman Ismat; Butt, Usman Ismat; Kakar, Aniqa Anser Tufail Khan; Malik, Tashia; Siddiqui, Arif Mahmood

doi:10.29271/jcpsp.2018.02.115

Cited by 9 publications

(5 citation statements)

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“… 58 , 59 Probably the strongest evidence favoring the large-intestine site in humans is that unabsorbable disaccharides (eg, lactulose), which are assumed to act primarily via acidification of colonic contents, are nearly as effective as antibiotics in reducing blood NH 3 in patients with CLD. 86 , 87 The potential mechanisms by which lactulose reduces blood NH 3 are discussed in more detail in the “Gastrointestinal therapeutic approaches to lowering blood ammonia “ section.…”

Section: Gi-tract N Balancementioning

confidence: 99%

A model of blood-ammonia homeostasis based on a quantitative analysis of nitrogen metabolism in the multiple organs involved in the production, catabolism, and excretion of ammonia in humans

Levitt¹,

Levitt²

2018

CEG

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Increased blood ammonia (NH3) is an important causative factor in hepatic encephalopathy, and clinical treatment of hepatic encephalopathy is focused on lowering NH3. Ammonia is a central element in intraorgan nitrogen (N) transport, and modeling the factors that determine blood-NH3 concentration is complicated by the need to account for a variety of reactions carried out in multiple organs. This review presents a detailed quantitative analysis of the major factors determining blood-NH3 homeostasis – the N metabolism of urea, NH3, and amino acids by the liver, gastrointestinal system, muscle, kidney, and brain – with the ultimate goal of creating a model that allows for prediction of blood-NH3 concentration. Although enormous amounts of NH3 are produced during normal liver amino-acid metabolism, this NH3 is completely captured by the urea cycle and does not contribute to blood NH3. While some systemic NH3 derives from renal and muscle metabolism, the primary site of blood-NH3 production is the gastrointestinal tract, as evidenced by portal vein-NH3 concentrations that are about three times that of systemic blood. Three mechanisms, in order of quantitative importance, release NH3 in the gut: 1) hydrolysis of urea by bacterial urease, 2) bacterial protein deamination, and 3) intestinal mucosal glutamine metabolism. Although the colon is conventionally assumed to be the major site of gut-NH3 production, evidence is reviewed that indicates that the stomach (via Helicobacter pylori metabolism) and small intestine and may be of greater importance. In healthy subjects, most of this gut NH3 is removed by the liver before reaching the systemic circulation. Using a quantitative model, loss of this “first-pass metabolism” due to portal collateral circulation can account for the hyperammonemia observed in chronic liver disease, and there is usually no need to implicate hepatocyte malfunction. In contrast, in acute hepatic necrosis, hyperammonemia results from damaged hepatocytes. Although muscle-NH3 uptake is normally negligible, it can become important in severe hyperammonemia. The NH3-lowering actions of intestinal antibiotics (rifaximin) and lactulose are discussed in detail, with particular emphasis on the seeming lack of importance of the frequently emphasized acidifying action of lactulose in the colon.

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Section: Gi-tract N Balancementioning

confidence: 99%

A model of blood-ammonia homeostasis based on a quantitative analysis of nitrogen metabolism in the multiple organs involved in the production, catabolism, and excretion of ammonia in humans

Levitt¹,

Levitt²

2018

CEG

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“… Blank 10D 10D Higuera-de-la-Tijera F 2018 [ 41 ] Mexico 87 Cirrhosis with variceal bleeding 400 mg t.i.d. Placebo 7d 28D Butt NI 2018 [ 42 ] Pakistan 130 HE due to decompensated chronic liver disease 550 mg b.i.d. Blank 10D 10D Khokhar N 2015 [ 43 ] Pakistan 306 Chronic cirrhosis with a previous episode of HE.…”

Section: Resultsmentioning

confidence: 99%

Preventive and therapeutic effects of rifaximin on hepatic encephalopathy with differential application dosages and strategies: a network meta-analysis

Fang,

Liu,

Liu

2024

BMC Gastroenterol

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Background Hepatic encephalopathy (HE) is a neuropsychiatric syndrome that affects the prognosis of patients with liver disease and is considered an independent risk factor for hospitalization and death. Rifaximin has been approved for HE treatment. This review will analyze the effect of rifaximin on different stages of HE with differential application dosages and strategies by traditional and network meta-analyses. Methods We performed a systematic search of PubMed, EmBase, and Cochrane Library databases up to February 26, 2023, to identify randomized controlled trials (RCTs) about rifaximin for the prevention and treatment of HE. The outcomes included incidence of HE and HE progression, HE reversal, mortality, and adverse effects. Results A total of 21 studies were included. In the primary prevention of HE, rifaximin significantly reduced the incidence of HE (OR: 0.66; 95% CI: 0.45, 0.96; p = 0.032). In secondary prevention, rifaximin significantly reduced the risk of recurrence in patients who were in remission (OR: 0.38; 95% CI: 0.28, 0.52; p < 0.001). In the treatment of minimal HE, rifaximin significantly reduced the breakthrough of MHE to OHE (OR: 0.17; 95% CI: 0.04,0.63; p = 0.008). Rifaximin also significantly improved the clinical symptoms of MHE and OHE patients (OR: 3.76; 95% CI: 2.69, 5.25; p < 0.001). However, rifaximin did not reduce mortality at any stage in HE patients (OR: 0.79; 95% CI: 0.58, 1.08; p = 0.133). Additionally, rifaximin did not increase the risk of adverse effects (OR: 0.96; 95% CI: 0.74, 1.24; p = 0.749). In the network meta-analysis, the 400 mg T.I.D. intervention had a relative advantage for HE risks in primary and secondary prevention. In the treatment of MHE, 600 mg b.i.d. was superior in preventing the breakthrough from MHE to OHE. Conclusion Rifaximin prevented HE risks and progression and improved clinical symptoms in patients with MHE but did not reduce mortality. For primary and secondary prevention, 400 mg t.i.d. could be considered. 600 mg b.i.d. could be considered in patients with MHE.

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“…However, the preventive effects of rifaximin on sarcopenia incidence or progression in LC patients remain unclear. Table 2 demonstrates randomized controlled trials (RCTs) published since 2010 regarding the effects of rifaximin on outcomes in patients with decompensated LC [ 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 , 140 , 141 , 142 , 143 , 144 , 145 , 146 , 147 , 148 , 149 , 150 , 151 , 152 , 153 ]. RCTs with the improvement of sarcopenia as a primary endpoint are not found.…”

Section: Antibiotics Dysbiosis Ammonia-lowering Strategies and mentioning

confidence: 99%

Liver Cirrhosis and Sarcopenia from the Viewpoint of Dysbiosis

Nishikawa

Enomoto

Nishiguchi

et al. 2020

IJMS

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Sarcopenia in patients with liver cirrhosis (LC) has been attracting much attention these days because of the close linkage to adverse outcomes. LC can be related to secondary sarcopenia due to protein metabolic disorders and energy metabolic disorders. LC is associated with profound alterations in gut microbiota and injuries at the different levels of defensive mechanisms of the intestinal barrier. Dysbiosis refers to a state in which the diversity of gut microbiota is decreased by decreasing the bacterial species and the number of bacteria that compose the gut microbiota. The severe disturbance of intestinal barrier in LC can result in dysbiosis, several bacterial infections, LC-related complications, and sarcopenia. Here in this review, we will summarize the current knowledge of the relationship between sarcopenia and dysbiosis in patients with LC.

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Is Lactulose Plus Rifaximin Better Than Lactulose Alone In The Management Of Hepatic Encephalopathy?

Abstract: There was no difference in effectiveness of lactulose plus rifaximin and lactulose alone in treatment of hepatic encephalopathy.

Cited by 9 publications

References 0 publications

A model of blood-ammonia homeostasis based on a quantitative analysis of nitrogen metabolism in the multiple organs involved in the production, catabolism, and excretion of ammonia in humans

A model of blood-ammonia homeostasis based on a quantitative analysis of nitrogen metabolism in the multiple organs involved in the production, catabolism, and excretion of ammonia in humans

Preventive and therapeutic effects of rifaximin on hepatic encephalopathy with differential application dosages and strategies: a network meta-analysis

Liver Cirrhosis and Sarcopenia from the Viewpoint of Dysbiosis

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