Effect of antibiotics, prebiotics and probiotics in treatment for hepatic encephalopathy.
In order to reduce ammonia production by urease-positive bacteria Solga recently hypothesised (S.F. Solga, Probiotics can treat hepatic encephalopathy, Medical Hypotheses 2003; 61: 307-13), that probiotics are new therapeutics for hepatic encephalopathy (HE), and that they may replace antibiotics and lactulose. This influenced our view of the effect of antibiotics, prebiotics, e.g., lactulose, and probiotics on intestinal bacteria in the treatment of HE. Intestinal ammonia arises from aminoacids after bacterial de-amination and not from urea making urease-positive bacteria irrelevant. Antibiotics are not preferred in the treatment of HE, since ammonia-producing antibiotic-resistant bacteria may survive and replace ammonia-producing antibiotic-susceptible bacteria. Intestinal prebiotics are carbohydrate-like compounds, such as lactulose and resistant starch, that beneficially affects host's health in a different manner than normal food. In the small bowel prebiotics are not absorbed and digested, but are fermented in the colon by colonic bacteria. Fermentation of prebiotics yields lactic, acetic and butyric acids, as well as gas especially hydrogen (H2). The massive H2 volumes cause rapid intestinal hurry and thus massive amounts of colonic bacteria, not only urease-positive bacteria, but also deaminating bacteria, are removed and intestinal uptake of toxic bacterial metabolites, e.g., ammonia, reduced. As living non-pathogenic micro-organisms, probiotics beneficially affect the host's health by fermenting non-absorbed sugars, especially in the small bowel. Thus, they reduce the substrate of the other bacteria, and simultaneously they create a surplus of fermentation products which may affect the non-probiotic flora. Regarding the fermentation products (lactic acid, ethanol, acetic acid and CO2) five groups of probiotic micro-organisms are known. It is argued that probiotic, CO2-producing (facultatively) heterolactic lactobacilli, i.e., lactobacilli, that produce both lactic acid and CO2 from sugars, such as glucose, are preferred in the treatment of HE. Our ideas concur with the practice guidelines regarding HE as formulated by Blei, Cordoba and the Practice Parameters Committee of the American College of Gastroenterology, and does not alter the final conclusion of Solga as regards the beneficial use in future treatment of HE.
Bongaerts
Ger
G
Department of Medical Microbiology, Radboud University Nijmegen Medical Centre, P.O. Box 9101, Nl-6500 HB, Nijmegen, The Netherlands. g.bongaerts@mmb.umcn.nl
Severijnen
René
R
Timmerman
Harro
H
D000641:Ammonia / Q000378:metabolism; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D002986:Clinical Trials as Topic; D006501:Hepatic Encephalopathy / Q000178:diet therapy* / Q000382:microbiology*; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000187:drug effects / Q000382:microbiology*; D007792:Lactulose / Q000627:therapeutic use*; D008954:Models, Biological; D019936:Probiotics / Q000627:therapeutic use*; D016896:Treatment Outcome
D000900:Anti-Bacterial Agents; D007792:Lactulose; D000641:Ammonia