Re: Re: Management of hepatic encephalopathy: role of rifaximin.

[Guest guest]

Thanks Jill, I am taking heaps of probiotics incl bifidus.

Read part of your article, congrats! my husband is in the USA at the moment I will get him to buy the mag so I can read it and show it to friends (people believe things that have been published much more than stuff they read on-line:)!)

Nelly

[infections] Re: Management of hepatic encephalopathy: role of rifaximin.

I can't answer the main question but I will say probiotics like bifidus (www.customprobiotics.com is the best) are known to stop the ammonia/even liver cirrosis...> > "...The observation that intestinal bacterial flora is involved in the production of both primary agent of HE (ammonia) and precipitating factors (NBZDs) suggests that the use of nonabsorbable antibiotics such as rifaximin may be useful in preventing episodes of HE in patients with liver cirrhosis."> > I have questions for you people here:> > Are you aware of other abx that may have a similar effect on ammonia and natural benzodiazepine-like compounds (NBZDs) in the gut?> > I experienced time and time again almost instant relief from brain fog when I use tinidazole (within hours sometimes of taking the first dose), but then I get a terrible headache a few days after I start tinidazole (Herx?).> > I keep trying to understand what is really happening when I use tinidazole. Is it killing bugs in my brain I know it (and metronidazole) crosses the BBB well? or is it doing "something else" like mopping up something that is causing my constant encephalopathy? > > Thanks> > Nelly> > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=15855752 & query_hl=1> > Chemotherapy. 2005;51 Suppl 1:90-5. > > > Management of hepatic encephalopathy: role of rifaximin.> > Zeneroli ML, Avallone R, Corsi L, Venturini I, Baraldi C, Baraldi M.> > Department of Medicine and Medical Specialities, University of Modena and Reggio Emilia, Modena, Italy. zeneroli.marialuisa@u...> > Hepatic encephalopathy (HE) is a neuropsychiatric syndrome, which develops in patients with acute or chronic liver failure. It is widely accepted to be due to impairment of hepatic clearance of toxic products from the gut such as ammonia. Accumulation of ammonia induces a glutamate neurotoxicity leading to an increased tone of the gamma-aminobutyric acid A (GABA-A) receptor system in the brain which results in HE. Factors either increasing the ammonia levels (protein load, constipation, sepsis, or gastrointestinal bleeding) or potentiating the functional activity of the GABAergic system [natural benzodiazepine-like compounds (NBZDs) or exogenous benzodiazepines] may act as precipitating factors of HE. NBZDs are present in trace amounts in the blood of normal subjects and have been found to be increased in the blood of patients with liver cirrhosis, with or without HE. These compounds may derive either from the diet since they have been found in plants, vegetables and animals or from gut bacteria. The observation that intestinal bacterial flora is involved in the production of both primary agent of HE (ammonia) and precipitating factors (NBZDs) suggests that the use of nonabsorbable antibiotics such as rifaximin may be useful in preventing episodes of HE in patients with liver cirrhosis. Copyright © 2005 S. Karger AG, Basel.> > Publication Types: > a.. Review > b.. Review, Tutorial > > PMID: 15855752 [PubMed - indexed for MEDLINE]