Hepatic encephalopathy Edit

No problem shroom, surely there could be some aspects of the body using\converting ammonia but most likely not in any amounts we see with this.
As you know I have some history in treating this and the ammonia accumulation going at least a year back.
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from: http://en.wikipedia.org/wiki/Hepatic_encephalopathy


The toxic substances which accumulate in the setting of liver failure and affect the brain are still not well understood. They have been thought to include ammonia (NH3) and mercaptans. Ammonia is normally converted to urea by the liver and, as with mercaptans, is produced by the bacterial breakdown of protein in the intestines.

Ammonia can cross the blood-brain barrier, where it causes the support cells of the brain (astrocytes) to swell. The swelling of the brain tissue increases intracranial pressure, and can lead to coma or death via herniation of the brainstem.


Treatment
Even 'minimal hepatic encephalopathy' may benefit from treatment. [5]


Reduce protein intake
It is important to prevent and/or remove excess protein from the inside (lumen) of the gut. This prevents its absorption into the bloodstream and subsequent conversion to ammonia (and other potentially toxic substances) which, in the setting of severe liver impairment, will accumulate and worsen the hepatic encephalopathy. Hence, dietary intake of protein should be minimised. Likewise, if there has been bleeding into the lumen of the esophagus or stomach, or small intestine (for instance, ruptured esophageal varices and bleeding ulcer, respectively) it should be treated promptly since blood is full of protein (hemoglobin). In this light, it should be kept in mind that both liver disease per se and portal hypertension predispose to just such bleeding.


Correction of hypokalemia
Concommittent hypokalemia should be corrected as hypokalemia increases renal ammonia production and may promote conversion into ammonium into ammonia which can cross the blood-brain barrier.[6]


Lactulose
Lactulose is a compound that will cause osmotic diarrhoea, thus lessening the time available for intestinal bacteria to metabolise protein into ammonia within the bowel. Further, it acidifies the environment in the lumen of the bowel. This promotes the conversion of lumenal ammonia (NH3) to ammonium (NH4+) which, by which virtue of its net charge, should be less readily absorbed into the bloodstream from the bowel lumen. Despite this theoretical and appealing mechanism, a meta-analysis of randomized controlled trials by the international Cochrane Collaboration found benefit, but suggests there is little evidence for its preferred use to treat hepatic encephalopathy.[7] Indeed, any drug (laxative) which speeds up transit through the bowel thereby lessening the time available for bacteria to metabolize protein into ammonia, works just as well.

Lactulose can be given rectally for patients who cannot take oral medications.[8][9][10] One regimen is 300 mL (200 gm) of lactulose syrup (10 gm/15 ml) in 1 L of water which is retained for 1 hour, with the patient in the Trendelenburg position.[11]


Antibiotics
Antibiotics may be given to kill bacteria present in the bowel thereby decreasing bacterial conversion of protein to ammonia (and other toxic substances) there. Although effective, neomycin, a non-absorbable aminoglycoside antibiotic, is essentially contraindicated; it has been found that a proportion of the ingested dose is indeed absorbed due to increased gut permeability, thus increasing the risk of renal failure and hearing loss (i.e. two of the potential side effects of neomycin). The former side-effect, in particular, is especially worrisome given the already increased likelihood of renal failure in cirrhosis and portal hypertension (i.e. hepatorenal syndrome). Metronidazole has also been studied.[12]


Rifaximin
Rifaximin (Xifaxan®), receieved orphan drug status in 2005 for the treatment of hepatic encephalopathy. In contrast to neomycin, its tolerability profile is comparable to placebo.[13] Multiple clinical trials have demonstrated that rifaximin at a dose of 400 mg taken orally 3 times a day was as effective as lactulose or lactilol at improving hepatic encephalopathy symptoms.[14] Similarly, rifaximin was as effective as neomycin and paromomycin.[15] Rifaximin was better tolerated than both the cathartics and the other nonabsorbable Antibiotics . A number of concerns remain regarding rifaximin's role in the treatment of hepatic encephalopathy. It remains to be determined if rifaximin can improve severe encephalopathy symptoms as rapidly as lactulose. There are also concerns regarding the cost-effectiveness of the medication.


Benzodiazepine receptor antagonists
A meta-analysis of randomized controlled trials by the international Cochrane Collaboration found benefit from flumazenil.[16] The doses of flumazenil varied around a median of 2 milligrams over 10 minutes: 'Flumazenil was given as a continuous infusion (12 trials), preceded by bolus injections in two trials. One trial used only bolus injections. Patients received flumazenil at a total dose ranging from 0.2 to 19.5 milligram (median 2 milligram). The median duration of treatment was 10 minutes (range one minute to 72 hours)'. However, the benefit was short.


L-ornithine-L-aspartate
L-ornithine-L-aspartate stimulates the urea cycle, and has shown encouraging results in randomized controlled trials