Ionic Mobilities in Ammonia-Hydrogen Mixtures and an Anomalous Effect of Ammonia.
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EXPERIMENTAL BIOLOGY OF AMMONIA-RICH ENVIRONMENTS: OPTICAL AND ISOTOPIC EVIDENCE FOR VITAL ACTIVITY IN Penicillium IN LIQUID AMMONIA-GLYCEROL MEDIA AT -40 degrees C.
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Staging properties of potassium-ammonia ternary graphite intercalation compounds at high ammonia pressure.
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Some Effects of Ammonia on Plant Metabolism and a Possible Mechanism for Ammonia Toxicity.
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l-Phenylalanine Ammonia-lyase (Maize): Partial Purification and Response to Gibberellic Acid and Cycloheximide of l-Phenylalanine and l-Tyrosine Ammonia-lyase Activities.
Extracts of maize leaf sheath tissue deaminate both l-phenylalanine and l-tyrosine. The activities with both substrates are enhanced by treating the plant with gibberellic acid. Both activities decrease rapidly at the same rate when tissue is incubated in a moist atmosphere, and this decrease can be slowed by treatment with cycloheximide. The ratio of the activities was constant throughout a series of purification steps which included acetone and ammonium sulfate precipitation, and passage through an agarose column. The two activities could not be separated by isoelectric focusing. These results support our earlier conclusion that both activities occur at the same catalytic site.
Journal Article↗
The distribution of ammonia between hepatocytes and extracellular fluid.
1. Some factors determining the distribution of ammonia between hepatocytes and the suspension medium and between mitochondria and cell cytosol were examined. 2. Intracellular [ammonia] of isolated hepatocytes was similar to that in freeze-clamped rat liver. The intra- to extracellular [ammonia] ratio ('ammonia ratio') of cells incubated without added substrates was as great as 70. 3. High ammonia ratios were found only within the physiological range of extracellular [ammonia] i.e. 0.03 mM. At higher external [NH4Cl] the ammonia ration decreased until at 20 mM it approached 1.0. 4. On addition of NH4Cl (10.0 mM) ammonia entered hepatocytes rapidly until at about 2.5 min internal and external ammonia concentration were similar. The final steady state distribution of ammonia was not reached until 60 min, when the internal concentration was slightly higher than that externally. 5. Intracellular [K+] decreased when intracellular [ammonia] increased. The sum of intracellular [K+] plus [NH4(+)] remained approximately constant. 6. In anaerobic cells the high endogenous ammonia ratio was not maintained. 7. The high physiological ammonia ratio was not abolished by ouabain. Thus the (Na+ + K+)-ATPase does nt appear to be responsible for the maintenance of the ammonia ratio. 8. A high ammonia ratio also existed between hepatocyte cytosol and mitochondria. 9. On addition of fructose, which depletes the cells of Pi and adenine nucleotides, the ammonia content of the cells decreased parallel with Pi and ATP. In the presence of fructose much ammonia was removed by the formation of alanine. However, when pyruvate was added to stimulate alanine formation there was no effect on the ammonia distribution. This showed that alanine formation alone was not responsible for decreased intracellular [ammonia] with fructose. 10. Incubation with adenosine led to a large increase in intracellular ATP and ammonia content as well as in the ammonia ratio. Incubation with alanine also led to increased intracellular ammonia production but in this case ammonia was released into the medium and high ammonia ratios did not occur. 11. Some mechanisms for maintenance of a high ammonia ratio between cells and medium are discussed.
Ammonia↗
Strategies for surviving high concentrations of environmental ammonia in the swamp eel Monopterus albus.
The swamp eel Monopterus albus lives in muddy ponds, swamps, canals, and rice fields in the tropics. It encounters high concentrations of environmental ammonia (HEA) during dry seasons or during agricultural fertilization in rice fields. This study aimed at determining the tolerance of M. albus to environmental ammonia and at elucidating the strategies that it adopts to defend against ammonia toxicity in HEA. In the laboratory, M. albus exhibited very high environmental ammonia tolerance; the 48-, 72-, and 96-h median lethal concentrations of total ammonia at pH 7.0 and 28 degrees C were 209.9, 198.7, and 193.2 mM, respectively. It was apparently incapable of actively excreting ammonia against a concentration gradient. In addition, it did not detoxify ammonia to urea, the excretion of which would lead to a loss of nitrogen and carbon, during ammonia loading. The high tolerance of M. albus to HEA was attributable partially to its exceptionally high tolerance to ammonia at the cellular and subcellular levels. During the 144 h of exposure to 75 mM NH(4)Cl at pH 7.0, the ammonia contents in the muscle, liver, brain, and gut of M. albus reached 11.49, 15.18, 6.48, and 7.51 mu mol g(-1), respectively. Such a capability allowed the accumulation of high concentrations of ammonia in the plasma (3.54 mu mol mL(-1)) of M. albus exposed to HEA, which would reduce the net influx of exogenous ammonia. Subsequent to the buildup of internal ammonia levels, M. albus detoxified ammonia produced endogenously to glutamine. The glutamine contents in the muscle and liver reached 10.84 and 17.06 mu mol g(-1), respectively, after 144 h of exposure to HEA, which happened to be the highest known for fish. Unlike urea, the storage of glutamine in the muscle during ammonia loading allowed its usage for anabolic purposes when the adverse environmental condition subsides. Glutamine synthetase activity increased significantly in the liver and gut (2.8- and 1.5-fold, respectively) of specimens exposed to HEA for 144 h. These results suggest that the liver was the main site of ammonia detoxification and the gut was more than a digestive/absorptive organ in M. albus. Monopterus albus did not undergo a reduction in amino acid catabolism during the first 24 h of ammonia exposure. However, assuming a total inhibition of excretion of endogenous ammonia, there was a deficit of -312 mu mol N between the reduction in nitrogenous excretion (3,360 mu mol N) and the retention of nitrogen (3,048 mu mol N) after 72 h of aerial exposure. The deficit became much greater after 144 h, reaching a value of -3,243 mu mol N. These results suggest that endogenous ammonia production in M. albus was suppressed in order to prevent the newly established internal steady state concentration of ammonia from rising to an intolerable level after an extended period of exposure to HEA.
Amino Acids↗
Ammonia production by intestinal bacteria: the effects of lactose, lactulose and glucose.
Ammonia production by eight groups of intestinal bacteria was measured, and the effect on ammonia production of lowered pH and ambient ammonia concentration was determined. Endogenous ammonia production from bacterial protoplasm was also examined. To examine the mechanisms by which fermentable substrates reduce ammonia formation in a faecal incubation system, the effect of lactose, lactulose or glucose on ammonia release by pure cultures of intestinal bacteria was studied. The largest amounts of ammonia were generated by gram-negative anaerobes, clostridia, enterobacteria, and Bacillus spp. Gram-positive non-sporing anaerobes, streptococci and micrococci formed modest amounts, and lactobacilli and yeasts formed very little ammonia. All groups of bacteria formed less ammonia at pH 5.0 than at pH 7.0 and production of ammonia was not inhibited when 30 mmol ammonia/litre was included in the medium. Small amounts of ammonia were formed due to endogenous metabolism of bacterial cells. Washed cell suspensions of four isolates of Bacteroides, one clostridial isolate and two streptococcal isolates formed less ammonia from alanine, methionine or histidine after growth in the presence of either lactose or lactulose. In contrast, the Bacteroides isolates formed more ammonia from aspartate than from either lactose or lactulose. Also, cultures of gram-negative anaerobes and enterobacteria, and to a lesser extent clostridia and streptococci, formed significantly less ammonia in nutrient broth when lactose, lactulose or glucose was included in the medium. This decrease in ammonia formation was not due to a fall in pH of the medium. Ammonia production by gram-positive non-sporing anaerobes was not affected by carbohydrate fermentation. These results suggest that gram-negative anaerobic bacteria make a major contribution to ammonia generated from peptides and amino acids in vivo, and that ammonia may be formed from bacterial cells in the colon. Fermentation of lactose and lactulose may repress the formation and inhibit the activity of enzymes responsible for ammonia release. In the human colon these substrate effects may decrease the amount of ammonia available to exert a toxic effect on the host, and thus contribute to the beneficial effects of lactulose when it is used in the treatment of portosystemic encephalopathy.
Amino Acids↗
Interorgan ammonia metabolism in liver failure.
In the post-absorptive state, ammonia is produced in equal amounts in the small and large bowel. Small intestinal synthesis of ammonia is related to amino acid breakdown, whereas large bowel ammonia production is caused by bacterial breakdown of amino acids and urea. The contribution of the gut to the hyperammonemic state observed during liver failure is mainly due to portacaval shunting and not the result of changes in the metabolism of ammonia in the gut. Patients with liver disease have reduced urea synthesis capacity and reduced peri-venous glutamine synthesis capacity, resulting in reduced capacity to detoxify ammonia in the liver. The kidneys produce ammonia but adapt to liver failure in experimental portacaval shunting by reducing ammonia release into the systemic circulation. The kidneys have the ability to switch from net ammonia production to net ammonia excretion, which is beneficial for the hyperammonemic patient. Data in experimental animals suggest that the kidneys could have a major role in post-feeding and post-haemorrhagic hyperammonemia.During hyperammonemia, muscle takes up ammonia and plays a major role in (temporarily) detoxifying ammonia to glutamine. Net uptake of ammonia by the brain occurs in patients and experimental animals with acute and chronic liver failure. Concomitant release of glutamine has been demonstrated in experimental animals, together with large increases of the cerebral cortex ammonia and glutamine concentrations. In this review we will discuss interorgan trafficking of ammonia during acute and chronic liver failure. Interorgan glutamine metabolism is also briefly discussed, since glutamine synthesis from glutamate and ammonia is an important alternative pathway of ammonia detoxification. The main ammonia producing organs are the intestines and the kidneys, whereas the major ammonia consuming organs are the liver and the muscle.
Ammonia↗
Exhaled breath condensate pH assays are not influenced by oral ammonia.
BACKGROUND: Measurement of pH in exhaled breath condensate (EBC) is robust and simple. Acidic source fluid (airway lining fluid) traps bases while volatilising acids, leading to EBC acidification in many lung diseases. Lower airway ammonia is one determinant of airway lining fluid pH, raising the concern that addition of the base ammonia by contamination from the mouth might confound EBC pH assays. METHODS: Three discrete methods were used to limit oral ammonia contamination of EBC collections: endotracheal intubation, oral rinsing, and -40 degrees C condenser temperatures. Separately, ammonia was removed from collected EBC samples by lyophilisation and resuspension. Intraweek and intraday variability of ammonia concentration was determined in 76 subjects, and ammonia and pH from a further 235 samples were graphically compared. Ammonia was assayed spectrophotometrically and pH was assessed after deaeration. RESULTS: Data from 1091 samples are presented. Ammonia was reduced in EBC by all methods. Endotracheal intubation decreased EBC ammonia from a mean (SD) of 619 (124) microM to 80 (24) microM (p<0.001, n=32). Oral rinsing before collection also led to a decline in EBC ammonia from 573 (307) microM to 224 (80) microM (p=0.016, n=7). The colder the condensation temperature used, the less ammonia was trapped in the EBC. Lyophilisation removed 99.4 (1.9)% of ammonia. Most importantly, the pH of EBC never decreased after removal of ammonia by any of these methods. Intraweek and intraday coefficients of variation for ammonia were 64 (27)% and 60 (32)%, which is substantially more variable than EBC pH assays. CONCLUSIONS: Although ammonia and pH appear to correlate in EBC, the oral ammonia concentration is not an important determinant of EBC pH. No precautions need to be taken to exclude oral ammonia when EBC pH is of interest. The low pH and low ammonia found in EBC from patients with lung diseases appear to be independent effects of volatile compounds arising from the airway.
Adult↗
Cerebral herniation in patients with acute liver failure is correlated with arterial ammonia concentration.
Cerebral edema leading to cerebral herniation (CH) is a common cause of death in acute liver failure (ALF). Animal studies have related ammonia with this complication. During liver failure, hepatic ammonia removal can be expected to determine the arterial ammonia level. In patients with ALF, we examined the hypotheses that high arterial ammonia is related to later death by CH, and that impaired removal in the hepatic circulation is related to high arterial ammonia. Twenty-two patients with ALF were studied retrospectively. In addition, prospective studies with liver vein catheterization were performed after development of hepatic encephalopathy (HE) in 22 patients with ALF and 9 with acute on chronic liver disease (AOCLD). Cerebral arterial-venous ammonia difference was studied in 13 patients with ALF. In all patients with ALF (n = 44), those who developed CH (n = 14) had higher arterial plasma ammonia than the non-CH (n = 30) patients (230 +/- 58 vs. 118 +/- 48 micromol/L; P <. 001). In contrast, galactose elimination capacity, bilirubin, creatinine, and prothrombin time were not different (NS). Cerebral arterial-venous differences increased with increasing arterial ammonia (P <.001). Arterial plasma ammonia was lower than hepatic venous in ALF (148 +/- 73 vs. 203 +/- 108 micromol/L; P <.001). In contrast, arterial plasma ammonia was higher than hepatic venous in patients with AOCLD (91 +/- 26 vs. 66 +/- 18 micromol/L; P <.05). Net ammonia release from the hepatic-splanchnic region was 6.5 +/- 6. 4 mmol/h in ALF, and arterial ammonia increased with increasing release. In contrast, there was a net hepatic-splanchnic removal of ammonia (2.8 +/- 3.3 mmol/h) in patients with AOCLD. We interpret these data that in ALF in humans, vast amounts of ammonia escape hepatic metabolism, leading to high arterial ammonia concentrations, which in turn is associated with increased cerebral ammonia uptake and CH.
Acute Disease↗
Ammonia exposure and hazard assessment for selected household cleaning product uses.
There is scant information pertaining to airborne ammonia exposures from either spills or common household uses of ammonia-containing floor and tile cleaners or from spray-on glass cleaners. We assessed instantaneous and event-specific time-weighted average (TWA) exposures to airborne ammonia during spills and use (per label directions) of a household floor and tile cleaner and two spray-on window cleaners. Airborne ammonia levels measured at breathing zone height (BZH) above the spilled floor and tile cleaner product reached 500 p.p.m. within 5 min, while levels for spilled window cleaner were below 8 p.p.m. TWA exposures were assessed while tile walls and floors were cleaned in three different bathrooms of a residence, and during use of a spray-on glass cleaner while washing several large windows in an office setting. NIOSH Method 6015 was utilized with concurrent field measurements every 60 s using a Drager PAC III monitor with an electrochemical cell detector. Peak ammonia levels ranged from 16 to 28 p.p.m. and short-term TWA concentrations ranged from 9.4 to 13 p.p.m. during mixing (0.1% ammonia) and cleaning tiles in the three bathrooms. Ammonia exposures while using spray-on window cleaner were over 10-fold lower (TWA=0.65 p.p.m.). Use of the floor and tile cleaner mixed at 0.2% ammonia led to peak airborne ammonia levels within 3-5 min at 36-90 p.p.m., and use of full strength cleaner (3% ammonia) led to peak ammonia levels of 125 to >200 p.p.m. within 2-3 min. Spillage or intentional use of the full strength floor and tile cleaner led to airborne ammonia concentrations that exceed occupational short-term exposure limits, while spillage or use of the spray-on window cleaner did not approach potentially hazardous airborne ammonia levels and likely represents a minimal inhalation health hazard. We conclude that routine household uses of ammonia are unlikely to produce significant exposures when using standard cleaning solutions (0.1-0.2%), but spillage or use of concentrated ammonia solutions (e.g., 3%) in poorly ventilated areas can lead to potentially hazardous airborne ammonia exposures.
Ammonia↗
Ammonia movement in the small intestine: preferential transport by the ileum.
Isolated, surviving sacs of everted small intestine were used to characterize ammonia transport in the golden hamster. Jejunal and ileal sacs incubated aerobically in ammonia-free test solution liberated the same quantity of ammonia as did sacs that were filled and immediately emptied of their contents, indicating no significant evolution of metabolic ammonia. Under aerobic conditions, ileal sacs transferred a solution of high ammonia content from the mucosal surface to the serosal surface against a concentration gradient. This transport was not glucose dependent and exhibited first-order Michaelis-Menten kinetics. Inhibition of absorption occurred with anaerobiosis, 2,4-dinitrophenol, and sodium cyanide. In jejunal segments ammonia was not transported against an adverse chemical gradient. Ileal ammonia absorption was accompanied by bicarbonate secretion and acidification of the serosal solution. Both bicarbonate movement and pH gradients were abolished by inhibitors of ammonia transport. In the jejunum, the absence of ammonia movement occurred in association with minimal bicarbonate secretion and no appreciable change in serosal pH. Despite the creation of hydrogen ion gradients tending to augment or to retard ammonia absorption by nonionic diffusion, ammonia movement was unaffected, i.e., relative acidification of serosal contents did not augment ammonia absorption, and relative alkalinization of serosal fluid caused no inhibition of ammonia transport. In the absence of bicarbonate ion, ammonia transport did not occur. The significance of these findings is discussed with consideration of both ionic and nonionic mechanisms of ammonia movement. It is suggested that ammonia is absorbed in the ileum by active ionic transport.
Ammonia↗
Effect of intrahepatic portal-systemic shunting on hepatic ammonia extraction in patients with cirrhosis.
Increased plasma ammonia levels in patients with advanced cirrhosis have been attributed to reduced conversion of enteric ammonia to urea by the diseased liver and to entry of enteric ammonia into systemic circulation by way of portal-systemic shunts. Because single-pass extraction is high for portal venous ammonia, reduction of portal blood supply to hepatocytes may have detrimental effects on the hepatic extraction of ammonia. To assess how the development of intrahepatic portal-systemic shunts alters hepatic ammonia metabolism, we determined portal and hepatic venous ammonia levels along with measurements of intrahepatic portal-systemic shunts using 99mTc-macroaggregated albumin in 46 patients with portal hypertension. Hepatic venous ammonia levels in the groups of patients with idiopathic portal hypertension, Child class A cirrhosis and Child class B or C cirrhosis were 36 +/- 17, 75 +/- 26 and 93 +/- 52 micrograms/dl, respectively, in increasing order, and portal venous ammonia extraction rates as calculated with the equation (portal venous ammonia-hepatic venous ammonia)/portal venous ammonia x 100% were decreased in the same order (77% +/- 14%, 50% +/- 21%, 40% +/- 25%, respectively). Furthermore, we noted a significant negative correlation between the intrahepatic shunt indexes as calculated by counts per minute in lungs/counts per minute in lungs and liver x 100% and the ammonia extraction rates. It was noteworthy that among Child class C patients, the ammonia extraction rates were significantly lower in patients with high intrahepatic shunt indexes than in those with low shunt indexes. These results demonstrate a significant direct relationship between hepatic ammonia extraction rates and intrahepatic shunting in cirrhosis.
Adult↗
Brain metabolism of 13N-ammonia during acute hepatic encephalopathy in cirrhosis measured by positron emission tomography.
Animal studies and results from 13N-ammonia positron emission tomography (PET) in patients with cirrhosis and minimal hepatic encephalopathy suggest that a disturbed brain ammonia metabolism plays a pivotal role in the pathogenesis of hepatic encephalopathy (HE). We studied brain ammonia kinetics in 8 patients with cirrhosis with an acute episode of clinically overt HE (I-IV), 7 patients with cirrhosis without HE, and 5 healthy subjects, using contemporary dynamic 13N-ammonia PET. Time courses were obtained of 13N-concentrations in cerebral cortex, basal ganglia, and cerebellum (PET-scans) as well as arterial 13N-ammonia, 13N-urea, and 13N-glutamine concentrations (blood samples) after 13N-ammonia injection. Regional 13N-ammonia kinetics was calculated by non-linear fitting of a physiological model of brain ammonia metabolism to the data. Mean permeability-surface area product of 13N-ammonia transfer across blood-brain barrier in cortex, PS(BBB), was 0.21 mL blood/min/mL tissue in patients with HE, 0.31 in patients without HE, and 0.34 in healthy controls; similar differences were seen in basal ganglia and cerebellum. Metabolic trapping of blood 13N-ammonia in the brain showed neither regional, nor patient group differences. Mean net metabolic flux of ammonia from blood into intracellular glutamine in the cortex was 13.4 micromol/min/L tissue in patients with cirrhosis with HE, 7.4 in patients without HE, and 2.6 in healthy controls, significantly correlated to blood ammonia. In conclusion, increased cerebral trapping of ammonia in patients with cirrhosis with acute HE was primarily attributable to increased blood ammonia and to a minor extent to changed ammonia kinetics in the brain.
Acute Disease↗
On the deposition of volatiles and semivolatiles from cigarette smoke aerosols: relative rates of transfer of nicotine and ammonia from particles to the gas phase.
The hypothesis that elevated levels of ammonia-releasing compounds in tobacco and ammonia in mainstream (MS) smoke increase the rate and amount of nicotine evaporation from the particles of MS smoke aerosol was examined by kinetic modeling and experiments with MS cigarette smoke. Computational simulation of a kinetic mechanism describing volatile loss of nicotine, ammonia, and acetic acid from an aqueous solution was used to compute the time-dependent concentration of all species in the model. Because of the high volatility of ammonia relative to that of nicotine, variation over a wide range of initial ammonia concentration had no significant effect upon the rate of loss of nicotine from the model system. The effects of a variation in the volatile loss rate constant for ammonia and for the acid were examined. The simulations show that ammonia is lost from the model solution at a greater rate than nicotine and acid, and the loss of volatile acid has a significant role in the rate and amount of nicotine loss. Simulations with a model system undergoing a continuous steady addition of ammonia showed that high rates of ammonia addition could significantly increase the rate of nicotine volatile loss from the model solution. A series of smoking experiments was performed using blended cigarettes connected to a denuder tube. Deposition of smoke constituents can occur directly from the gas phase and by the deposition of smoke aerosol particles themselves. As nicotine exists >99% in the particle phase of MS smoke, in the absence of particle deposition, denuder tube deposition of nicotine occurs via the evaporation-deposition pathway. Solanesol, a nonvolatile tobacco and smoke terpene, was used to quantify the amount of particle deposition onto the denuder tube. The amount of ammonia deposited on the denuder tube was an order of magnitude greater than that of nicotine, showing that ammonia evaporates from the MS smoke particles much faster than does nicotine. The experimental results were supported and explained by the aqueous model simulations. Included in these experiments are cigarettes that differ in their MS smoke ammonia content by a factor of ca. five. However, an increased amount of MS smoke ammonia does not increase the rate of nicotine loss from the particles. The combined results support the conclusion that ammonia in mainstream smoke has little effect, if any, upon the rate and amount of nicotine evaporation from MS smoke particles.
Aerosols↗
Ammonia saturation constants for predominant species of rumen bacteria.
Ammonia saturation constants were determined for representative pure cultures of predominant, anaerobic, fermentative rumen bacteria. Based on growth experiments with ammonia limited continuous cultures, average estimates for ammonia saturation constants of Bacteroides amylophillus and Bacteroides ruminicola were 10.5 and 23.5 microM ammonia-nitrogen, respectively. With ammonia-limited linear-growth cultures, the estimates for the ammonia saturation constants of B. amylophilus, B. ruminicola, and Selenomonas ruminantium were, respectively, 6, 33.5, and 18 microM ammonia nitrogen. By a third method, which involved estimation of ammonia concentration in the medium when the growth rate of ammonia-limited batch cultures reached half maximal, the ammonia saturation constant was determined for the species mentioned as well as Megaspaera elsdenii and Ruminococcus flavefaciens. Except for M. elsdenii, saturation constants of the other bacteria were less than 50 microM ammonia nitrogen. An organism with a saturation constant for ammonia of 50 microM growing in a medium containing 1 mM ammonia should achieve 95% of its maximum specific growth rate. Many of the predominant species of rumen bacteria are efficient scavengers of ammonia.
Ammonia↗
Breath and blood ammonia in liver cirrhosis.
BACKGROUND/AIMS: Hyperammonemia causes dysfunction of multiple organs in patients with cirrhosis, including hepatic encephalopathy. Blood ammonia concentrations are monitored with respect to disease progression and efficacy of treatment. Fetor hepaticus, the characteristic breath odor in hepatic encephalopathy has called little quantitative attention to breath ammonia. We studied the dynamics of ammonia metabolism in cirrhosis in terms of the relationship between breath and blood ammonia. METHODOLOGY: Breath and blood ammonia levels were measured simultaneously in 20 cirrhotic patients and in 10 healthy volunteers. Breath ammonia was measured using ammonia electrodes in collected expired air. Helicobacter pylori serum antibody titers were also measured, since the organism produces ammonia. RESULTS: Blood ammonia correlated positively with breath ammonia in patients with cirrhosis. Breath ammonia levels were significantly higher in cirrhotic patients (0.745 ppm) than in controls (0.278 ppm), and higher in cirrhotic patients with hyperammonemia (0.997 ppm) than in those without (0.558 ppm). Breath and blood ammonia decreased together with treatment of hyperammonemia. H. pylori seropositivity was 20% in controls, 27.3% in cirrhotic patients with normal blood ammonia, and 66.7% in those with hyperammonemia. CONCLUSIONS: Breath ammonia measurement may be useful in diagnosis, treatment assessment, and follow-up in hepatic encephalopathy.
Adult↗