Plasma ammonia concentration

Hnber, M., Rossle, M., Siegerstetter, V., Ochs, A., Haag, K., Kist, M., Blnm, H.E. Helicobacter pylori infection does not correlate with plasma ammonia concentration and hepatic encephalopathy in patients with cirrhosis. Hepato-Gastroenterol. 2001 48 541 -544... 

The fasting venous plasma ammonia concentration is useful in the differential diagnosis of encephalopathy when it is unclear if encephalopathy is of an hepatic origin. It is especially helpful in diagnosing Reye s syndrome and the inherited disorders of urea metabolism. However, it is not a useful test to use in patients with laiown liver disease. 

The pathophysiology of hepatic encephalopathy is not completely understood but includes an increased sensitivity to dietary proteins. Ammonia concentrations are always increased with acute encephalopathy and usually increased with chronic encephalopathy. A reduction of plasma ammonia is often associated with symptomatic improvement. However, since plasma ammonia concentrations do not correlate with the severity of the encephalopathy, it has been suggested that other factors are involved. It is now recognized that a variety of neurotransmitter systems are dysfunctional in hepatic encephalopathy, but the exact cause for the changes is not known. One important contributor is the endogenous benzodiazepine agonist system, but other abnormalities must be invoked to explain all the findings. ... 

The diagnosis of hepatic encephalopathy is made on clinical grounds. Plasma ammonia concentrations are rarely helpful, either for diagnosis or for monitoring the patient s disorder normal ammonia concentrations are helpful in excluding hepatic encephalopathy as a cause of cerebral dysfunction. An exception is a patient who presents with acute encephalopathy of unknown cause. Elevated ammonia concentrations in that situation suggest acute hepatic failure or Reye s syndrome. 

Means to reduce the rate of nitrogen release from urea in the rumen (and subsequent post-feeding peak in rumen and plasma ammonia concentrations) have been... 

Colombo JP, Peheim E, Kretschmer R, Dauwalder H, Sidiropoulos D. Plasma ammonia concentrations in newborns and children. Clinica Chimica Acta 1984 138 283-191... 

Divalproex sodium extended-release has been evaluated in a 12-month, open extension of a 3-month, double-blind, placebo-controlled, multicenter study in 112 adolescents with migraine [339. The most common symptomatic adverse events were weight gain (15%), nausea (14%), somnolence (12%), upper respiratory tract infection (11%), and sinusitis (8%). Five subjects had serious adverse events, and 15 prematurely withdrew because of an adverse event. Plasma ammonia concentrations were increased in 8% but there were no other clinically significant changes in laboratory values, vital signs, or electrocardiography. 

In a 6-month open study of divalproex sodium extended-release (15 mg/kg/day on day 1 with increases allowed to a maximum of 35 mg/kg) in 226 children and adolescents with acute mania associated with bipolar I disorder the most common adverse events were weight gain (16%), nausea (9%), and increased appetite (8%) raised plasma ammonia concentrations were non-symptomatic in all cases [340 J. 

In a 28-day, double-blind, placebo-controlled study, followed by a 6-month open extension study of divalproex extended-release in 150 children and adolescents with bipolar disorders, there were no significant differences in efficacy [344 ]. Four of those who took divalproex extended-release and three of those who took placebo withdrew because of adverse effects. Mean plasma ammonia concentrations increased with divalproex extended-release, but only one patient was symptomatic. In the 6-month open extension study, the most common adverse events were headache and vomiting. 

Urease. An enzyme of the hydrolase class that catalyzes the hydrolysis of urea to COj and ammonia. It is nickel protein found in micro-organisms and plant that is frequently used in clinical assays of plasma urea concentrations. 

Ammonia is normally present in all tissues of the body. The distribution and metabolic fate of absorbed ammonia depends on the route of administration. The distribution of endogenous and absorbed ammonia in various body compartments is influenced by pH. The lower the pH of a compartment, the greater its total ammonia content (NRC 1979). The normal concentration of ammonia in human blood is approximately 1 milligram per liter (mg/L) (Wands 1981). Total ammonia concentrations in humans are 70-113 micromoles (pmol) in arterial blood and plasma, 5-40 /rmol in venous blood and plasma, and 20-100 /imol in cerebrospinal fluid (Cooper and Plum 1987). 

The determination of ammonia in blood is carried out enzymatically, which is considered to be specific, precise and simple. (48) Serious mistakes can easily occur during the preanalytical phase of ammonia determination, making it imperative to comply with the standardized method of taking a blood sample, (s. p. 91) EDTA blood should be taken with the addition of sodium borate and L-serine. Furthermore, elevated serum y-GT activity and increased thrombocytes cause the ammonia level to rise, as does cigarette smoking prior to blood collection. Even minor haemolysis (e. g. in the event of prolonged transport) will spoil the blood for ammonia determination, since the ammonia concentration of erythrocytes is three times that found in plasma. Besides these interfering factors, ammonia concentration is influenced by (7.) the metabolic performance of the urea cycle, (2.) the extrahepatic formation and elimination of ammonia, and (5.) the acid-base status. 

Owing to the multitude of factors interfering with the ammonia concentration as well as to the multifactorial pathogenesis of hepatic encephalopathy (HE), it is understandable that there is no correlation between the levels of ammonia and the prevailing HE stage. Nevertheless, a hyperammonia syndrome is generally presumed if concentrations in the venous or arterial plasma reach 135-170 4g/dl. A value of > 150 gg/dl can be attributed to coma stage I. Here, the arterial ammonia level correlates better with HE than do the values found in venous blood, (s. pp 56, 266)... 

Thus changes in the zinc concentration of plasma, erythrocytes, leucocytes, and urine and changes in the activities of zinc-dependent enzymes such as alkaline phosphatase, RNase in the plasma, and deoxythymidine kinase in the tissue during the zinc restriction phase, appear to have been induced specifically by a mild deficiency of zinc in the volunteers. One unexpected finding was with respect to plasma ammonia level which appeared to increase during the zinc-restricted period. We recently have reported a similar finding in zinc deficient rats (88). This... 

Both enzymatic and chemical methods are used to measure ammonia in body Buids. Enzymatic assay with glutamate dehydrogenase is the most frequently used method. Plasma ammonia measurement is particularly susceptible to contamination, leading to falsely elevated concentrations. Some of the common samphng problems are discussed in the third edition of this textbook. 

Endocrine Effects. Adrenaline levels in urine, 17-oxycorticosteroids in the urine, and 11-oxycorticosteroid levels in blood were increased in humans exposed to 3.0 ppm ammonia for 37 days (Kalandarov et al. 1984). Exposure to 7.2 ppm for 17 days also increased adrenaline levels in urine and 17-oxycorticosteroids in the urine, and increased free, but not total, 11-oxycorticosteroid levels in blood (Kalandarov et al. 1984). Experimental details were lacking in this study additionally, no clinical or histological data were provided for this or other end points in this study and no supporting data are available in the literature. Therefore, the significance of these effects is unclear. Exposure of pigs to up to 100 ppm ammonia for 6 days did not significantly alter the plasma cortisol concentration (Gustin et al. 

As a catabolic waste product ammonia must be translocated from the different tissues to liver for conversion into urea, and to the kidneys for excretion. Circulating blood, however, contains practically no free ammonia (Parnas, Conway). Glutamine, present in blood plasma in concentrations of 5-12 mg.% (86, 87, 7), acts as the vehicle of ammonia. 

CH 10 METABOLISM OF AMMONIA AND NUCLEIC ACIDS Table 10.5 Changes in the concentration of various intermediates of the urea cycle or their metabolites in plasma or urine in various enzyme deficiency diseases in humans ... 

Various methods for lowering the concentrations of NO in combustion products have been proposed lowering the temperature,13 which decreases NO output from both sources introduction of ammonia additives,1, 15 which reacts readily with NO and use of a plasma jet of nitrogen atoms.16 In coal combustion the nitrogen oxide is removed in a heterogeneous reaction on the surface of the coal particles.17... 

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