Studies of the Blood Ammonia in Liver Disease

Stahl, J

doi:10.7326/0003-4819-58-1-1

Cited by 176 publications

(26 citation statements)

References 22 publications

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“…The correlation between plasma ammonia levels and severity of hepatic encephalopathy is not consistent in the literature, and this may be due to differences in sampling sites and assays used (6)(7)(8). Venous ammonia measurement is subject to variability due to a number of factors including contamination of the laboratory with ammoniacontaining compounds, smoking by patient or technician, delay or turbulence in transport, and patient factors such as muscle mass, urinary pH, and hypokalemia (4,9).…”

Section: Discussionmentioning

confidence: 96%

“…Venous ammonia measurement is subject to variability due to a number of factors including contamination of the laboratory with ammoniacontaining compounds, smoking by patient or technician, delay or turbulence in transport, and patient factors such as muscle mass, urinary pH, and hypokalemia (4,9). Arterial ammonia is thought to provide a more accurate assessment of the amount of ammonia at the blood-brain barrier and fewer false-negative results compared to ve- nous ammonia measurements (8). The partial pressure of ammonia (pNH 3 ) can be calculated from the total ammonia and pH, and has been found to correlate more strongly with stage of hepatic encephalopathy than total arterial ammonia (6).…”

Section: Discussionmentioning

confidence: 99%

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Breath Ammonia Testing for Diagnosis of Hepatic Encephalopathy

et al. 2005

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Measurement of arterial ammonia has been used as a diagnostic test for hepatic encephalopathy, but obtaining an arterial specimen is an invasive procedure. The aim of this study was to evaluate the ability of a minimally invasive, highly sensitive optical sensing device to detect ammonia in the breath of patients with end-stage liver disease and to evaluate the correlation of breath ammonia levels, arterial ammonia levels, and psychometric testing. Fifteen subjects with liver cirrhosis and clinical evidence of hepatic encephalopathy underwent mini-mental status examination, number connection test, focused neurological examination, and arterial ammonia testing. On the same day, breath ammonia testing was performed using an apparatus that consists of a sensor (a thin membrane embedded with a pH-sensitive dye) attached to a fiberoptic apparatus that detects optical absorption. Helicobacter pylori testing was performed using the 14C urea breath test. A positive correlation was found between arterial ammonia level and time to complete the number connection test (r = 0.31, P = 0.03). However, a negative correlation was found between breath ammonia level and number connection testing (r = -0.55, P = 0.03). Furthermore, no correlation was found between breath and arterial ammonia levels (r = -0.005, P = 0.98). There is a significant correlation between the trailmaking test and arterial ammonia levels in patients with cirrhosis. However, no correlation was found between breath and arterial ammonia levels using the fiberoptic ammonia sensor apparatus in this small study.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Breath Ammonia Testing for Diagnosis of Hepatic Encephalopathy

et al. 2005

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“…A relation between ammonia levels and the risk of cerebral edema in cirrhosis (17) has not been examined. Ammonia levels should be promptly assayed in an experienced laboratory to avoid pitfalls in its determination (18).…”

Section: Hepatic Encephalopathy Is a Diagnosis Of Exclusionmentioning

confidence: 99%

Hepatic encephalopathy

Blei¹

2001

The American Journal of Gastroenterology

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“…4 Many investigators have described a close correlation between ammonia levels and cerebral function (for review, see Butterworth et al 3 ), whereas others have questioned either the strength of such a correlation or even any causal relationship between ammonia and HE. [5][6][7] Some of this discrepancy can be resolved by accounting for the frequent use of venous ammonia levels, which are appreciably lower than arterial ammonia, to which the brain is exposed. 4 A further important reason may be related to ammonia kinetics.…”

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confidence: 99%

Partial pressure of ammonia versus ammonia in hepatic encephalopathy

et al. 2000

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Ammonia is considered the major pathogenetic factor of cerebral dysfunction in hepatic failure. The correlation between total plasma ammonia and the severity of hepatic encephalopathy (HE), however, is variable. Because ammonia that is present in gaseous form readily enters the brain, the correlation with the grade of HE of the pH-dependent partial pressure of gaseous ammonia (pNH 3 ) could be better than that of total arterial ammonia levels. To test this hypothesis, 56 cirrhotic patients with acute episodes of clinical HE (median age, 54 years; range, 21-75) were studied by clinical examination and by long-latency mediannerve sensory-evoked potentials (SEPs) N70 peak, an objective and sensitive electrophysiological measure of HE. pNH 3 was calculated from arterial blood according to published methods. The clinical grade of HE correlated (P F .001) with both pNH 3 and total ammonia, but correlation was stronger with pNH 3 (r ‫؍‬ .79 vs. .69, P ‫؍‬ .01). A similar correlation was found for N70 peak latency (r ‫؍‬ .71 with pNH 3 vs. .64 with total ammonia, respectively, P ‫؍‬ .08). In summary, arterial pNH 3 correlates more closely than total ammonia with the degree of clinical and electrophysiological abnormalities in HE. These findings support the ammonia hypothesis of HE and suggest that pNH 3 might be superior to total ammonia in the pathophysiological evaluation of HE. (HEPATOLOGY 2000;31:30-34.)Although there is little doubt that ammonia plays a major role in the pathogenesis of hepatic encephalopathy (HE), 1-3 the relation between plasma ammonia and the severity of cerebral dysfunction is variable. 4 Many investigators have described a close correlation between ammonia levels and cerebral function (for review, see Butterworth et al. 3 ), whereas others have questioned either the strength of such a correlation or even any causal relationship between ammonia and HE. 5-7 Some of this discrepancy can be resolved by accounting for the frequent use of venous ammonia levels, which are appreciably lower than arterial ammonia, to which the brain is exposed. 4 A further important reason may be related to ammonia kinetics. In biological fluids, ammonia exists in 2 forms: as ammonium ion and as gaseous, unionized ammonia (NH 3 ). 8 At a physiological pH of 7.4, 98% of total plasma ammonia is ionized and 2% is present as gaseous NH 3 . 8 In intracellular fluid where the pH is about 7.0, an even smaller fraction exists as unionized NH 3 . Because biological membranes are much more permeable to nonionized than to ionized molecules, 8 only the nonionized NH 3 freely diffuses through the blood-brain barrier. 9 Partial pressure of NH 3 (pNH 3 ) can be calculated from total ammonia and pH 10 and increases with pH. Despite an almost universal validity across species, 8 the phenomenon of pH-dependent ammonia toxicity has been largely ignored in the clinical setting. In this study, arterial pNH 3 was compared with total arterial ammonia levels regarding their correlation with the severity of HE. Cerebral dysfunction was assesse...

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Studies of the Blood Ammonia in Liver Disease

Cited by 176 publications

References 22 publications

Breath Ammonia Testing for Diagnosis of Hepatic Encephalopathy

Breath Ammonia Testing for Diagnosis of Hepatic Encephalopathy

Hepatic encephalopathy

Partial pressure of ammonia versus ammonia in hepatic encephalopathy

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