Literature DB >> 15963970

Evaluation of plasma ammonia levels in patients with acute liver failure and chronic liver disease and its correlation with the severity of hepatic encephalopathy and clinical features of raised intracranial tension.

Arun Kundra1, Anil Jain, Alok Banga, Girish Bajaj, Premasish Kar.   

Abstract

OBJECTIVES: The present study was designed to (a) evaluate and compare plasma ammonia levels (PAL) in patients with acute liver failure (ALF) and chronic liver disease (CLD) with or without hepatic encephalopathy (HE); (b) correlate the severity of HE with PAL; and (c) correlate PAL with clinical features of raised intracranial tension in ALF. DESIGN AND METHODS: A total of 40 patients, comprised of 20 patients with ALF (Group A) and 20 patients with CLD (Group B, which was comprised of 8 patients with HE (subgroup B1) and 12 patients without HE (subgroup B2)), were studied. PAL was estimated using an enzymatic UV-method (RANDOX). The clinical and biochemical profile of all the patients was recorded. Correlation between the grade of HE and PAL was derived using Pearson's correlation coefficient. The mean PAL of ALF patients with and without raised intracranial tension was compared using the standard error of difference between the two means.
RESULTS: The mean PAL (micromol/L) +/- SD was as follows: Group A: 172.1 +/- 52.55, subgroup B1: 58.75 +/- 29.38, subgroup B2: 42.17 +/- 18.19 (normal levels = 10-47 micromol/L). All patients with ALF showed PAL more than the upper limit of the normal range, and there was good correlation between the severity of HE and PAL [r = 0.91 at P < 0.05]. In subgroup B1 (CLD with HE), 3/8 patients (37.5%), and in subgroup B2 (CLD with HE), 4/12 patients (33.3%) patients had PAL more than the upper limit of normal range. Within Group A, 14 patients had clinical features of raised intracranial tension/cerebral edema, and the mean PAL of these patients (188.21 +/- 49.15 micromol/L) was significantly higher than those who did not have features of raised intracranial tension (134.5 +/- 42.36 micromol/L) (SE of difference between two means).
CONCLUSIONS: Raised PAL appears to be an important laboratory abnormality seen in patients with ALF, and there seems to be a significant correlation between the severity of encephalopathy and PAL in these patients. However, among patients with CLD, the proportion of patients with PAL more than the upper limit of normal range is not significantly different between those with or without HE. Our study also suggests that high PAL in ALF patients appears to correlate with clinical features of cerebral edema and raised intracranial tension.

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Year:  2005        PMID: 15963970     DOI: 10.1016/j.clinbiochem.2005.04.013

Source DB:  PubMed          Journal:  Clin Biochem        ISSN: 0009-9120            Impact factor:   3.281


  21 in total

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Review 4.  Pathophysiology, diagnosis, and management of hepatic encephalopathy.

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Authors:  Adam Back; Kelsey Y Tupper; Tao Bai; Paulpoj Chiranand; Fernando D Goldenberg; Jeffrey I Frank; James R Brorson
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6.  Recovery of awareness after hyperacute hepatic encephalopathy with "flat" EEG, severe brain edema and deep coma.

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Authors:  Santosh Singh; Surendra K Trigun
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8.  Absence of neuropsychological impairment in hyperammonaemia in healthy young adults; possible synergism in development of hepatic encephalopathy (HE) symptoms?

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9.  Clinical impact of arterial ammonia levels in ICU patients with different liver diseases.

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Review 10.  Hyperammonemia in Hepatic Encephalopathy.

Authors:  A R Jayakumar; Michael D Norenberg
Journal:  J Clin Exp Hepatol       Date:  2018-06-20
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