• Title of article

    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

  • Author/Authors

    Arun Kundra، نويسنده , , Anil Jain، نويسنده , , Alok Banga، نويسنده , , Girish Bajaj، نويسنده , , Premasish Kar، نويسنده ,

  • Issue Information
    روزنامه با شماره پیاپی سال 2005
  • Pages
    4
  • From page
    696
  • To page
    699
  • 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 Pearsonʹs 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 (μmol/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 μmol/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 μmol/L) was significantly higher than those who did not have features of raised intracranial tension (134.5 ± 42.36 μmol/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.
  • Keywords
    Hepatic encephalopathy , chronic liver disease , Acute liver failure , Plasma ammonia
  • Journal title
    Clinical Biochemistry
  • Serial Year
    2005
  • Journal title
    Clinical Biochemistry
  • Record number

    482753