الفهرس 
AcknowledgementsOnly 14 pages are availabe for public view
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Abstract
Minimal hepatic encephalopathy is defined as HE which can’t be detected by routine clinical and neurological examination, however it can be dignosed by neurological and psychometric test. The prevalence of MHE has been reported to vary between 30% and 84% in patients with liver cirrhosis. Patients with MHE may improve, remain unchanged or deteriorate and develop overt HE over a long-term follow up.
MHE is an important disorder that impairs patients daily functioning and HRQOL. Various tools have been evaluated for the diagnosis of MHE.
Zinc is integrally involved in the metabolism of ammonia. Zinc deficiency markedly decreases the activity of urea cycle enzyme, ornithine transcarbamylase. Similarly, zinc deficiency has been reported to impair the activity of muscle glutamine synthetase, which causes hyperammonemia
Our study aims to study serum zinc concentration in cirrhotic patients with and without subclinical hepatic encephalopathy and correlate it with the results of neuropsychological tests and auditory P300 event-related potential.
This study was conducted on 55 cirrhotic patients, their ages ranged between 45 to 60 years. After signing a written consent, all patients were submitted to clinical assessment; liver function test; serum zinc level; serial dotting test; line tracing test and auditory P300 event related potential.
Patients were divided into 3 groups:
Group I: Seventeen patients with liver cirrhosis without hepatic encephalopathy.
Group II: Thirteen patients with liver cirrhosis with minimal hepatic encephalopathy diagnosed based on the results of psychometric tests (serial dotting and line tracing test) and P300 event related potential.
Group III: Twenty-five cirrhotic patients with overt hepatic encephalopathy.
The control group: included thirty healthy individuals (without any evidence of liver disease) matched for age and sex.
The time needed for serial dotting test and line tracing test was highly significantly prolonged for patients with MHE than healthy controls. The time needed for serial dotting test and line tracing test was prolonged for patients with MHE than patient with no HE but with no statistical significance.
The P300 latency was highly significantly prolonged in patients with MHE than no HE (P= 0.000). There was a highly significantly reduction in the serum zinc level in patients with liver cirrhosis than healthy controls. Serum zinc levels were significantly reduced in higher grades of hepatic encephalopathy
There was a positive correlation between serum zinc levels and serum albumin levels. However, there was no correlation between the serum zinc levels and results of serial dotting test and line tracing test (time and errors).
Conclusion:
• The P300 latency was highly significantly prolonged in patients with MHE.
• Patients with cirrhosis have depressed serum zinc levels, and those with hepatic encephalopathy have statistically reduced serum zinc concentrations. Thus, zinc may be involved in the pathogenesis of MHE.
• There was a positive correlation between serum zinc levels and serum albumin levels. Thus, improvement of the nutritional state may improve the serum zinc levels.
Recommendation:
• Screening all patients with liver cirrhosis for MHE using psychometric tests and P300 event related potential.
• Using serum zinc level as a predictor for minimal hepatic encephalopathy.
• Early assessment o f malnutrition and zinc deficiency are of crucial importance in patients with liver cirrhosis to avoid significant derangements in the health status.
• Further studies are needed to test the long term effect of zinc supplementation on MHE and patients with overt HE associated with zinc deficiency.