الفهرس 
Hepatic EncephalopathyOnly 14 pages are availabe for public view
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Abstract
Apart from increased blood ammonia, alterations in various other
substances have been implicated in the pathogenesis of hepatic
encephalopathy (HE). The role of trace elements like zinc and manganese
has been described recently (Chetri K and Choudhuri G, 2003). The
purpose of this case control study is to investigate the possible
relationship between hepatic encephalopathy and serum levels of
manganese (Mn), zinc (Zn), and copper (Cu) in Egyptian cirrhotic
patients compared with age- and sex-matched control subjects and
correlate them with various clinical and laboratory parameters.
This case control study was carried out in Sohag General Hospital
from January to March 2012. It included 30 cirrhotic patients and 10
healthy subjects as controls that were matched for age and gender.
Cirrhotic patients were classified into 2 groups:
Group I: which included 15 cirrhotic patients with hepatic
encephalopathy.
Group II: which included 15 cirrhotic patients without hepatic
encephalopathy.
All participants were subjected to full history taking, thorough clinical
examination, abdominal ultrasonography and routine laboratory
investigations. Serum levels of manganese (Mn), zinc (Zn), and copper
(Cu) and also blood ammonia levels were estimated in all subjects. All
patients were classified according to modified Child-Pugh’s classification
to asses the severity of liver cirrhosis. Severity of hepatic encephalopathy
was assessed according to West Haven (W-H) criteria.results of this research showed that serum levels of
studied trace elements differ significantly in patients with liver cirrhosis
compared to healthy subjects as there was significant increase in serum
levels of manganese and copper, whereas, there was significant decrease
in serum zinc levels in cirrhotic patients (regardless presence or absence
of HE) compared to control subjects. However, there were no significant
differences in serum levels of studied trace elements in cirrhotic patients
with HE compared to those without HE.
There were significant differences in serum levels of zinc and copper
with more severe clinical state of liver cirrhosis according to Child-Pugh
classification in cirrhotic patients with HE as there was significant
decrease in serum zinc levels, whereas, there was significant increase in
serum copper levels in patients with child C class compared to those with
child B class. However, serum manganese levels did not differ
significantly with progression of liver cirrhosis according to Child-Pugh
classification. This indicated that serum levels of zinc and copper were
affected by the degree of hepatic decompensation according to Child-
Pugh classification rather than presence or absence of HE. Serum
manganese levels, on the other hand, showed no significant change along
the course of liver cell failure. It is recommended that further researches
involving larger number of patients with different child classes may be
helpful for better assessment of the relation between those trace elements
and HE.
There were no significant differences in serum levels of studied trace
elements in cirrhotic patients with ascites compared to those without
ascites. Also, serum levels of studied trace elements did not influenced by
amount of ascites or grade of HE according to West-Haven criteria.
There was significant inverse correlation between serum zinc levels
and blood ammonia levels in cirrhotic patients. So, it is suggested that
zinc supplementation will correct hypozincemia in cirrhotic patients
leading to decrease in blood ammonia levels probably by activating
muscle glutamine synthetase and hepatic ornithine transcarbamoylase and
inhibiting AMP deaminase in skeletal muscles.
Of the studied trace elements, only serum copper was significantly
correlated with HE grade. In addition, there was significant direct
correlation between blood ammonia levels and both serum manganese
and copper levels in cirrhotic patients with HE. So, chelation therapy of
both manganese and copper may be of value in treatment of HE. But, the
role of both manganese and copper in the pathogenesis of HE and the
possible use of their chelation as treatment need further study before any
recommendations can be made.
In conclusion, decreased serum concentrations of zinc and increased
levels of manganese and copper in patients with liver cirrhosis could have
an important role in the pathogenesis of liver cirrhosis and its
complications, especially in hepatic encephalopathy. The
supplementation of zinc could improve hepatic encephalopathy. The
decrease in manganese and copper levels could also have a beneficial
effect on the neurological status in patients with liver cirrhosis and
hepatic encephalopathy.
Considering all that, the correction of serum trace elements
concentrations would have a beneficial effect on some complications of
liver cirrhosis and may be on progression of the disease, so it would be
recommendable to provide laboratory analysis of trace elements as a
routine.