الفهرس 
Liver CirrhosisOnly 14 pages are availabe for public view
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Abstract
Hepatic encephalopathy is a serious neuropsychiatric complication of both acute and chronic liver disease. This disease encompass a broad range of neuropsychiatric abnormalities of varying severity; affected patients exhibit alterations in psychomotor, intellectual, cognitive, emotional, behavioral and fine motor functions. HE can be classified as either overt or minimal. Overt HE is a syndrome of neurological and neuropsychiatric abnormalities that can be detected by bed side clinical tests. By contrast, patients with minimal HE present with normal mental and neurological status upon clinical examination but specific psychometric tests yield abnormal results.
Despite much scientific research, the exact pathophysiological mechanisms leading to HE are not clearly understood. The most widely accepted theory of the pathogenesis of HE is that nitrogenous substances derived from the gut adversely affect the cerebral function. The main substance implicated is ammonia, There is accumulating evidence that a number of pathophysiological mechanisms exist or co-exist; however, there is no doubt that increased ammonia concentration is integral in the pathogenesis of HE.
Patients with HE often have other manifestations of end-stage liver disease, such as ascites, jaundice or gastrointestinal variceal bleeding. HE can also develop as an isolated manifestation of decompensated cirrhosis. HE usually signals advanced liver failure and is often considered a clinical indication for evaluation for liver transplantation.
Several scoring systems have been used to determine the severity of hepatic encephalopathy. However, all scoring systems for determining the severity of hepatic encephalopathy have inherent weakness, since several, if not all, aspects of scoring criteria are highly subjective.
The approach to HE comprises exclusion of other causes of encephalopathy, identification of the precipitating cause and a trial of empiric treatment for HE. Many different assessments including brain imaging and neuropsychometric tests can be used to diagnose HE. OHE is conventionally graded by clinical scales. MHE, by contrast, can only be diagnosed by specific neuropsychometric tests.
Most studies have shown that the removal of ammonia from the body is critical to the treatment of HE as hyperammonemia is detected in over 80% of patients with HE. Therefore, treatment is aimed at excluding non hepatic causes of altered mental function, treating precipitating factors, initiating treatment based on the ammonia hypothesis, managing severe encephalopathy in the intensive care unit with full medical support.
In other side of this study is to find a non-invasive method for early detection of acute deterioration of kidney functions in patients with decompensated advanced liver cirrhosis and ascites (defined as 50% rise of serum creatinine from baseline within 48 hours).
Comparison between laboratory data of study group (n = 18) and non HRS group (42) revealed significant differences between 2 groups in laboratory data especially regarding mean urinary NAG levels 12 & 48 hours after admission with statistically significant P value = 0.0001.
Comparison between urinary NAG levels 12 hours (mean SD = 88.7 39.9) and 48 hours (mean SD = 100 44.1) for patients of study group revealed statistically significant P value = 0.0001.
So, our recommendation for assessment of kidney functions in these patients by urinary NAG measurement due to it is a reliable and non-invasive method for early detection of AKI in these patients.
We conclude that urinary NAG is a reliable biomarker for detection of AKI in patients with chronic liver disease and that it allows early detection of AKI before serum urea and creatinine. Our study showed that there is a statistically significant increase in urinary NAG when measured in patients with liver cirrhosis at 12 hours and at 48 hours from exposure to factors that can precipitate hepatorenal syndrome (P =0.0001) compared to normal controls. The rise at 48 hours was statistically significant when compared to 12 hours in patients with liver cirrhosis exposed to factors that can precipitate hepatorenal syndrome; however, the rise at 12 hours was statistically significant when compared to non HRS (P =0.0001).
It also showed that there is statistically significant increase when compared with serum urea and creatinine at same time point when measured in patients with liver cirrhosis at 12 hours and at 48 hours from exposure to factors that can precipitate hepatorenal syndrome (P=0.0001). However, urinary NAG showed a statistically significant increase when measured in patients with liver cirrhosis at 12 hours compared to urea and creatinine. So, we concluded that serial measurement of urinary NAG may allow early detection of AKI in patients with liver cirrhosis long enough before serum creatinine and urea.