الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
HCV can eventually result in cirrhosis and HCC. Egypt possesses the highest recorded cases of HCV globally, mainly caused by genotype 4. HCV infections usually progress to chronicity.
Cirrhosis of the liver is the terminal point of chronic liver disease. It is the 11th cause of death worldwide. Cirrhosis can be divided into compensated and decompensated phase which progresses towards death from complications, ACLF or LT.
A key element in physiopathology is cirrhosis-associated immune dysfunction syndrome (CAID). It is a state of immune deficiency and exacerbated systemic inflammation. In decompensated cirrhosis, the amount of pro-inflammatory cytokines and leukocyte activation antigens increases, while the anti-inflammatory cytokines decrease. This is called the pro-inflammatory phase. In late stages of cirrhosis, the immune system becomes exhausted and an “immunodeficient” phase is observed in which there is increased amounts of anti-inflammatory cytokines and leukocyte inhibitory antigens and deteriorated immune cell function.
Leukotrienes are chief mediators in cirrhosis. LTs intensify vascular permeability and neutrophil recruitment, Moreover, increased hepatic concentration of LTs contributes to liver insult in cholestasis.
LTs are potent biological mediators, are formed when arachidonic acid is changed into either CysLTs or LTB4. LTB4 displays strong proinflammatory chemoattractant properties. Increased LTB4 was incriminated in lots of inflammatory and allergic diseases and levels correlates with disease activity in some of these.
This study was held to evaluate the value of LTB4 as a marker of decompensation in cirrhosis and its relation to complications and disease progression.
This study was carried out on 80 candidates in Alexandria main university hospital, Tropical medicine Department, Subjects were divided into three groups, group I (n=30) compensated cirrhotic patients, group II (n=30) decompensated cirrhotic patients and group III (n=20) apparently healthy individuals. All patients were HCV positive.
Patients with concurrent allergic diseases, diabetes mellitus, obesity, malignancies, and history of anti-inflammatory and immunosuppressive drugs were excluded.
All patients were subjected to the following:
• Thorough history taking & clinical examination.
• Laboratory investigations:
1. Complete Blood Picture.
2. Liver function: Albumin, bilirubin, INR and liver enzymes.
3. FBS.
4. Electrolyte study: serum sodium and potassium.
5. Urea and creatinine.
6. ESR & CRP.
7. Virology: HBsAg, HCV Ab.
8. PCR Test for HCV RNA.
9. AFP.
10. Serum LEUKOTRIEN B4 level by ELISA.
• Radiological investigations:
a. Ultrasound abdomen and pelvis
b. CT Triphasic: In case of presence of focal hepatic lesions to exclude hepatocellular carcinoma.
Analysis of data obtained from the current study revealed the following:
• As regards hematological findings, Hb was higher in controls than the patients with higher values in compensated patients than the decompensated ones. Platelets were lower in patients than in control with lower values in decompensated patients than the compensated ones. WBCs were not of statistical difference between the three studied groups.
• As regards liver enzymes, they were higher in patients than control. Bilirubin was higher in patients than in control with higher values in decompensated group than compensated one. Albumin was lower in patients than in control and lower in decompensated group than compensated one. INR was statistically higher in decompensated group than compensated group.
• Serum creatinine was higher in decompensated group than compensated group.
• Na was statistically lower in decompensated group than compensated group and control.
• CRP was statistically significant higher in the patients and control. Moreover, it was statistically significant higher in decompensated group than compensated group.
• Child score was higher in decompensated cirrhosis group than compensated cirrhosis group.
• MELD/Na was higher in decompensated cirrhosis group than compensated cirrhosis group.
• Serum LTB4 showed remarkably higher values in decompensated cirrhosis group than the compensated and the control groups. Despite that, there was no significant difference between the compensated and the control groups.
• There was positive correlation between LTB4 and degree of ascites.
• There was no correlation between HE and LTB4.
• There was positive correlation between serum level of creatinine and LTB4.
• There was negative correlation between serum level of sodium and LTB4.
• There was positive correlation between CRP and LTB4.
• The Child score and MELD/Na score showed positive correlation with LTB4.
• The ROC curve for Serum LTB4 was significant (p 0.002*) and showed that the cutoff point discriminating decompensated patients from compensated patients was >16.2, with sensitivity of 93.33%, specificity of 43.33%, positive predictive value of 62.2% and negative predictive value of 86.7%.
• LTB4 is a sensitive tool for hepatic decompensation in liver cirrhosis.