الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Liver cirrhosis has become one of the major causes of morbidity and mortality. Global Burden of Disease reported that over one million people died due to cirrhosis in 2010 worldwide, compared with 676,000 deaths in 1980. Since the survival rate of cirrhosis is relatively low, data on the incidence of geographical variations are essential to prevent its related disability and mortality.
Portal vein thrombosis (PVT) is characterized by interruption of normal blood flow in the PV because of blood clot formation. Thrombophilic conditions, abdominal inflammation, tumorous invasion, and liver cirrhosis are among the most common causes of PVT. Less commonly, PVT has been described after bariatric surgery, radiofrequency ablation (RFA) for hepatocellular carcinoma (HCC).
Protein S is a vitamin K-dependent anticoagulant protein. Its major function is as a cofactor to facilitate the action of activated protein (A P C) on its substrates, activated factor V (FVa) and activated factor VIII (FVIIIa). Protein S deficiencies are associated with thrombosis.
Protein S possesses both APC-dependent and independent anticoagulant properties and thus is an important guardian in controlling thrombin generation and fibrinolysis, although the contribution of these properties to the anticoagulant functions of PS is still unclear. Concentrations of protein S decline with deteriorating liver function. It may also be involved in PVT formation in patients with cirrhosis.
This work aimed to study serum protein S levels in cirrhotic patients with portal vein thrombosis.
The present study conducted on 90 persons enrolled in study about of 36 cirrhotic patients without PVT and 34 cirrhotic patients with PVT as well as 20 healthy persons as a control.
Patients on anticoagulant therapy, age below 18 years, inflammatory or bleeding events in previous 2 months, history of personal (or familial, in first degree relatives) unprovoked, thromboembolism, DM, hepatocellular carcinoma are excluded from the study.
All subjects had been subjected to:
1. Demographic Data assessment: (age, sex, height and BMI).
2. History taking: Full history taking focusing on history of hepatic encephalopathy.
3. Thorough clinical examination:
a. General examination: focusing on jaundice, pallor, cyanosis, petichea, lower limb edema, palmar erythema and clubbing.
b. Local examination: focusing on for liver size, consistency, spleen, ascites, dilated abdominal veins and umbilical hernia.
4. Complete blood picture.
5. Liver function tests including ALT, AST, serum bilirubin, albumin and prothrombin time.
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6. Renal function tests including blood urea and serum creatinine.
7. Serum level of protein-S
8. Abdominal Ultrasonography: to confirm diagnosis of liver cirrhosis by giving idea about liver echogenicity, irregularity of liver outline, liver size, presence of liver nodules, also portal vein diameter and presence of portal vein thrombosis.
Results:
— There was no significant difference between LC group and LC+PVT group regard gender, history of hepatic encephalopathy, history of gastrointestinal bleeding and Child-Pugh score.
— There was no significant difference among studied groups regarding WBC (p=0.1).
— Platelet count and HB level were significantly lower in LC and LC+PVT groups than control (p>0.05).
— There was no significant difference between LC group and LC+PVT group regard platelet count and HB level (p<0.05).
— There was no significant difference between LC group and LC+PVT group regard blood urea and creatinine(p<0.05).
— FIB- 4 score was significantly higher in cirrhosis group than cirrhosis group with PVT (p>0.05).
— There was no significant difference between LC group and LC+PVT group regard APRI score(p<0.05).
— There was no significant difference between LC group and LC+PVT group regard ALT, AST, bilirubin and albumin (p<0.05).
— Statistical analysis of the studied groups revealed no significant difference as regarding liver and spleen diameter in ultrasonography. However, regarding portal vein diameter, liver cirrhosis with portal vein thrombosis group was higher than the mean of liver cirrhosis group (P<0.0001). Regarding grade of portal vein thrombosis in group liver cirrhosis and portal vein thrombosis, there were 28 (82.4%) patients with grade I PVT and 4 (11.8%) patients with grade II PVT and 2 (5.9%) patients with grade III PVT.
— Regarding protein S, the mean of protein S in the liver cirrhosis group was significantly lower than the mean of the control group (P1= 0.0123) and the mean of protein S in the liver cirrhosis with portal vein thrombosis group was significantly lower than the mean of control group (P2 <0.0001) and the mean of protein S in the liver cirrhosis with portal vein thrombosis group was highly significant lower than the mean of liver cirrhosis group (P3=0.0001).
— In correlation between protein S and different clinical, biochemical and radiological parameters in liver cirrhotic group, there was significant positive correlation between protein S and serum urea (p=0.006), serum creatinine (p=0.048) and FIB-4 (p=0.027). There was insignificant correlation between protein S and age, PT, AST, APRI, TLC, HB, PLT, albumin, ALT, bilirubin, spleen size and PV diameter (p>0.05).
— In correlation between protein S and different clinical, biochemical and radiological parameters in liver cirrhotic group with portal vein thrombosis group, there was significant positive correlation between protein S and PT (p=0.0293), APRI (p=0.0281) and FIB-4 (p- value =0.0463). There was significant negative correlation
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between protein S and PV diameter (p=0.0223). There was insignificant correlation between protein S and TLC, HB, albumin, AST, urea, creatinine, and spleen size, age, PLT, ALT and bilirubin (p<0.05).
— Protein S showed a high sensitivity (91%) and specificity (98%) with Area under curve of 0.97 at a cut-off value of < 3.15 for detection of PVT in cirrhosis.