الفهرس 
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Abstract
Cirrhosis is defined as liver regenerative nodule formation surrounded by fibrous bands in response to chronic liver injury that disrupts the entire normal architecture of the liver. The most contributing causes include viral infection, autoimmune disorders, cholestatic and metabolic disease which lead to portal hypertension and end-stage liver disease. Liver cirrhosis follows an indolent course and eventually patients represent the complications of liver decompensation characterized by variceal bleeding from portal hypertension, ascites, hepatorenal syndrome, hepatic encephalopathy and spontaneous bacterial peritonitis Portal hypertension is a frequently occurring clinical syndrome caused by intrinsic liver disease, obstruction, or structural changes that result in increased portal blood flow or increased hepatic resistance. The increased portal pressure causes an increase in the pressure gradient between the portal vein and the hepatic veins which leads to the formation of portosystemic collaterals that divert portal blood to the systemic circulation, bypassing the liver. Gastroesophagealvarices are submucosal veins, acting as vascular channels that link the portal venous and the systemic venous circulation and are usually caused by portal hypertension. Hemorrhage from ruptured esophageal varices is one of the most common causes of gastrointestinal bleeding and is the most common cause of death among individuals with cirrhosis. The bleeding risk for small varices and large varices is around 5% and 15% per year respectively All patients who are newly diagnosed with cirrhosis should be screened by upper GI endoscopy to detect esophageal varices at the time of diagnosis and after that, surveillance endoscopies should be performed every 2 to 3 years in cirrhotic patients without varices, every 1-2 years in patients with small varices, and annually in the setting of decompensation. There is a need for non-invasive markers for predicting esophagealvarices in patients with cirrhosis as endoscopy is an uncomfortable, costly and time consuming procedure and therefore lays a heavy burden upon endoscopy units and leads to low patient compliance. Currently, the predictive accuracy of noninvasive markers is still considered to be unsatisfactory, and the search for the optimal predictor is ongoing. The aim of this study was to predict presence of esophageal varices among Egyptian hepatitis C cirrhotic patients by combination of albumin bilirubin grade and platelet count score (ALBI Platelet score). The score depends on cheap, readily available routine laboratory parameters that reflect the degree of liver dysfunction. This was a cross sectional study, carried out on 150 consecutive HCV cirrhotic patients coming to the endoscopy unit of the Tropical medicine and infectious diseases department, Tanta University hospitals during a period of 6 months for screening of esophageal varices. They were divided into the following groups: • group (A): Eighty- seven patients with HCV related cirrhosis and esophageal varices. • group (B): Sixty-three patients with HCV related cirrhosis and no esophageal varices. Inclusion criteria: Adult Egyptian patients with post-hepatitis C cirrhotic liver. Exclusion criteria: • Patients in hepatic encephalopathy or coma • Patients with portal vein thrombosis. • Patients in active bleeding or having a previous history of upper GI bleeding. • Patients who has previously received endoscopic treatment for esophageal varices. • Patients on prophylactic medications to lower portal hypertension such as non –selective beta blockers. • Patient with hepatocellular carcinoma. • Patients taking any medication that could affect platelet counts or bilirubin levels. All patients were subjected to the following: 1. Full history taking 2. Thorough clinical examination 3. Laboratory investigation of patients: • Liver function tests (Total and differential serum bilirubin-serum albumin- Alanine transaminase (ALT), Aspartate transaminase (AST)) • Prothrombin time and activity and international normalized ratio (INR). • Renal function tests (Urea and creatinine). • Complete blood picture. • Erythrocyte sedimentation rate (ESR). 4. MELD score was calculated using the formula: -3.78 × (serum bilirubin) + 11.2 × (INR) + 9.57 × (s.creatinine) + 6.43 5. The ALBI score was calculated using the formula: −0.085×(albumin g/L + 0.66 × log (bilirubinμmol/L) • ALBI grades: ALBI I ≤ − 2.60 ALBI II > − 2.60 to ≤ − 1.39 ALBI III > − 1.39 (Johnson et al.,2015) • Albumin-Bilirubin Grade and Platelet count (ALBI-PLT score): The ALBI-PLT score is calculated by adding the ALBI grade and points for platelet count (1 point if platelet count >150,000/mm3 and 2 points if ≤150,000/mm3). The ALBI PLT range is 2–5. 6. Child-Pugh score calculation 7. Pelvi-abdominal US: Ultrasound examination of the liver, portal venous system, spleen, splenic vein diameter, splenic longitudinal diameter, presence of collaterals, kidney and other abdominal organs was performed for all patients. 8. Upper GI endoscopy The following results were obtained: There was a significant difference between studied groups (group A which represent variceal group, group B non variceal group) regarding to serum bilirubin, serum albumin and platelet count (P value =0.001, 0.048, 0.001 respectively). There was a significant association between studied groups as regard to Child class, clinical examination results (ascites, lower limb edema, splenomegaly) (P value=0.054, <0.001, <0.001, 0.001 respectively). The cutoff point of platelets count as a predictor for esophageal varices among studied groups is <154.5, P value=0.046 with a sensitivity 30.2% and a specificity 79.8%, the negative predictive value (NPV) 45% and positive predictive value (PPV) 68%. The cutoff value for ALBI score is -1.67 as the point for prediction of patients with esophageal varices, P value=0.046, sensitivity 52.9%, specificity 59.6%, positive predictive value (PPV) 64%, and negative predictive value( NPV) 47%. ALBI-Plt score>3 for prediction of patients with esophageal varices whatever the size. P value =0.04, sensitivity 42.5%, specificity of 63.5%, NPV 40% and PPV 65%. At ALBI score cutoff point -1.27 in which the value assessed by the area under the ROC curve represents large high risk esophageal varices, sensitivity 69.7%, specificity 42.9%, PPV 40%, and NPV of 52%. The ALBI-Plt cutoff point for large sized varices>4 has sensitivity 61.9% , specificity 55%, NPV 59% , PPV50%, P value= 0.07.