Serum Kallistatin Level as a Predictor of Esophageal Varices in Patients of Liver Cirrhosis

Abstract

Abstract Background Esophageal varices are porto-systemic collaterals resulting from portal hypertension, and considered the most lethal complication of liver cirrhosis so early diagnosis of varices can improve prognosis of liver cirrhosis. Kallistatin a tissue kallikrein-binding protein and a serine proteinase inhibitor (serpin) is mainly formed and secreted in liver and its serum level diminished in liver cirrhosis. It has anti-angiogenic, anti-oxidant, anti-inflammatory and anti-tumor effects. Kallistatin level is believed by many literature to be related to the severity of liver disease. Aim of the Work The aim of this study was to assess the relation between serum kallistatin level and presence of OVs. This study also aimed to evaluate serum kallistatin level as a non-invasive predictor of OVs. Patients and Methods This study was conducted in the Gastro-enterology unit, Internal medicine department, Ain Shams University hospitals &Theodor Bilharz Institute. This is a case control study including 60 cirrhotic patients and 20 healthy. Results There was no significant differences between the studied groups regarding demographic data. There was no significant differences between the studied groups as regards Hb, WBCs, ALT, AST, creatinine and, urea but there was highly significant differences between cirrhotic groups and healthy group in the means of platelet count, serum albumin, serum sodium, total and direct bilirubin but no significant difference between groups I and II. Regarding to prothrombin time, there was highly significant differences between the 3 groups as it was higher in group I more than II more than III. There was also no significant difference between the cirrhotic groups regarding to Child Pugh score, MELD score and portal hypertensive gastropathy (PHG). There were significant differences between the 3 studied groups regarding to the means of splenic diameter and portal vein diameter. Kallistatin level showed significant decrease in both patients with OVs and patients without OVs vs. healthy individuals and there was highly significant difference between patients with OVs and patients without OVs. The level of Kallistatin concentration is not correlated with size of varices or risky signs suggesting that Kallistatin level can predict presence of O.V but it can’t reflect the size and severity of varices. There was no significant correlation between serum level of Kallistatin and age, gender and smoking. There was positive correlation to hemoglobin, platelet count, albumin level and negative correlation with PT, INR and urea. There was positive correlation to portal hypertensive gastropathy (PHG) and negative correlation with MELD score and portal vein diameter. Conclusion Serum level of Kallistatin level may express the degree of liver dysfunction. It is correlated with presence of O.V but not correlate to size or risky signs of OVs suggesting that Kallistatin level can’t reflect the presence of O.V. It can predict the presence of severe PHG.