Relation between fecal calprotectin concentration and severity of hepatitis c (HCV) related chronic liver disease

Abstract

HCV was first identified as the major causative agent of parentally transmitted and community acquired non-A non-B hepatitis. Recently; chronic hepatitis C virus infection turned out to be a major cause of chronic liver disease and death throughout the world. Egypt has one of the highest prevalence rates of hepatitis C virus (HCV) infection in the world, where the seroprevalence is 10-20 folds higher than that in United States and Europe. The course and outcome of HCV infection is highly variable, at one end of spectrum are patients who have no signs or symptoms of liver disease and completely normal serum liver enzymes and at the other end are patients with sever hepatitis C who have symptoms, elevated liver enzymes and who ultimately develop cirrhosis and end stage liver disease. The time from the onset of the infection to the end-stages of disease may be decades. The course and prognosis for HCV infected patient varies with the individual. Genetic makeup and immunologic status alter the course and duration of the disease. Calprotectin is a calcium and zinc-binding peptide, proposed as a biomarker for various inflammatory diseases due its potential role in pathophysiology of inflammation and associated outcomes like tissue destruction, apoptosis and growth impairment. As an acute phase reactant, calprotectin increases more than 100 folds during inflamed conditions. Calprotectin is found in monocytes, keratinocytes, muscle tissue and infiltrating tissue macrophages. Calprotectin is also found abundant in neutrophils and it constitutes 30-60% of the cytosolic proteins. Once get stimulated by an injury or cell disruption, neutrophils and monocytes start secreting calprotectin into the extra cellular fluid. Accordingly, the presence of fecal calprotectin quantitatively relates to intestinal neutrophil migration and is therefore, it may be considered as a valid marker of intestinal inflammation. As the gastrointestinal tract of cirrhotic patients shows various alterations of its mucosal barrier including infiltrates of neutrophils, calprotectin might be a promising diagnostic parameter to diagnose the onset of hepatic encephalopathy. The aim of this work was to study of fecal calprotectin concentration in patients with chronic hepatitis C virus infection and to correlate it with the severity of liver disease as judged by Child-Pugh score. To achieve this goal, the present study was conducted on forty five HCV-related chronic liver disease patients, diagnosed by serological, biochemical and ultrasonographic evidence. This group was subdivided according to Modified Child_Pugh's classification into: Group(1) Child A: includes 15 patients (33% of patients). Group(2) Child B: includes 15 patients (33% of patients). Group(3) Child C: includes 15 patients (33% of patients). Twenty healthy volunteers were selected as controls. All participants were subjected to detailed history taking, thorough clinical examination as well as laboratory investigations (complete blood picture, liver function tests, ESR, CRP, hepatitis markers, FCCs and abdominal ultrasonography). From the statistical analysis of the present study, we can summarize the following results:  There was a positive correlation between FCCs and serum ammonia only in cases groups.  A highly significant positive correlation between FCCs and INR, S.albumin, total and direct bilirubin in total patient, while there were no significant correlation between FCCs and AST, ALT.  There was no significant correlation between FCCs and history of previous GIT bleeding.  We found that there was highly positive correlation between FCCs, ESR, CRP and serum ferritin in total patients, while there were no significant correlation between FCCs and WBCs  We noted that there was no significant correlation between FCCs and HE in patient groups.  The comparison between cases groups and control group as regard FCCs, showed that it was significantly higher among patient's groups with a mean FCCs (52.19 ± 16.99), (182.50 ± 74.81) and (311.47 ± 90.92) in child A, child B and child C respectively compared to (20.55 ± 13.58) in control group.