Identification of some Helicobacter species in patients with hepatitis C virus-related liver cirrhosis with and without hepatocellular carcinoma; a retrospective study

The progression of hepatitis C virus [HCV] positive liver disease from hepatitis to cirrhosis and hepatocellular carcinoma [HCC] involves factors other than the virus itself. An etiologic agent capable of inducing chronic active hepatitis and hepatocellular tumors in mouse was discovered belonging to the genus Helicobacter, and was named Helicobacter Hepaticus. Several research have reported high seroprevalence of helicobacter pylori antibodies in patients with hepatitis C virus. Since then, the relation between helicobacter species and liver disease in human was investigated. The aim of the present work was to identify and study the prevalence of some helicobacter species [helicobacter pylori [HP] and helicobacter pullorum] in HCV positive liver cirrhosis with and without hepatocellular carcinoma [HCC] in humans. The study was carried out on liver biopsies of 45 patients classified into 3 equal groups; Group I [control group]: where the liver biopsy specimens were taken from grossly normal areas of 15 hepatectomy specimens resected for hepatic benign tumours/cysts or metastatic tumours; Group II: 15 liver biopsy specimens from patients with HCV positive liver cirrhosis; and Group III which included 15 liver biopsy specimens belonging to HCV positive patients diagnosed by histopathology as hepatocellular carcinoma [HCC]. Identification of Helicobacter species as well as detection of Cag A positive and glm M positive strains was done in liver biopsies using polymerase chain reaction. Staining of helicobacter pylori in liver biopsies with immune stain was carried out. Helicobacter genus DNA was detected in 15 cases out of 45 studied cases: 6 cases out of 15 [40%] in group II [liver cirrhosis group], 8 cases out of 15[53. 33%] in group III [HCC group], and only one case out of 15 [6.67%] in the control group. The prevalence of helicobacter positive cases were significantly higher in group II [liver cirrhosis group] and in group III [HCC group] than in group I [control group] [P=0.02].No significant difference between the three studied groups was found regarding the Cag A and the glmM gene status. Helicobacter pullorum was detected in only two cases; one in group II and the other in group III. Helicobacter pylori was detected by immune stain in 4 cases out of 15 cases positive for HP by PCR in group III [HCC]. Helicobacter DNA is present in liver tissue of HCV positive liver disease. Further research is recommended to explore the role of Helicobacter species in the progression of HCV positive liver disease to HCC

Plasma and ascitic fluid level of calprotectin in chronic liver disease: malignant and non malignant

Calprotectin was widely investigated in alcoholic liver disease and proved to be a new prognostic marker of survival independent of the severity of liver disease as well as marker of malignancy. However it was not widely investigated in other causes of liver cirrhosis. Of the present work was to study the level of calprotectin both in plasma and ascitic fluid in patients with hepatitis C [HCV] related chronic liver disease with and without malignancy, and to find out whether one or both of them correlate with the severity of liver damage and presence of malignancy. This study was conducted at the Faculty of Medicine, Alexandria University and the National Liver Institute, Menoufiya University. Thirty patients with Hepatitis C related liver cirrhosis were recruited. Fifteen of these patients suffered from concomitant hepatocellular carcinoma [HCC] diagnosed by elevated alpha foeto-protein [AFP] and one imaging technique OR by two imaging techniques in the case of normal AFP. Calprotectin was significantly elevated in patients with cirrhosis and cirrhosis/HCC than in controls [p=<0.01]. However there was no significant difference in the levels of plasma or ascitic calprotectin between the cirrhotic group and the group with HCC. There was no correlation between plasma and ascitic calprotectin levels. Ascitic calprotectin correlated significantly with bilirubin, and markers of synthetic liver function [p=<0.05], but plasma calprotectin correlated only with prothombin activity [p=<0.05]. In patients with spontaneous bacterial peritonitis, ascitic calprotectin was significantly higher in patients having this complication [879.8 +/- 67.5] than patients without SBP [534.2 +/- 59.3 [p<0.01] and a highly significant correlation was found between ascitic calprotectin and total leucocytic count in ascitic fluid [p=<0.01]. Calprotectin is elevated in HCV-related cirrhosis but not further elevation with the occurrence of hepatocellular carcinoma. Ascitic calprotectin correlated with the degree of hepatocellular injury and was significantly higher in patients with SBP. Further studies are warranted to establish a role of plasma calprotectin for the risk assessment of infectious complications secondary to bacterial translocation in patients with HCV- related liver cirrhosis

study of expression of matrix metalloproteinase-1 [MMP-1] and tissue inhibitor of metalloproteinase-1 [TIMP-1] in inflammatory bowel disease

Extracellular matrix [ECU] degradation and remodeling are major features of inflammatory bowel disease [IBD]. Matrix metalloproteinase-1 [MMP-1] is an important enzyme in ECM degradation. Its activity is controlled by tissue inhibitor ofmetalloproteinase-1 [TIMP-1]. To study the expression of MMP-1 and TIMP-1 in intestinal biopsies of patients with IBD and to determine its correlation with the endoscopic and histological scores of inflammation. Immunohistochemistry was used to study the expression of MMP-1 and TIMP-1 in 30 patients with IBD [16 patients with ulcerative colitis [UC] and 14 patients with Crohn's disease [CD]]. In addition, a control group of 10 non inflamed intestinal biopsies from these patients was studied. A semi-quantitative [ordered] method based on both the degree of staining and the percentage of positive cells was used to score immunohistochemical results. 76.67% and 90% of the studied cases of IBD showed positive staining for MMP-1 and TIMP-1 respectively. The mean staining scores of both MMP-1 and TIMP-1 were significantly higher in IBD [3.27 +/- 2 and 3.6 +/- L61 respectively] than control [0.8+0.92 and 1.9+ and .88 respectively] [p=0.001 and p-0.004 respectively]. A significant correlation was found between MMP-1 and TIMP-1 expression [p<0.001]. The expression of both MMP-1 and TIMP-1 was higher in UC [3.38 +/- 1.93 and 3.63 +/- 1.71 respectively] than CD [3.14+2.14 and 3.57 +/- 1.56 respectively], yet the difference was not significant [p=0.8 and p=0.9 respectively]. A significant correlation was detected between both MMP-1 and TIMP-1 expression and each of histological score [p<0.001] and endoscopic score [p < 0.001] of inflammation. MMP-1 and TIMP-1 are overexpressed in the affected mucosa of IBD and their expression correlates with the endoscopic and histological scores of inflammation. Thus, MMP-1 and TIMP-1 are likely to play a major role in the process of tissue destruction and remodeling in IBD. MMP-1 inhibitor therapy may prove useful in modulation of mucosal inflammation and promotion of healing in IBD