Detection of Helicobacter pylori infection in Egyptian patients with chronic calcular cholecystitis.

Reports of Helicobacter pylori in biliary tract diseases in humans are very fragmentary, and therefore there is a need for further investigations. This study aims to detect H. pylori in the bile and gall bladder (GB) of patients with chronic calcular cholecystitis (CCC), and to determine the association of H. pylori infection with gallstone type. Thirty patients with CCC admitted for laparoscopic cholecystectomy were investigated, including upper gastro-endoscopy before cholecystectomy. Rapid urease test and histopathological examination were performed on gastric biopsies. The GB specimens were investigated for the presence of H. pylori by immunohistochemistry (IHC). H. pylori antigen in bile was detected by enzyme immunoassay. Chemical analysis of gallstones was performed to determine type. Immunohistochemistry testing showed 73.3% and 66.7% positivity among GB neck and body biopsies, respectively, demonstrating high sensitivity and specificity. A significant association was found between gastric and GB H. pylori positivity (P < 0.01). H. pylori antigen was detected in bile from three CCC cases. The greatest number of stones were of the calcium bilirubinate type. Gall bladder positivity for H. pylori was accompanied by chronic quiescent gastritis (40.9%). In conclusion, H. pylori infection may be an aetiological factor leading to cholecystitis. Gastric colonisation with H. pylori could be a source for GB infection, and the organism may act as a lithogenic component, especially in the context of pure pigmented gallstones.

Differences in circulating MMP-9 levels with regard to viral load and AST:ALT ratio between chronic hepatitis B and C patients.

Hepatitis B virus (HBV) and hepatitis C virus (HCV) are the two major causes of chronic liver inflammation, fibrosis and cirrhosis. They have the ability to cause persistent infection in susceptible hosts and severely damage liver function. Matrix metalloproteinase-9 (MMP-9) is one of the gelatinases that may be important in liver fibrosis. This study aims to evaluate whether or not MMP-9 in relation to viral load is involved in the development of liver dysfunction in HBV and HCV Blood samples from 20 patients chronically infected with HBV and 30 with HCV, along with 15 healthy individuals as controls, were investigated. Viral load was assessed by real-time polymerase chain reaction (PCR). Serum MMP-9 levels were evaluated by enzyme-linked immunosorbent assay (ELISA). Alanine transaminase and aspartate aminotransferase (ALT and AST) activities were measured spectrophotometrically. Levels of MMP-9 were significantly higher in HCV than in HBV patients (P < 0.01), and positively correlated with HBV viral load (r = 0.842, P < 0.01) and AST:ALT ratio (r = 0.614, P < 0.05). Conversely, MMP-9 levels did not correlate with HCV viral load but did correlate with AST:ALT ratio (r = 0.652, P < 0.01). Therefore, MMP-9 levels could reflect progressive liver damage in HBV and HCV infection. However, a distinction between the pathological mechanism of HCV and HBV is suggested, as HCV probably promotes hepatocyte damage and fibrosis through mechanisms other than replication. Continuous expression of the HBV genome through replication and secretion of viral antigens may contribute to the transcriptional regulation of MMP-9, thus promoting liver damage and fibrosis.