ABSTRACT
Recent studies have suggested that bacterial coinfection with Helicobacter species in patients with hepatitis C virus [HCV] may increase the burden of both infections on the hepatobiliary and gastrointestinal tracts. The aim of this study was to evaluate the association between H. pylori infection and gastric apoptosis in patients with hepatitis C cirrhosis. One hundred consecutive patients with dyspepsia; 50 with posthepatitis C cirrhosis and 50 without hepatitis C or cirrhosis, were studied. The presence of H. pylori was tested by urease test and Gram staining of gastric biopsies. The apoptotic index was calculated in gastric biopsies stained with hematoxylin and eosin. A statistical analysis was done to correlate H. pylori infection with gastric apoptosis in both groups. A verbal consent was taken from all patients after explaining the need for endoscopy and H. pylori testing to diagnose their illness. The accuracy of rapid urease test and Gram staining was almost similar in detection of H. pylori. The results of this study have shown that gastric apoptosis increased significantly in cirrhotic patients with H. pylori infection than non-cirrhotic patients with H. pylori infection. This increase was highly significant in comparison with cirrhotic and non- cirrhotic patients without H. pylori infection. Also, non-cirrhotic patients with H. pylori injection had significantly more gastric apoptosis than cirrhotic and non-cirrhotic patients without H. pylori infection. On the other hand, no significant difference was found in gastric apoptosis between cirrhotic and non-cirrhotic patients without H. pylori infection. In conclusion, H. pylori was associated with more gastric apoptosis. Hepatitis C cirrhosis increases gastric apoptosis in patients with H. pylori infection independent of the degree of cirrhosis and concomitant endoscopic findings including portal hypertensive gastropathy [PHG]. There was an association between H. pylori infection and gastric apoptosis specially in hepatitis C cirrhotic patients. This result warrants prospective studies to determine the possible interaction between H. pylori and HCV in increasing gastric lesions in patients with cirrhosis
ABSTRACT
Helicobacter pylori [H. Pylori] is a human bacterial pathogen capable of surviving in the hostile environment of the stomach and duodenum. The bacterium has been linked to a number of gastric and extra gastric diseases. Recent reports of gastric infections caused by helicobacters other than H. Pylori created a clinical and research significance for a rapid, sensitive and specific diagnostic method. This is particularly important to make the laboratory-supported clinical diagnosis and follow up easier and specific. In this study, we used a multiplex PCR for the simultaneous detection and identification of Helicobacter genus and Helicobacter pylon in gastric fluid from patients with chronic non-ulcer dyspepsia. Patients with chronic dyspepsia of more than one month duration were recruited through the outpatient clinic in the university of Tanta hospital-Egypt for upper gastrointestinal endoscopy, only patients with no ulcer were involved in this study. Gastric fluid was obtained from 40 patients at the end of diagnostic upper gastrointestinal endoscopy, peripheral blood samples were also obtained and used to prepare serum for serodiagnosis. Gastric fluid was used for DNA preparation and inoculation of Skirrow's medium. Isolated pure colonies of H. pylori were used to prepare bacterial DNA to be used as positive control. Two pairs of primers; Hcom1, Hconn2 specific for Helicobacter genus, and Hicd1, Hicd2 specific for H. pylori species were used in the multiplex PCR. Two fragments of PCR products of 389 bp and 1200 bp were obtained from 34 specimen [85%] using Hcom1-Hcom2 and Hicd1-Hicd2 primers respectively. In five specimens [12.5%] a single band corresponding to the genus-specific gene and not the species-specific gene was obtained. In one specimen [2.5%], no DNA amplification was obtained. No DNA amplification of the negative control Gram-positive or Gram-negative bacteria was detected. The detection limit of the assay used in this study was 0.04 pg of DNA. The results obtained from this study demonstrate that 85% of the symptomatic gastric helicobacter infections are due to helicobacter pylori. They also demonstrate that this used protocol is a rapid, specific and sensitive assay for simultaneous detection of Helicobacter genus members and Helicobacter pylori species in gastric juice samples. This protocol reduces the number of PCR amplifications needed for specific diagnosis of the helicobacter infections. This can help physicians to have accurate and rapid diagnosis to cases of non ulcer dyspepsia, so that the right treatment can be precisely planned