BACKGROUND: Helicobacter pylori strains possessing the cagA gene have been postulated to have a disease-specific relationship to peptic ulcer. The purpose of this study was to investigate the relationship between the infection with Helicobacter pylori expressing the cagA gene and the development of peptic ulcer diseases in Korean patients. METHODS: Genomic DNA and bacterial mRNA in the gastric mucosa were amplified by polymerase chain reaction (PCR) and reverse transcription PCR, using synthetic oligonucleotide primers to cagA genes to compare the prevalence of cagA genes in 35 patients with non-ulcer gastritis and 99 patients with gastric or duodenal ulcer disease (53 and 46, respectively). Two different primer sets for the cagA gene were used. The first primer set amplified a 298-bp region (nucleotides 1751-2048), and the second set amplified a 349-bp region (nucleotides 1228-1249). RESULTS: The expected 298 and 349-bp PCR amplicons were identified as follows: 1) 32 (91.4%) and 30 (85.7%) of 35 non-ulcer gastritis patients; 2) 5 1 (96.2%) and 50 (94.3%) of 53 benign gastric ulcer patients; and 3) 46 (100.0%) and 40 (87.0%) of 46 duodenal ulcer patients, respectively. CONCLUSION: These results strongly suggest that the cagA gene will not prove to be a useful marker to distinguish disease-specific H. pylori strains in the development of peptic ulcer diseases in Korean patients.
BACKGROUND:Helicobacter pylori strains possessing the cagA gene have been postulated to have a disease-specific relationship to peptic ulcer. The purpose of this study was to investigate the relationship between the infection with Helicobacter pylori expressing the cagA gene and the development of peptic ulcer diseases in Korean patients. METHODS: Genomic DNA and bacterial mRNA in the gastric mucosa were amplified by polymerase chain reaction (PCR) and reverse transcription PCR, using synthetic oligonucleotide primers to cagA genes to compare the prevalence of cagA genes in 35 patients with non-ulcer gastritis and 99 patients with gastric or duodenal ulcer disease (53 and 46, respectively). Two different primer sets for the cagA gene were used. The first primer set amplified a 298-bp region (nucleotides 1751-2048), and the second set amplified a 349-bp region (nucleotides 1228-1249). RESULTS: The expected 298 and 349-bp PCR amplicons were identified as follows: 1) 32 (91.4%) and 30 (85.7%) of 35 non-ulcer gastritispatients; 2) 5 1 (96.2%) and 50 (94.3%) of 53 benign gastric ulcerpatients; and 3) 46 (100.0%) and 40 (87.0%) of 46 duodenal ulcerpatients, respectively. CONCLUSION: These results strongly suggest that the cagA gene will not prove to be a useful marker to distinguish disease-specific H. pylori strains in the development of peptic ulcer diseases in Korean patients.