Association of smoking, alcohol and NSAIDs use with expression of cag A and cag T genes of Helicobacter pylori in salivary samples of asymptomatic subjects

Objective:To determine the association of smoking, alcohol and nonsteroidal anti-inflammatory drugs (NSAIDs) use with presence and virulence of Helicobacter pylori (H. pylori) infection in a representative sample of a random adult population of asymptomatic subjects. Methods:Non virulent 16S rRNA and virulent cag A and T genes from salivary samples of 854 asymptomatic subjects were determined using polymerase chain reaction. The presence and absence of virulent and non virulent infection was statistically compared with consumption of smoking, alcohol and NSAIDs. Results:The prevalence of infection in male and female subjects was found to be 69.25%and 66.90%, respectively. The prevalence of infection in the population of asymptomatic subjects with respect to consumption of alcohol was as follows:current (31.22%), former (52.20%) and never (43.58%). The prevalence of infection in the population of asymptomatic subjects with respect to smoking of cigarettes was as follows:current (88.80%), former (57.14%) and never (33.33%). The prevalence of infection in the subject population consuming NSAIDs and not consuming NSAIDs frequently was found to be 82.75%and 21.16%, respectively. Virulence in male and female subjects was found to be 60.00%and 50.00%, respectively. The presence of virulent infection in the population of asymptomatic subjects with respect to consumption of alcohol was as follows:current (28.57%), former (40.15%) and never (50.00%). The prevalence of virulent infection in the population of asymptomatic subjects with respect to smoking of cigarettes was as follows:current (79.32%), former (75.00%) and never (50.00%). The prevalence of virulent infection in the subject population consuming NSAIDs and not consuming NSAIDs frequently was found to be 88.23%and 66.66%, respectively. Conclusions:It can be concluded that smoking and NSAIDs consumption are aggravating factors for virulence of H. pylori and alcohol can inhibit H. pylori infection in asymptomatic subjects.

Association of Helicobacter pylori with colorectal cancer development.

Background: Helicobacter pylori (H. pylori) may be associated with colorectal cancer. However, the underlying mechanisms are still unclear. Objectives: Explore the serostatus of H. pylori cytotoxicity-associated gene A product (CagA) in patients with colorectal carcinoma, and assess the association of H. pylori with colorectal cancer via c-Myc and MUC-2 proteins at tumor tissues. Methods: H. pylori CagA IgG antibodies were screened using enzyme-linked immunosorbent assay (ELISA) in 30 patients with colorectal carcinoma and 30 cancer-free control subjects. Paraffin-embedded blocks were examined for the expression of c-Myc and MUC-2 protein by immunohistochemistry. Results: H. pylori CagA seropositivity increased significantly among colorectal cancer patients (p <0.05). The expression of c-Myc and MUC-2 in colorectal carcinoma patients was over-expressed (80%), and downexpressed (63%) in resection margins (p <0.05). c-Myc over-expression and MUC-2 down-expression were associated with CagA-positive rather than CagA-negative H. pylori patients. In 16 CagA seropositive vs. 14 CagA seronegative patients, the expression rate was 97.3% vs. 64.2% and 33.3% vs. 78.5% for cMyc and MUC-2, respectively. CagA IgG level was significantly higher in positive than in negative c-Myc patients (p= 0.036), and in negative than in positive MUC-2 patients (p= 0.044). c-Myc and MUC-2 were positively and inversely correlated with CagA IgG level (p <0.05). Conclusions: CagA-seropositive H. pylori is most probably associated with colorectal cancer development. Part of the underlying mechanism for such association might be via alterations in expression of MUC-2, which depletes the mucous protective layer in the colo-rectum, and c-Myc, which stimulates the growth of cancerous cells.

Genotipo cag A+ en cepas de Helicobacter pylori asociadas a úlcera péptica, gastritis crónica y cáncer gástrico / Cag A+ genotype in Helicobacter pylori strains associated with peptic ulcer, chronic gastritis and gastric cancer

Se estudiaron 171 pacientes con úlcera duodenal, úlcera gástrica, gastritis crónica y cáncer gástrico; los 3 últimos confirmados histológicamente. Se analizaron 56 casos con úlcera duodenal, 48 con úlcera gástrica, 47 con gastritis crónica y 20 con cáncer gástrico. Se detectó la presencia de Helicobacter pylori mediante PCR en el 98,2 por ciento de las úlceras duodenales; en el 95,8 por ciento de las úlceras gástricas; en el 95,0 por ciento de los cánceres gástricos y en el 93,6 por ciento de las gastritis crónicas, para una prevalencia total del 95,9 por ciento. El genotipaje cag A de las cepas detectadas reportó positividad en el 80,0 por ciento de las úlceras duodenales; en el 72,7 por ciento de las gastritis crónicas; en el 69,6 por ciento de las úlceras gástricas y en el 42,1 por ciento de los cáncer gástricos, para una prevalencia total del 70,7 por ciento. Tanto las úlceras en su conjunto, como la gastritis crónica presentaron una prevalencia de cepas Helicobacter pylori cag A+ significativamente superior al cáncer gástrico (p = 0,19).

171 patients with duodenal ulcer, gastric ulcer, chronic gastritis and gastric cancer were studied. The last 3 were histologically confirmed. 56 cases with duodenal ulcer, 48 with gastric ulcer, 47 with chronic gastritis and 20 with gastric cancer were analyzed. The presence of Helicobacter pylori was detected by PCR in 98.2 percent of the duodenal ulcers; in 95.8 percent of the gastric ulcers; in 95.0 percent of the gastric cancers; and in 93.6 percent of the chronic gastritis. The cag A genotyping of the strains found proved to be positive in 80.0 percent of the duodenal ulcers; in 72.7 percent of the chronic gastritis; in 69.6 percent of the gastric ulcers; and in 42.1 percent of the gastric cancers, for a total prevalence of 70.7 percent. Both, the ulcers as a whole and the chronic gastritis showed a prevalence of cag A+ strains of Helicobacter pylori significantly higher than gastric cancer (p = 0,19).

Analyze the associativity between Helicobacter pylori infection and cholecystolithiasis / 重庆医科大学学报

Objective:To investigate the relationship of H pylori with cholecystolithiasis,to collect the evidence of Hp existing in biliary tract,and to study the detective method of Hp DNA in billiary tract.Methods:Hp which existing in bile,mucosa and gallstone of 120 cholecystolithiasis patients were cultured according to the literature.Then they were amplified by the primer of Ure A and cagA.Amplified products were analyzed.Results:All of the 120 samples were negative.No Hp grew in the medium.No Hp DNA and Hp Cag A antibody were found with PCR method.Conclusion:(1) It was restricted by many factors that Hp DNA in bile and gallstone wereexamined with PCR.(2) Hp maybe entered biliary tract regressively through Oddi's sphincter andhad no relationship with cholecystolithiasis.