An evaluation of a serologic test with a current infection marker of Helicobacter pylori before and after eradication therapy in Chinese.

BACKGROUND AND AIMS: Development of an accurate and less cumbersome noninvasive method to detect current Helicobacter pylori infection is essential in clinic. The aim of this study was to evaluate the performance of the CIM test, also known as the Assure H. pylori Rapid Test (Genelabs Diagnostics Pty. Ltd., Singapore), for the diagnosis of current H. pylori infection before and after eradication therapy in Chinese population. METHODS: A total of 452 eligible people were recruited for this study in Jiangsu Province, China. Each individual underwent a 13C urea breath test (13C-UBT). For the evaluation of CIM test after eradication, 115 H. pylori-positive outpatients were treated with 1-week triple therapy. One month after the end of therapy, the patients underwent 13C-UBT again, and the CIM-test was performed 1, 3, and 6 months after the end of therapy. Its performance (sensitivity, specificity, positive and negative predictive values, and accuracy) were determined using the 13C-UBT as a gold standard for H. pylori diagnosis. RESULTS: H. pylori was detected in 221 (65.6%) of the 337 people by 13C-UBT. The sensitivity, specificity, positive and negative predictive values, and accuracy of the CIM test were 93.2%, 90.5%, 94.9%, 87.5%, and 92.3%, respectively, using 13C-UBT as a gold standard. One month after eradication therapy, the sensitivity, specificity of CIM test were only 50% and 66.7%, 66.7% and 84.6% 3-month after eradication therapy and the sensitivity, specificity increased to 85.7% and 96.9%, respectively, when CIM test was used 6 months after the end of anti-H. pylori therapy. CONCLUSIONS: The CIM test is a simple, rapid, accurate, cheap, and near-people test. It may be satisfactory for detecting H. pylori infection in cases without eradication therapy, but it could not differentiate the past or current infection correctly within 6 months after anti-H. pylori therapy.

Coordinate increase of telomerase activity and c-Myc expression in Helicobacter pylori-associated gastric diseases.

AIM: To detect the telomerase activity and c-Myc expression in gastric diseases and to examine the relation between these values and Helicobacter pylori (H pylori) as a risk factor for gastric cancer. METHODS: One hundred and seventy-one gastric samples were studied to detect telomerase activity using a telomerase polymerase chain reaction enzyme linked immunosorbent assay (PCR-ELISA), and c-Myc expression using immunohistochemistry. RESULTS: The telomerase activity and c-Myc expression were higher in cancers (87.69% and 61.54%) than in noncancerous tissues. They were higher in chronic atrophic gastritis with severe intestinal metaplasia (52.38% and 47.62%) than in chronic atrophic gastritis with mild intestinal metaplasia (13.33% and 16.67%). In chronic atrophic gastritis with severe intestinal metaplasia, the telomerase activity and c-Myc expression were higher in cases with H pylori infection (67.86% and 67.86%) than in those without infection (21.43% and 7.14%). c-Myc expression was higher in gastric cancer with H pylori infection (77.27%) than in that without infection (28.57%). The telomerase activity and c-Myc expression were coordinately up-regulated in H pylori infected gastric cancer and chronic atrophic gastritis with severe intestinal metaplasia. CONCLUSION: H pylori infection may influence both telomerase activity and c-Myc expression in gastric diseases, especially in chronic atrophic gastritis.

Enhancement of osteopontin expression in HepG2 cells by epidermal growth factor via phosphatidylinositol 3-kinase signaling pathway.

AIM: Osteopontin (OPN) is a phosphorylated glycoprotein with diverse functions including cancer development, progression and metastasis. It is unclear how osteopontin is regulated in HepG2 cells. The aim of this study was to investigate the effect of epidermal growth factor on the expression of osteopontin in HepG2 cells, and to explore the signal transduction pathway mediated this expression. METHODS: Osteopontin expression was detected by RNAase protection assay and Western blot. Wortmannin, a specific inhibitor of PI3K, was used to see if PI3K signal transduction was involved in the induction of osteopontin gene expression. RESULTS: HepG2 cells constitutively expressed low levels of osteopontin. Treatment with epidermal growth factor increased osteopontin mRNA and protein level in a dose- and time-dependent manner. Application of wortmannin caused a dramatic reduction of epidermal growth factor-induced osteopontin expression. CONCLUSION: Osteopontin gene expression can be induced by treatment of HepG2 cells with epidermal growth factor. Epidermal growth factor may regulate osteopontin gene expression through PI3K signaling pathway. Several potential targets in the pathway can be manipulated to block the synthesis of osteopontin and inhibit liver cancer metastasis.