| Theme | Risk Factors and Prevention of Gastric Cancer | |
|---|---|---|
| Title | Secondary Stomach Cancer after Gastrectomy Persistence of H. pylori Infection and the Refluxes of the Bile and Pancreas Juices into the Stomach | |
| Publish Date | 2009/04 | |
| Author | Shunji Kato | Department of Surgery, Nippon Medical School |
| Author | Norio Matsukura | Department of Surgery, Nippon Medical School |
| Author | Zenya Naito | Pathology, Nippon Medical School |
| Author | Hitoshi Kanno | Department of Surgery, Nippon Medical School |
| Author | Itsuo Fujita | Department of Surgery, Nippon Medical School |
| Author | Teruo Kiyama | Department of Surgery, Nippon Medical School |
| Author | Takashi Tajiri | Department of Surgery, Nippon Medical School |
| [ Summary ] | The persistence of H. pylori infection and reflux of bile and pancreatic juice into the stomach supposed to be the cause of secondary stomach cancer. It is well known that secondary stomach cancer occurrs in many remnant stomach lesion. This occurs relatively soon after gastrectomies employing the Biliroth I re-construction procedure. Frequent occurrences were also observed in anastomosis sites at longer periods after Billroth II re-construction. On the other hand, neutralization of pH levels possibly to reproduce the nitroso-carcinogenic compounds is also important for the stomach carcinogenesis. Cumulative regenerating morbidity was higher with post-endoscopic mucosal resection (5 / 35 ; 14.3 %). Patients, who received Billroth II re-construction had rates of : (3 / 40 ; 7.5 %), and those who had the Billroth I re-construction procedure had rates of : (2 / 107 ; 1.9 %). Information concerning stomach mucosa was evaluated by using updated Sydney System Scores. The information gathered suggested the possibility of being able to predict secondary stomach cancer. The regions of the stomach without H. pylori infection due to eradication therapy or natural elimination through bile reflux were found to have no or low inflammation scores. These lymphocyte migrations in at risk stomach mucosa and higher mRNA levels of IL-8 and COX 2 may induce secondary tumors in remnant stomachs. There ia a risk of secondary cancer which relative risk is 4.1 (95 % C. I. : 2.4 - 7.1). These results indicated that patients who did not exhibit improvements in inflammations after the eradication or eliminate of H. pylori, were at higher risk of new carcinogenesis of the stomach. Inflammation scores after H. pylori eradication will be good biomarkers to formulate not only risk assessments for secondary gastric carcinogenesis, but also may be used for determining clinical benefits to determine intervals for endoscopic screening observations after gastrectomies. |
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