| Summary: | 碩士 === 國立臺灣大學 === 預防醫學研究所 === 91 === Abstract
Background Notwithstanding multistate and multifactorial model for gastric cancer was proposed in early studies quantitative models for throwing light on the mechanism of disease progression were barely addressed.
Aims The present study was therefore (1) to elucidate risk factors accounting for gastric cancer and its precursor and; (2) to model the progression rates from superficial gastritis to gastric cancer.
Material and Methods
Data used in this study were derived from a community-based screening for gastric cancer in Matzu with high prevalence of gastric cancer. A total of 2201 residents participated in a two-stage screening project using H pylori infection, PGI, and PGII as screening criteria. Those who had positive results were referred to receive endoscopy and biopsy. We identified 434 biopsy-proven precursors and gastric cancers, including 229 superficial gastrisits, 53 atrophy gastritis, 119 intestinal meta-plasia, and 33 gastric cancers. Serum samples for testing anti-HP, PGI, PGII were collected. Information on life-style factors, family history, personal disease, dietary factors were obtained from a structured questionnaire. Cox regression model was used to assess the effect of risk factors on the severity of gastric neoplasm. Markov model was proposed to estimate the progression rates from superficial gastritis to gastric cancer.
Results In the multivariate analysis, H pylori infection (OR=3.10, 95% CI: 1.10-3.72), family history of gastric cancer or esophageal ca (OR=3.39, 95% CI: 2.42-4.75), history of UGI disease (OR=4.72, 95% CI: 3.57-6.26), cooked seafood intake (OR=3.48, 95% CI: 1.49-8.15) were significant factors for occurrence of SG. The effects of PGIon SG were modified by smoking or drinking.
H pylori infection (OR=11.17, 95% CI: 4.32-28.90), family history of gastric cancer or esophageal ca (OR=3.31, 95% CI: 1.51-7.22), history of UGI disease (OR=4.87, 95% CI: 2.68-8.85), salted meat intake (OR=3.00, 95% CI: 0.71-12.73) were also statistically significant for AG. H pylori infection (OR=1.66, 95% CI: 1.13-2.43), level of PGI(OR=2.63, 95% CI: 1.74-3.95), family history of gastric cancer or esophageal ca (OR=5.02, 95% CI: 3.08-8.20), history of UGI disease (OR=4.35, 95% CI: 2.93-6.46), and fermented bean intake (OR=3.06, 95% CI: 1.24-7.56) remained statistically significant for IM. For gastric cancer, only leaf vegetable intake (OR=0.16, 95% CI: 0.04-0.78), and meat intake (OR=6.94, 95% CI: 2.04-23.65) remained statistically significant (Table 4.14).
Annual progression rate from SG to AG was 2.45% (95% CI: 1.57%-3.33%). Annual progression rates from AG to IM or from IM to gastric cancer were 12.70% (95% CI: 5.23%-20.16%) and 11.95% (95% CI: 3.49%-20.41%), respectively. This gives average dwelling times for staying at AG and IM were 7.87 years and 8.37 years, respectively. The effects of H pylori, PGI&II or other dietary factors on different stages of precursor and gastric cancer were also modeled. Annual rates of malignant transformation for IM, AG and GS were 0.63%, 0.44% and 0%. Intervention efficacy for treating precursors can be calculated.
Conclusions The present study elucidated risk factors associated with precursor and invasive carcinoma of stomach. The findings fit in with Correa multi-factor and multi-stage carcinogenesis model, indicating the initiator role of H pylori and the promoter of salty food and inhibitor of vegetables in late stage of carcinogenesis. Progression rates from superficial gastritis to invasive carcinoma were also quantified. The results have significant implications for early detection of precursor of gastric cancer.
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