Liu Cheng-Ying, Wu Chia-Yun, Lin Jaw-Town, Lee Yi-Chia, Yen Amy Ming-Fang, Chen Tony Hsiu-Hsi
Health Bureau of Lienchiang County, Matzu, Taiwan.
J Med Screen. 2006;13 Suppl 1:S2-5.
Although multistate progression models for gastric cancer have been proposed, estimation of quantitative parameters of such models is yet to be done. The present study was conducted to elucidate risk factors for gastric cancer and its precursors, and to model the progression rates from superficial gastritis to gastric cancer. Data were derived from a community-based screening programme for gastric cancer in the Matzu region of Taiwan. A total of 2184 residents participated in a two-stage screening project. Subjects testing positive for Helicobacter pylori infection or pepsinogen (PGI or PII/PGII ratio) and immunoglobulin G (IgG), and subjects with a history of peptic ulcer or other upper gastrointestinal disease or with a family history of gastric cancer were referred to endoscopy. We identified 325 biopsy-proven precursors and gastric cancers, including 148 superficial gastritis (SG), 42 atrophic gastritis (AG), 117 intestinal metaplasia (IM) and two gastric cancers. Three further cancers were diagnosed on endoscopy alone and 14 were later diagnosed in those who did not comply with referral to endoscopy. A Markov process model was used to estimate the progression rates from superficial gastritis through to gastric cancer, with exponential regression to assess the effect of covariates on progression rates. The annual progression rate from SG to AG was 0.0670 (95% confidence interval [CI] 0.0446-0.0895). Annual progression rates from AG to IM and from IM to gastric cancer were 0.2775 (0.1665-0.3884) and 0.2265 (0.1315-0.3214), respectively. This gives average dwelling times in AG and IM of 3.60 years and 4.42 years, respectively. Progression from no disease to SG was significantly accelerated in those testing positive for H. pylori, those testing positive for PGI and in subjects with a family history of gastric cancer or a personal history of upper gastrointestinal disease. Further progression to AG and IM was significantly accelerated in those testing positive for PGI and in those with a history of upper gastrointestinal disease.
尽管已经提出了胃癌的多状态进展模型，但此类模型定量参数的估计尚未完成。本研究旨在阐明胃癌及其癌前病变的危险因素，并模拟从浅表性胃炎到胃癌的进展率。数据来源于台湾马祖地区一项基于社区的胃癌筛查项目。共有2184名居民参与了一个两阶段筛查项目。幽门螺杆菌感染或胃蛋白酶原（PGI或PII/PGII比值）及免疫球蛋白G（IgG）检测呈阳性的受试者，以及有消化性溃疡或其他上消化道疾病病史或有胃癌家族史的受试者被转诊进行内镜检查。我们确定了325例经活检证实的癌前病变和胃癌，包括148例浅表性胃炎（SG）、42例萎缩性胃炎（AG）、117例肠化生（IM）和2例胃癌。另外3例癌症仅在内镜检查时被诊断出，14例后来在未遵从转诊进行内镜检查的患者中被诊断出。使用马尔可夫过程模型估计从浅表性胃炎到胃癌的进展率，并采用指数回归评估协变量对进展率的影响。从SG到AG的年进展率为0.0670（95%置信区间[CI] 0.0446 - 0.0895）。从AG到IM以及从IM到胃癌的年进展率分别为0.2775（0.1665 - 0.3884）和0.2265（0.1315 - 0.3214）。这使得在AG和IM中的平均停留时间分别为3.60年和4.42年。幽门螺杆菌检测呈阳性的受试者、PGI检测呈阳性的受试者以及有胃癌家族史或有上消化道疾病个人史的受试者，从无疾病进展到SG的速度显著加快。PGI检测呈阳性的受试者以及有上消化道疾病病史的受试者，进一步进展到AG和IM的速度显著加快。
