Table 3. Associations of genetic variants with risk of advanced gastric lesions by H. pylori infection^*.

Variant	H. pylori infection	Genotype	SG/CAG†	IM/DYS†
			n (%)	n (%)	OR (95% CI)† ‡	P for trend§
rs2910164∥	Negative	GG	46 (15.2)	32 (17.6)	1.00 (referent)
		GC	165 (54.5)	91 (50.0)	0.86 (0.50–1.47)
		CC	92 (30.4)	59 (32.4)	0.93 (0.52–1.66)	0.90
	Positive	GG	124 (18.1)	145 (16.1)	1.00 (referent)
		GC	359 (52.4)	444 (49.2)	1.15 (0.86–1.53)
		CC	202 (29.5)	314 (34.8)	1.53 (1.12–2.08)	0.004
rs895819¶	Negative	TT	155 (51.2)	92 (50.6)	1.00 (referent)
		TC	129 (42.6)	77 (42.3)	1.03 (0.69–1.54)
		CC	19 (6.3)	13 (7.1)	1.12 (0.50–2.51)	0.79
	Positive	TT	358 (52.5)	472 (52.7)	1.00 (referent)
		TC	268 (39.3)	357 (39.8)	1.04 (0.84–1.29)
		CC	56 (8.2)	67 (7.5)	0.92 (0.62–1.36)	0.94

^*This analysis was restricted to 2078 participants who had diagnosis for H. pylori infection.

^†SG = superficial gastritis; CAG = chronic atrophic gastritis; IM = intestinal metaplasia; DYS = dysplasia; OR = odds ratio; CI = confidence interval.

^‡Odds ratios and 95% confidence intervals were estimated in reference to SG/CAG group, and adjusted for age, gender, smoking and drinking status. Participants with missing data on any of covariates were excluded from the analysis.

^§ P for trend was calculated by including the 3-level ordinal variable under codominant model for each genetic variant (0 = homozygote wild, 1 = heterozygote, 2 = homozygote variant) as a continuous variable to the multivariate models.

^∥Five participants with missing values on rs2910164 genotype were excluded from analysis.

^¶Fifteen participants with missing values on rs895819 genotype were excluded from analysis.