Effect of Helicobacter pylori infection on gastric mucosal pathologic change and level of nitric oxide and nitric oxide synthase

Table 1 H pylori positive rate in chronic gastric disease (%)

Group	n	H pylori positive	H pylori negative
CSG	96	37 (38.54)	59 (61.46)
CAG	119	61 (51.26)a	58 (48.74)
IM	41	30 (73.17)b	11 (26.83)
Dysplasia	26	22 (84.62)b	4 (15.38)
Total	282	150 (53.19)	132 (46.81)

^aP<0.05,

^bP<0.01 vs CSG.

Table 2 Positive rate of anti-CagA in 150 H pylori positive patients (%)

Group	CSG	CAG	IM	Dysplasia
n	37	61	30	22
Anti-CagA Positive (%)	15 (40.54)b	46 (75.41)	26 (86.67)	20 (90.91)

^bP<0.01 vs Cag, IM, dysplasia.

Table 3 Serum concentration of No and NOS(mean±SD)

Group	n	NO(μmol/L)	NOS(μmol/L)
H pylori positive	50	87.6±16.1b	51.4±13.3b
H pylori negative	35	69.8±19.4	35.2±13.3

^bP<0.01 vs H pylori negative group.

Table 4 Serum concentration of NO in different pathological groups(μmol/L, mean±SD)

Group	H pylori positive		H pylori negative
	n	Concentration	n	Concentration
CSG	16	80.0±14.6a	11	62.2±16.9a
CAG	25	95.4±8.4	21	74.6±19.2
IM	12	91.2±13.9	4	75.5±27.7
Dysplasia	9	95.3±10.3	3	71.5±19.6

^aP<0.05 vs atrophic gastritis group, intestinal metaplasia group, and dysplasia group.

Table 5 Serum concentration of NOS in different pathological groups(μmol/L, mean±SD)

Group	H pylori positive		H pylori negative
	n	Concentration	n	Concentration
CSG	16	38.0±12.4a	11	31.7±9.4
CAG	25	57.6±8.3	21	35.4±13.0
IM	12	54.8±8.3	4	26.1±4.4
Dysplasia	9	59.6±9.4	3	46.1±22.9

^aP<0.05 vs atrophic gastritis group, intestinal metaplasia group, and dysplasia group.