Association between cag-pathogenicity island in Helicobacter pylori isolates from peptic ulcer, gastric carcinoma, and non-ulcer dyspepsia subjects with histological changes

Table 5 Distribution of cagE, T, LEC1, and LEC2 in H pylori isolates

Clinical status (n)	cagE (%)	cagT (%)	LEC1 (%)	LEC2 (%)
DU (58)	47 (81)	56 (96.5)	44 (75.8)	33 (56.8)
GU (46)	46 (100)	46 (100)	46 (100)	46 (100)
NUD (56)	36 (64.2)	36 (64.2)	38 (67.8)	18 (32.1)
GC (14)	14 (100)	14 (100)	14 (100)	14 (100)
Total (174)	143 (82.1)	152 (87.3)	142 (81.6)	111 (63.7)

For cagE, GU vs NUD is highly significant at 0.1% level (P<0.001), DU vs GU, NUD vs GC combinations are significant at 1% level (P<0.01), DU vs NUD combination is significant at 5% level (P<0.05) and DU vs GC . For cagT, DU vs NUD, GU vs NUD combinations are highly significant at 0.1% level (P<0.001), NUD vs GC combination is significant at 1% level (P<0.01) and DU vs GU, DU vs GC, GU vs GC are not significant at 1% level. For LEC1, DU vs GU, GU vs NUD combinations are highly significant at 0.1% level (P<0.001), NUD vs GC is significant at 1% level (P<0.01), DU vs GC is significant at 5% level (P<0.05). For LEC2, DU vs GU, GU vs NUD, NUD vs GC combinations are highly significant at 0.1% level (P<0.001), DU vs NUD, DU vs GC combinations are significant at 1% level (P<0.01) and GU vs GC is not significant at 1% level.