Table 2. Lewis phenotypes and cag status of clinical H. pylori isolates obtained from the Kalixanda study.

Individual	Histopathology at year 0 and 4	Lex+y+	Lex+y−	Lex−y+	Lex−y−	cag status
Kx438	Moderate atrophy	13	0	2	0	+
	Gastric adenocarcinoma	15	0	0	0	+
Kx201	Normal	8	0	7	0	+
	Mild atrophy	11	1	3	0	+
Kx345	Normal	6	6	2	1	+
	High grade atrophy	4	6	0	5	+
Kx439	Mild atrophy	4	0	11	0	+
	High grade atrophy	ND	ND	ND	ND	ND
Kx533	Moderate atrophy	4	0	11	0	+
	High grade atrophy	2	0	13	0	+
Kx1039	Mild atrophy	8	0	7	0	+
	High grade atrophy	14	0	1	0	+
Kx1167	Moderate atrophy	31	01	01	01	+1
	High grade atrophy	2	0	13	0	+
Kx1172	Moderate atrophy	4	0	11	0	+
	High grade atrophy	2	0	13	0	+
Kx208	Normal	2	1	7	5	+
	Normal	0	0	7	8	+
Kx239	Normal	0	0	15	0	+/− 3
	Normal	0	0	15	0	+
Kx364	Normal	11	0	4	0	-4
	Normal	13	2	0	0	-4
Kx491	Normal	0	15	0	0	-
	Normal	0	15	0	0	-
Kx573	Normal	5	1	4	5	+
	Normal	4	0	9	2	+
Kx595	Normal	0	0	15	0	-
	Normal	9	0	6	0	-
Kx1259	Normal	0	0	13	2	+
	Normal	0	0	2	13	+
Kx1353	Normal	12	02	132	02	+
	Normal	3	0	12	0	+
Kx1379	Normal	1	0	14	0	+
	Normal	6	0	9	0	+
Total		155	47	239	41
		(32%)	(9.8%)	(50%)	(8.5%)

¹3 isolates analyzed.

²14 isolates analyzed.

³80% positive for cagA and 20% positive for cag PAI empty site PCR in this individual.

⁴All isolates were negative for both cagA and cag PAI empty site PCR:s, indicating that part of the cag PAI may still be present in these isolates, although the cagA gene is deleted.