Antralization at the edge of proximal gastric ulcers: Does Helicobacter pylori infection play a role?

Table 1 The demographic clinical characteristics of the patients initially recruited, according to the location of gastric ulcers (n = 116)

	Ulcer location
	Incisura (n = 91)	Body (n = 23)	Fundus (n = 2)
Age (mean ± SD)	59.5 ± 13.3	69.3 ± 10.2	51.0 ± 11.2
Gender (male/female)	60/31	17/6	2/0
Smoking (yes/no)	44/46	11/12	1/1
H. pylori status (positive/negative)	81/10	19/4	1/1

Table 2 Changes of gastric mucosa at the edge of proximal gastric ulcers and gastric body one year after treatment, in relation to post-treatment H. pylori status, treatment regimens, ulcer relapse and ulcer location (n = 65)

	Mucosal type change (%)
	Ulcer edge			Gastric body
	Improvementa(n = 11)	No changeb(n = 49)	Worseningc(n = 5)	Improvement(n = 5)	No change(n = 58)	Worsening(n = 2)
H. pyloriinfection
Eradicated (n = 28)	35.7d	64.3	0	14.3	85.7	0
Persistent (n = 37)	2.7	83.8	13.5	2.7	91.9	5.4
Ulcer location
Incisura (n = 52)	15.4	76.9	7.7	5.8	90.4	3.8
Body (n = 13)	23.1	69.2	7.7	15.4	84.6	0

^a, Improvement, antral-type (A)→transitional type (T), A→body-type (B), or T→B;

^b, No change, A→A, T→T or B→B;

^c, Worsening, T→A, B→A or B→T.

^d, P < 0.001, compared with persistent infection.