Helicobacter pylori-induced inflammation masks the underlying presence of low-grade dysplasia on gastric lesions

doi:10.3748/wjg.v26.i26.3834

Advanced Search

BPG is committed to discovery and dissemination of knowledge

Home / Archive / Volume 26, Issue 26

This Article

Academic Content and Language Evaluation of This Article

CrossCheck and Google Search of This Article

Academic Rules and Norms of This Article

Supplementary Materials of This Article

Citation of this article

Corresponding Author of This Article

Research Domain of This Article

Article-Type of This Article

Open-Access Policy of This Article

Times Cited Counts in Google of This Article

Number of Hits and Downloads for This Article

Total Article Views (8768)

All Articles published online

The chart showing PDF series, WORD series, HTML series, Figures (1-4) series, Tables (1-4) series.

Item

Count

PDF

442

WORD

206

HTML

4105

Figures (1-4)

804

Tables (1-4)

310

Sum=5867

Publishing Process of This Article

The chart showing Browse series, Download series.

Item

Count

Browse

934

Download

1967

Sum=2901

Jul 14, 2020 (publication date) through Jan 11, 2025

Times Cited of This Article

Times Cited (4)

Journal Information of This Article

Publication Name

World Journal of Gastroenterology

ISSN

1007-9327

Publisher of This Article

Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Observational Study

World J Gastroenterol. Jul 14, 2020; 26(26): 3834-3850
Published online Jul 14, 2020. doi: 10.3748/wjg.v26.i26.3834

Table 1 Baseline demographic and clinical characteristics of patients who underwent Helicobacter pylori eradication

Parameters	Patients (n = 85)
Age, mean (SD), yr	56.1 (12.3)
Gender, n (%)
Female	53 (62.4)
BMI, mean (SD), kg/m²	25.1 (2.2)
Alcohol users (12-24 g/dL /die), n (%)	27 (31.8)
Previous smokers, n (%)	12 (14.1)
Drug users, n (%)	23 (27.1)
Family history of gastric cancer, n (%)	4 (4.7)
Family history of other cancer, n (%)	9 (10.6)
Autoimmune comorbidity
Autoimmune atrophic gastritis	12 (14.1)
Autoimmune thyroiditis	6 (7.1)
Type-1/2 diabetes mellitus	3 (3.5)
Skin psoriasis	1 (1.2)
Rheumatoid arthritis	1 (1.2)
Sjögren syndrome	1 (1.2)
A. thyroiditis + vitiligo	1 (1.2)
A. thyroiditis + Crohn’s disease	1 (1.2)
A. thyroiditis + Sjögren syndrome	1 (1.2)
APCA and/or AIF antibody positivity	12 (14.1)
Endoscopy indication, n (%)
Gastroesophageal reflux	17 (20)
Recurrent abdominal pain	12 (14.1)
Dyspepsia	41 (48.2)
Unexplained anemia	15 (17.7)
H. pylori eradication scheme, n (%)
Quadruple¹	53 (62.4)
Modified triple²	28 (32.9)
Triple³	3 (3.6)
Sequential⁴	1 (1.2)
H. pylori eradication cycles, n (%)
One-cycle	71 (83.5)
Two-cycles	14 (16.5)

Data are expressed as number of patients and percentage (in parenthesis).

¹Bismuth + Metronidazole + Tetracycline + Proton pump inhibitor.

²Amoxicillin + Levofloxacin + Proton pump inhibitor.

³Amoxicillin + Clarithromycin + Proton pump inhibitor.

⁴Amoxicillin + Clarithromycin + Proton pump inhibitor Amoxicillin (5 d), then Clarithromycin + Metronidazole (5 d) + Proton pump inhibitor. BMI: Body mass index; SD: Standard deviation; APCA: Anti-parietal cell antibody; AIF: Anti-intrinsic factor; H. pylori: Helicobacter pylori; PPI: Proton pump inhibitor.

Table 2 Endoscopic and histological characteristics of patients before and after Helicobacter pylori eradication

Parameters	*Before H. pylori* eradication (n = 85)**	*After H. pylori* eradication (n = 85)**	P value
Endoscopic atrophy¹, n (%)
Absent	5 (5.9)	4 (4.7)	1.0
Antrum	19 (22.4)	19 (22.4)	1.0
Antrum-predominant	18 (21.2)	12 (14.1)	0.23
Corpus-predominant	21 (24.7)	23 (27.1)	0.73
Pan-atrophy	22 (25.9)	27 (31.8)	0.40
OLGA-scale, n (%)
Stage 0	4 (4.7)	4 (4.7)	1.0
Stage 1	22 (25.9)	28 (32.9)	0.31
Stage 2	34 (40)	23 (27.1)	0.07
Stage 3	20 (23.5)	25 (29.4)	0.38
Stage 4	5 (5.9)	5 (5.9)	1.0
EGGIM-scale, n (%)
0-2	47 (55.3)	45 (52.9)	0.76
3-4	21 (24.7)	10 (11.8)	0.03^a
5-6	12 (14.1)	21 (24.7)	0.08
7-8	4 (4.7)	4 (4.7)	1.0
9-10	1 (1.2)	5 (5.9)	0.21
OLGIM-scale, n (%)
Stage 0	40 (47.1)	29 (34.1)	0.08
Stage 1	14 (16.5)	17 (20)	0.55
Stage 2	14 (16.5)	14 (16.5)	1.0
Stage 3	13 (15.3)	18 (21.2)	0.32
Stage 4	4 (4.7)	7 (8.2)	0.53
Gastritis at histology², n (%)
Quiescent	0	81 (95.3)	< 0.0001^b
Mild	19 (22.4)	4 (4.7)	0.001^b
Moderate	46 (54.1)	0	< 0.0001^b
Severe	20 (23.5)	0	< 0.0001^b
MALT-hyperplasia, n (%)
Absent	46 (54.1)	82 (96.5)	< 0.0001^b
Mild	25 (29.4)	3 (3.5)	< 0.0001^b
Moderate	11 (12.9)	0	0.007^b
Severe	3 (3.5)	0	0.24
Histological LGD³, n (%)
Absent	70 (82.4)	57 (67.1)	0.02^a
On random biopsies	15 (17.6)	9 (10.6)	0.19
On random + on lesions biopsies	0	6 (7)	0.03^b
Only on visible lesions	0	13 (15.3)	0.0001^b

Data are expressed as number of patients and percentage (in parenthesis).

¹By Kimura and Takemoto[32].

²By Sydney System.

³LGD: Low-grade dysplasia according to World Health Organization classification.

^aBy χ² test.

^bby Fisher’s exact test. H. pylori: Helicobacter pylori; EGGIM: Endoscopic grading of gastric intestinal metaplasia; MALT: Mucosa-associated lymphoid tissue; OLGA: Operative Link on Gastritis Assessment; OLGIM: Operative Link on Gastric Intestinal Metaplasia.

Table 3 Demographic and clinical characteristics of patients with low-grade dysplasia detected on visible gastric lesions or randomly and without low-grade dysplasia, before and after Helicobacter pylori eradication

Parameters	With LGD (n = 28)	Without LGD (n = 57)	P value
Age, mean (SD), yr	60.9 (8.2)	53.7 (13.4)	0.01^a
Gender, n (%)
Female	15 (53.6)	38 (66.7)	0.24
BMI, mean (SD), kg/m²	25 (2.4)	25 (2.3)	1.0
Alcohol users (12-24 g/dL/die), n (%)	15 (53.6)	12 (21.1)	0.002^b
Previous smokers, n (%)	10 (35.7)	2 (3.5)	< 0.0001^c
Family history of gastric cancer, n (%)	4 (14.3)	0	0.001^c
Family history of other cancer, n (%)	6 (21.4)	3 (5.3)	0.001^c
Autoimmune comorbidity
Autoimmune atrophic gastritis	8 (28.6)	4 (7)	0.02^c
Autoimmune thyroiditis	3 (10.7)	3 (5.3)	0.39
A. thyroiditis + vitiligo	1 (3.6)	0	0.33
A. thyroiditis + Crohn’s disease	1 (3.6)	0	0.33
A. thyroiditis + Sjögren syndrome	0	1 (1.7)	1.0
Sjögren syndrome	0	1 (1.7)	1.0
Type-1/2 diabetes mellitus	1 (3.6)	2 (3.5)	1.0
Skin psoriasis	1 (3.6)	0	0.33
Rheumatoid arthritis	0	1 (1.7)	1.0
APCA and/or AIF antibody positivity	8 (28.6)	4 (7)	0.02^c
H. pylori eradication scheme, n (%)
Quadruple¹	17 (60.7)	36 (63.2)	0.82
Modified triple²	9 (32.1)	19 (33.3)	0.91
Triple³	1 (3.6)	2 (3.5)	1.0
Sequential⁴	1 (3.6)	0	0.33
H. pylori eradication cycles, n (%)
One cycle	22 (78.6)	46 (86)	0.82
Two cycles	6 (21.4)	8 (14)	0.82
OLGA scale before⁵
Stage 0	0	4 (7)	0.3
Stage 1-2	8 (28.6)	48 (84.2)	< 0.0001^b
Stage 3-4	20 (71.4)	5 (8.8)	< 0.0001^c
OLGA scale after⁶
Stage 0	0	4 (7)	0.3
Stage 1-2	7 (25)	44 (77.2)	< 0.0001^b
Stage 3-4	21 (75)	9 (15.8)	< 0.0001^b
OLGIM scale before
Stage 0	0	40 (70.1)	< 0.0001^c
Stage 1-2	12 (42.8)	16 (28.1)	0.17
Stage 3-4	16 (57.1)	1 (1.8)	< 0.0001^c
OLGIM scale after
Stage 0	0	29 (50.9)	< 0.0001^c
Stage 1-2	7 (25)	24 (42.1)	0.12
Stage 3-4	21 (75)	4 (7)	< 0.0001^c
Gastritis at histology before, n (%)
Quiescent	0	0	1.0
Mild	3 (10.7)	16 (28.1)	0.10
Moderate-severe	25 (89.3)	41 (71.9)	0.10
Gastritis at histology after, n (%)
Quiescent	26 (92.9)	55 (96.5)	0.59
Mild	2 (7.1)	2 (3.5)	0.50
Moderate-severe	0	0	1.0
MALT hyperplasia before, n (%)
Absent	10 (35.7)	36 (63.2)	0.02^b
Mild	10 (35.7)	15 (26.3)	0.37
Moderate	6 (21.4)	5 (8.8)	0.17
Severe	2 (7.2)	1 (1.8)	0.25
MALT hyperplasia after, n (%)
Absent	10 (35.7)	36 (63.2)	0.02^b
Mild	18 (64.3)	21 (36.8)	0.02^b
Moderate	0	0	1.0
Severe	0	0	1.0

Data are expressed as number of patients and percentage (in parenthesis).

¹Bismuth + Metronidazole + Tetracycline + Proton pump inhibitor.

²Amoxicillin + Levofloxacin + Proton pump inhibitor.

³Amoxicillin + Clarithromycin + Proton pump inhibitor.

⁴Amoxicillin + Clarithromycin + Proton pump inhibitor Amoxicillin (5 d), then Clarithromycin + Metronidazole (5 d) + Proton pump inhibitor.

⁵Before Helicobacter pylori eradication (by Sydney System).

⁶After Helicobacter pylori eradication.

^aBy t-test.

^bBy χ² test.

^cBy Fisher’s exact test. BMI: Body mass index; SD: Standard deviation; APCA: Anti-parietal cell antibody; AIF: Anti-intrinsic factor; H. pylori: Helicobacter pylori; PPI: Proton pump inhibitor; OLGA: Operative Link on Gastritis Assessment; OLGIM: Operative Link on Gastric Intestinal Metaplasia; MALT: Mucosa-associated lymphoid tissue.

Table 4 Probability of detecting low-grade dysplasia randomly or on visible lesions after Helicobacter pylori eradication

	Univariate		Multivariate
Variable	OR (95% CI)	P value	OR¹ (95%CI)	P value
Age, yr	1.05 (1.01-1.11)	< 0.02	1.05 (1.00-1.10)	0.07
Gender
Female	1.00²		-
Male	1.73 (0.69-4.37)	0.24	-	-
BMI, kg/m²	0.93 (0.75-1.15)	0.49	-	-
Alcohol use
No	1.00²		1.00²
Yes	4.33 (1.63-11.51)	< 0.01	3.88 (1.31-11.49)	0.01
Drug use
No	1.00²		-
Yes	1.45 (0.54-3.94)	0.46	-	-
MALT hyperplasia regression/reduction
No	1.00²		-
Yes	3.90 (1.20-7.91)	< 0.02	3.10 (1.05-9.12)	0.04
APCA and/or AIF antibody positivity
No	1.00²
Yes	5.30 (1.44-19.56)	0.01	5.47 (1.33-22.39)	< 0.02

¹Ajusted for age, alcohol use, Mucosa-associated lymphoid tissue hyperplasia reduction/regression and anti-parietal cell antibody and/or anti-intrinsic factor antibody positivity.

²Reference group. LGD: Low-grade dysplasia; H. pylori: Helicobacter pylori; OR: Odds ratio; BMI: Body mass index; MALT: Mucosa-associated lymphoid tissue; APCA: Anti-parietal cell antibody; AIF: Anti-intrinsic factor.

Citation: Panarese A, Galatola G, Armentano R, Pimentel-Nunes P, Ierardi E, Caruso ML, Pesce F, Lenti MV, Palmitessa V, Coletta S, Shahini E. Helicobacter pylori-induced inflammation masks the underlying presence of low-grade dysplasia on gastric lesions. World J Gastroenterol 2020; 26(26): 3834-3850
URL: https://www.wjgnet.com/1007-9327/full/v26/i26/3834.htm
DOI: https://dx.doi.org/10.3748/wjg.v26.i26.3834