Risk of lymphoid follicle development in patients with chronic antral gastritis: role of endoscopic features, histopathological parameters, CagA status and interleukin-1 gene polymorphisms

B R Achyut; N Moorchung; A N Srivastava; N K Gupta; B Mittal

doi:10.1007/s00011-007-7033-2

Risk of lymphoid follicle development in patients with chronic antral gastritis: role of endoscopic features, histopathological parameters, CagA status and interleukin-1 gene polymorphisms

B R Achyut, N Moorchung, A N Srivastava, N K Gupta, B Mittal

Research output: Contribution to journal › Article › peer-review

16 Scopus citations

Abstract

OBJECTIVE: Helicobacter pylori infection causes gastritis, lymphoid follicle formation and development of MALT lymphoma. We evaluated endoscopic, histological, serological and genetic risk factors associated with lymphoid follicle development in gastritis.

MATERIALS AND METHODS: After upper GI endoscopy, 3 antral biopsies were taken from 120 patients for histological examination. H. pylori was diagnosed using rapid urease test (RUT), modified Giemsa stain and IgG anti-CagA ELISA. Genotyping of IL-1B (-511C/T) and IL-1RN (86 bp VNTR) genes were performed by PCR-RFLP/PCR.

RESULTS: In 120 patients, 45 (37.5%) showed presence of lymphoid follicles in antral gastric mucosa. H. pylori was positive by modified Giemsa stain (26%) RUT (50%) and anti-CagA IgG in 67.5%, The presence of nodularity (p = 0.030), neutrophilic infiltration (p = 0.010), lymphocytic infiltration (p = 0.002), glandular atrophy (p = 0.0001), glandular shortening (p = 0.001), fibrosis (p = 0.0001), plasma cells (p = 0.007), eosinophils (p = 0.012), anti-CagA antibodies (p = 0.003) and H. pylori density (p = 0.020) were associated with risk (odds ratio = 11.5, 3.8, 11.0, 8.4, 3.8, 4.6, 5.8, 16.0, 10.8 and 2.8 respectively) of lymphoid follicle. However, IL-1 gene polymorphisms did not influence lymphoid follicle development

CONCLUSION: The presence of modularity, lymphocytic infiltration, glandular atrophy, glandular shortening, fibrosis, plasma cells, eosinophils and anti-CagA IgG antibodies are risk factors for lymphoid follicle development in patients with gastritis.

Original language	English (US)
Pages (from-to)	51-6
Number of pages	6
Journal	Inflammation Research
Volume	57
Issue number	2
DOIs	https://doi.org/10.1007/s00011-007-7033-2
State	Published - Feb 2008
Externally published	Yes

Keywords

Adult
Antigens, Bacterial
Bacterial Proteins
Endoscopy
Female
Gastritis
Helicobacter pylori
Humans
Interleukin-1
Lymph Nodes
Lymphatic Diseases
Male
Middle Aged
Polymorphism, Genetic
Polymorphism, Restriction Fragment Length
Risk Factors
Journal Article
Research Support, Non-U.S. Gov't

Access to Document

10.1007/s00011-007-7033-2

Cite this

Risk of lymphoid follicle development in patients with chronic antral gastritis: role of endoscopic features, histopathological parameters, CagA status and interleukin-1 gene polymorphisms. / Achyut, B R; Moorchung, N; Srivastava, A N et al.
In: Inflammation Research, Vol. 57, No. 2, 02.2008, p. 51-6.

Research output: Contribution to journal › Article › peer-review

@article{b9c5c8db5c8d4608a82b97630ba20ce2,

title = "Risk of lymphoid follicle development in patients with chronic antral gastritis: role of endoscopic features, histopathological parameters, CagA status and interleukin-1 gene polymorphisms",

abstract = "OBJECTIVE: Helicobacter pylori infection causes gastritis, lymphoid follicle formation and development of MALT lymphoma. We evaluated endoscopic, histological, serological and genetic risk factors associated with lymphoid follicle development in gastritis.MATERIALS AND METHODS: After upper GI endoscopy, 3 antral biopsies were taken from 120 patients for histological examination. H. pylori was diagnosed using rapid urease test (RUT), modified Giemsa stain and IgG anti-CagA ELISA. Genotyping of IL-1B (-511C/T) and IL-1RN (86 bp VNTR) genes were performed by PCR-RFLP/PCR.RESULTS: In 120 patients, 45 (37.5%) showed presence of lymphoid follicles in antral gastric mucosa. H. pylori was positive by modified Giemsa stain (26%) RUT (50%) and anti-CagA IgG in 67.5%, The presence of nodularity (p = 0.030), neutrophilic infiltration (p = 0.010), lymphocytic infiltration (p = 0.002), glandular atrophy (p = 0.0001), glandular shortening (p = 0.001), fibrosis (p = 0.0001), plasma cells (p = 0.007), eosinophils (p = 0.012), anti-CagA antibodies (p = 0.003) and H. pylori density (p = 0.020) were associated with risk (odds ratio = 11.5, 3.8, 11.0, 8.4, 3.8, 4.6, 5.8, 16.0, 10.8 and 2.8 respectively) of lymphoid follicle. However, IL-1 gene polymorphisms did not influence lymphoid follicle developmentCONCLUSION: The presence of modularity, lymphocytic infiltration, glandular atrophy, glandular shortening, fibrosis, plasma cells, eosinophils and anti-CagA IgG antibodies are risk factors for lymphoid follicle development in patients with gastritis.",

keywords = "Adult, Antigens, Bacterial, Bacterial Proteins, Endoscopy, Female, Gastritis, Helicobacter pylori, Humans, Interleukin-1, Lymph Nodes, Lymphatic Diseases, Male, Middle Aged, Polymorphism, Genetic, Polymorphism, Restriction Fragment Length, Risk Factors, Journal Article, Research Support, Non-U.S. Gov't",

author = "Achyut, {B R} and N Moorchung and Srivastava, {A N} and Gupta, {N K} and B Mittal",

year = "2008",

month = feb,

doi = "10.1007/s00011-007-7033-2",

language = "English (US)",

volume = "57",

pages = "51--6",

journal = "Inflammation Research",

issn = "1023-3830",

publisher = "Birkhauser Verlag Basel",

number = "2",

}

TY - JOUR

T1 - Risk of lymphoid follicle development in patients with chronic antral gastritis

T2 - role of endoscopic features, histopathological parameters, CagA status and interleukin-1 gene polymorphisms

AU - Achyut, B R

AU - Moorchung, N

AU - Srivastava, A N

AU - Gupta, N K

AU - Mittal, B

PY - 2008/2

Y1 - 2008/2

N2 - OBJECTIVE: Helicobacter pylori infection causes gastritis, lymphoid follicle formation and development of MALT lymphoma. We evaluated endoscopic, histological, serological and genetic risk factors associated with lymphoid follicle development in gastritis.MATERIALS AND METHODS: After upper GI endoscopy, 3 antral biopsies were taken from 120 patients for histological examination. H. pylori was diagnosed using rapid urease test (RUT), modified Giemsa stain and IgG anti-CagA ELISA. Genotyping of IL-1B (-511C/T) and IL-1RN (86 bp VNTR) genes were performed by PCR-RFLP/PCR.RESULTS: In 120 patients, 45 (37.5%) showed presence of lymphoid follicles in antral gastric mucosa. H. pylori was positive by modified Giemsa stain (26%) RUT (50%) and anti-CagA IgG in 67.5%, The presence of nodularity (p = 0.030), neutrophilic infiltration (p = 0.010), lymphocytic infiltration (p = 0.002), glandular atrophy (p = 0.0001), glandular shortening (p = 0.001), fibrosis (p = 0.0001), plasma cells (p = 0.007), eosinophils (p = 0.012), anti-CagA antibodies (p = 0.003) and H. pylori density (p = 0.020) were associated with risk (odds ratio = 11.5, 3.8, 11.0, 8.4, 3.8, 4.6, 5.8, 16.0, 10.8 and 2.8 respectively) of lymphoid follicle. However, IL-1 gene polymorphisms did not influence lymphoid follicle developmentCONCLUSION: The presence of modularity, lymphocytic infiltration, glandular atrophy, glandular shortening, fibrosis, plasma cells, eosinophils and anti-CagA IgG antibodies are risk factors for lymphoid follicle development in patients with gastritis.

AB - OBJECTIVE: Helicobacter pylori infection causes gastritis, lymphoid follicle formation and development of MALT lymphoma. We evaluated endoscopic, histological, serological and genetic risk factors associated with lymphoid follicle development in gastritis.MATERIALS AND METHODS: After upper GI endoscopy, 3 antral biopsies were taken from 120 patients for histological examination. H. pylori was diagnosed using rapid urease test (RUT), modified Giemsa stain and IgG anti-CagA ELISA. Genotyping of IL-1B (-511C/T) and IL-1RN (86 bp VNTR) genes were performed by PCR-RFLP/PCR.RESULTS: In 120 patients, 45 (37.5%) showed presence of lymphoid follicles in antral gastric mucosa. H. pylori was positive by modified Giemsa stain (26%) RUT (50%) and anti-CagA IgG in 67.5%, The presence of nodularity (p = 0.030), neutrophilic infiltration (p = 0.010), lymphocytic infiltration (p = 0.002), glandular atrophy (p = 0.0001), glandular shortening (p = 0.001), fibrosis (p = 0.0001), plasma cells (p = 0.007), eosinophils (p = 0.012), anti-CagA antibodies (p = 0.003) and H. pylori density (p = 0.020) were associated with risk (odds ratio = 11.5, 3.8, 11.0, 8.4, 3.8, 4.6, 5.8, 16.0, 10.8 and 2.8 respectively) of lymphoid follicle. However, IL-1 gene polymorphisms did not influence lymphoid follicle developmentCONCLUSION: The presence of modularity, lymphocytic infiltration, glandular atrophy, glandular shortening, fibrosis, plasma cells, eosinophils and anti-CagA IgG antibodies are risk factors for lymphoid follicle development in patients with gastritis.

KW - Adult

KW - Antigens, Bacterial

KW - Bacterial Proteins

KW - Endoscopy

KW - Female

KW - Gastritis

KW - Helicobacter pylori

KW - Humans

KW - Interleukin-1

KW - Lymph Nodes

KW - Lymphatic Diseases

KW - Male

KW - Middle Aged

KW - Polymorphism, Genetic

KW - Polymorphism, Restriction Fragment Length

KW - Risk Factors

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1007/s00011-007-7033-2

DO - 10.1007/s00011-007-7033-2

M3 - Article

C2 - 18288454

SN - 1023-3830

VL - 57

SP - 51

EP - 56

JO - Inflammation Research

JF - Inflammation Research

IS - 2

ER -

Risk of lymphoid follicle development in patients with chronic antral gastritis: role of endoscopic features, histopathological parameters, CagA status and interleukin-1 gene polymorphisms

Abstract

Keywords

Access to Document

Fingerprint

Cite this