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 journalArticle

11 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)51-6
Number of pages6
JournalInflammation Research
Volume57
Issue number2
DOIs
StatePublished - Feb 2008
Externally publishedYes

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Gastritis
Interleukin-1
Helicobacter pylori
Azure Stains
Urease
Plasma Cells
Eosinophils
Genes
Atrophy
Fibrosis
Odds Ratio
Marginal Zone B-Cell Lymphoma
Polymerase Chain Reaction
Helicobacter Infections
Gastric Mucosa
Restriction Fragment Length Polymorphisms
Endoscopy
Anti-Idiotypic Antibodies
Enzyme-Linked Immunosorbent Assay
Biopsy

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

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; Gupta, N K; Mittal, B.

In: Inflammation Research, Vol. 57, No. 2, 02.2008, p. 51-6.

Research output: Contribution to journalArticle

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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",
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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.

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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

VL - 57

SP - 51

EP - 56

JO - Inflammation Research

JF - Inflammation Research

SN - 1023-3830

IS - 2

ER -