Helicobacter pylori and Upper Endoscopy in Systemic Sclerosis: A Cross-sectional Study in the Real World.
Autoantibodies
/ blood
Barrett Esophagus
/ pathology
Biopsy
/ methods
DNA Topoisomerases, Type I
Endoscopy, Digestive System
/ methods
Female
Gastric Mucosa
/ microbiology
Gastroesophageal Reflux
/ drug therapy
Helicobacter Infections
/ epidemiology
Helicobacter pylori
/ isolation & purification
Humans
Male
Middle Aged
Nuclear Proteins
/ immunology
Proton Pump Inhibitors
/ therapeutic use
Risk Assessment
Scleroderma, Systemic
/ blood
Upper Gastrointestinal Tract
/ diagnostic imaging
Journal
Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases
ISSN: 1536-7355
Titre abrégé: J Clin Rheumatol
Pays: United States
ID NLM: 9518034
Informations de publication
Date de publication:
01 Jan 2021
01 Jan 2021
Historique:
entrez:
21
12
2020
pubmed:
22
12
2020
medline:
5
1
2021
Statut:
ppublish
Résumé
A role for Helicobacter pylori in triggering systemic sclerosis (SSc) has been proposed, but data are conflicting. In previous studies, infection has been generally searched for by using serology. We designed this study to assess H. pylori prevalence in SSc patients with histology of gastric mucosa, considered the criterion standard for infection diagnosis. This cross-sectional study enrolled 30 SSc patients who complained of upper gastrointestinal symptoms. All underwent upper endoscopy with gastric biopsies. Endoscopic alterations were recorded, and gastric mucosa biopsies were used for both histological examination and searching for H. pylori. The role for proton-pump inhibitor (PPI) therapy was considered. Fisher exact test was used for statistical analysis. Data of 28 SSc patients were available, 14 with ongoing PPI therapy. Helicobacter pylori infection at histology was detected in 14.3% patients, and it equally occurred in patients with or without PPI therapy. Erosive esophagitis/Barrett esophagus was detected in 26.6% of cases. Among patients with PPI therapy, 30% received half dose only. The prevalence of intestinal metaplasia was low (14.3%). Endoscopic esophageal alterations were significantly more frequent in those patients showing anti-Scl70 antibody positivity. This study showed that prevalence of H. pylori is very low in SSc patients, so that it seems not having a role in triggering SSc. Management of gastroesophageal diseases in SSc patients needs to be improved, and looking to the autoimmune profile may be of help. Thus, collaboration between rheumatologist and gastroenterologist is highly recommended.
Sections du résumé
BACKGROUND/AIMS
OBJECTIVE
A role for Helicobacter pylori in triggering systemic sclerosis (SSc) has been proposed, but data are conflicting. In previous studies, infection has been generally searched for by using serology. We designed this study to assess H. pylori prevalence in SSc patients with histology of gastric mucosa, considered the criterion standard for infection diagnosis.
METHODS
METHODS
This cross-sectional study enrolled 30 SSc patients who complained of upper gastrointestinal symptoms. All underwent upper endoscopy with gastric biopsies. Endoscopic alterations were recorded, and gastric mucosa biopsies were used for both histological examination and searching for H. pylori. The role for proton-pump inhibitor (PPI) therapy was considered. Fisher exact test was used for statistical analysis.
RESULTS
RESULTS
Data of 28 SSc patients were available, 14 with ongoing PPI therapy. Helicobacter pylori infection at histology was detected in 14.3% patients, and it equally occurred in patients with or without PPI therapy. Erosive esophagitis/Barrett esophagus was detected in 26.6% of cases. Among patients with PPI therapy, 30% received half dose only. The prevalence of intestinal metaplasia was low (14.3%). Endoscopic esophageal alterations were significantly more frequent in those patients showing anti-Scl70 antibody positivity.
CONCLUSIONS
CONCLUSIONS
This study showed that prevalence of H. pylori is very low in SSc patients, so that it seems not having a role in triggering SSc. Management of gastroesophageal diseases in SSc patients needs to be improved, and looking to the autoimmune profile may be of help. Thus, collaboration between rheumatologist and gastroenterologist is highly recommended.
Identifiants
pubmed: 33347033
doi: 10.1097/RHU.0000000000001502
pii: 00124743-202101000-00008
doi:
Substances chimiques
Autoantibodies
0
Nuclear Proteins
0
Proton Pump Inhibitors
0
Scl 70 antigen, human
0
DNA Topoisomerases, Type I
EC 5.99.1.2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
40-41Informations de copyright
Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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