4.4 Article

Helicobacter pylori infection and gastroduodenal lesions in patients with systemic lupus erythematosus

Journal

CLINICAL RHEUMATOLOGY
Volume 39, Issue 2, Pages 463-469

Publisher

SPRINGER LONDON LTD
DOI: 10.1007/s10067-019-04805-w

Keywords

Endoscopy; Gastroduodenal lesions; Helicobacter pylori; Systemic lupus erythematosus

Categories

Funding

  1. [FIS/IMSS/PROT/G17/1663]

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Objective The aim of this study was to determine the frequency of Helicobacter pylori in SLE patients and to compare clinical characteristics and gastroduodenal lesions in patients with and without H. pylori infection. Methods Adult SLE patients were selected and subjected to endoscopy. Gastroduodenal lesions were examined by endoscopy and biopsy (antrum and corpus). Biopsies were evaluated by hematoxylin and eosin and Giemsa staining. Immunochromatographic membrane-based assay using amplification was used to test for H. pylori antigen (coproantigen) in stool samples in all participants. Clinical characteristics and gastroduodenal lesions were compared between patients with and without H. pylori infection. Results A total of 118 SLE patients were included (mean age 44.7 +/- 11.7 years, mean disease duration 11.6 +/- 6.0 years), of whom 101 (85.6%) were receiving non-steroidal anti-inflammatory drugs (NSAIDs). The coproantigen test was positive in 32 (27.1%) patients. H. pylori was present in twenty six patients (22.0%) in the gastric biopsy. The frequency of gastric erosions and gastric ulcers were 55.1% and 0.8%, respectively. Gastric erosions were less frequent in SLE patients with H. pylori infection than those without H. pylori (43.5.7% vs. 62.5%; p = 0.04). The age, disease duration, disease activity, chronic damage, gastroprotective drugs, and immunosuppressive therapy did not differ between the two groups. Conclusions We found a high frequency of H. pylori infection in SLE patients. The severity of SLE and reception of gastroprotective therapy do not seem to be related to H. pylori infection. Immunosuppressive therapy may not be protective against H. pylori infection in SLE patients.

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