The Contribution of Drugs and Helicobacter pylori to Gastric Mucosa Changes in Patients with Systemic Lupus Erythematosus and Antiphospholipid Syndrome.

Tatiana M Reshetnyak,Irina A Doroshkevich,Vasiliy I Reshetnyak,Evgeny L Nasonov,Igor V Maev,Natalia V Seredavkina

doi:10.1155/2019/9698086

Abstract

Background The nature and rate of gastric mucosal (GM) damage in systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) remain to be among the unsolved problems. Objective To define the role of H. pylori and drugs in the development of GM damages in SLE and APS. Methods A study was conducted on 85 patients with SLE and APS. All the patients underwent esophagogastroduodenoscopy with targeted biopsy of the mucosa of the gastric body and antrum. The presence of H. pylori in the gastric biopsy specimens was determined using polymerase chain reaction. Results Endoscopic examination revealed that the patients with SLE and APS on admission had the following GM changes: antral gastritis (82.4%), erosions (24.7%), hemorrhages (8.2%), and pangastritis (8.2%). SLE and APS patients showed no direct correlation between the found GM damages and the presence of H. pylori. The use of glucocorticoid, low-dose acetylsalicylic acid, nonsteroidal anti-inflammatory drug, and anticoagulant in SLE and APS patients is accompanied by GM damage. Conclusion There was no evidence of the role of H. pylori in GM damage in the SLE and APS patients. More frequent detection of H. pylori was observed in anticoagulants or low-dose acetylsalicylic acid users than in glucocorticoids and nonsteroidal anti-inflammatory drugs ones.

Highlights

Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease characterized by exacerbations and remissions, as well as by diverse clinical manifestations that can range from minor signs, such as fatigue, weight loss, and arthralgia, to life-threatening damage to the kidneys or central nervous system [1,2,3]
The survey of the patients indicated that epigastria pain was recorded significantly (χ2 = 3.65; OR = 2.50; 95% CI, 1.11-10.10; P = 0.05) more frequently in patients with antiphospholipid syndrome (APS) (38/46) compared to those with systemic lupus erythematosus (SLE) without APS (23/39)
The findings suggest that the administration of GCs and nonsteroidal anti-inflammatory drugs (NSAIDs) is accompanied by a decline in the amount of H. pylori in the gastric mucosal (GM) of SLE and APS patients

Summary

Introduction

Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease characterized by exacerbations and remissions, as well as by diverse clinical manifestations that can range from minor signs, such as fatigue, weight loss, and arthralgia, to life-threatening damage to the kidneys or central nervous system [1,2,3]. There is no clear idea: whether the clinical signs of digestive system damage are a sequel of SLE, or whether they are nonspecific and associated with infection, thrombosis, and medication [7,8,9]. The study of this issue in SLE is of great importance since digestive system damage can affect the course of the disease [10,11,12]. The use of glucocorticoid, low-dose acetylsalicylic acid, nonsteroidal anti-inflammatory drug, and anticoagulant in SLE and APS patients is accompanied by GM damage. More frequent detection of H. pylori was observed in anticoagulants or low-dose acetylsalicylic acid users than in glucocorticoids and nonsteroidal anti-inflammatory drugs ones

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