International research has been conducted to determine whether the causative organism of some gastrointestinal disease symptoms (such as, indigestion, nausea, vomiting, stomach and/or duodenal ulcers, gastric relux, gastritis, stomach cancer), called Helicobacter pylori (HP), may be implicated as an infectious cause of rheumatoid arthritis (RA) and its progression. HP is gram-negative, helical-shaped organism, a spirochete of the genus Campylobacter. Although 50% of the world’s population harbors this transmissible infection in the gastrointestinal tract, some researchers contend that it may trigger and perpetuate RA (and other rheumatic diseases) via antigenic stimulation of the inflammatory cascade. As some of the studies below demonstrate, successful HP-eradication therapy may lead to improved outcomes in RA patients.
For further information on HP infection and appropriate treatment protocols, please visit The Helicobacter Foundation, which was founded by the Australian researcher, Professor Barry J. Marshall, discoverer of this infection as a major cause of stomach ulcers.
Implications for induction of autoimmunity via activation of B-1 cells by Helicobacter pylori urease. Infect Immun. 2006 Jan;74(1):248-56.
Japanese researchers studied how the causative organism of stomach ulcers, Helicobacter pylori (HP), induces autoimmune reactions, such as rheumatoid arthritis (RA) or idiopathic thrombocytopenic purpura (ITP). Their findings suggest that B-1-cells, found in the pleural cavity or mucosal compartment, are stimulated by H. P. urease-specific immunoglobulin A (IgA), leading to innate immune system responses. Additionally, that auto-reactive antibodies (IgM rheumatoid factor, anti-single-stranded DNA, and anti-phosphatidyl choline antibody) were produced when splenic B-cells were stimulated with the HP enzyme, urease, in-vitro. These researchers conclude that HP urease-activation of B-1-cells and the subsequent production of auto-reactive antibodies, indicates that this infection may be a trigger of autoimmunity, providing new insights into autoimmune pathogenesis.
Case study of a 62-year old Japanese woman with rheumatoid arthritis (RA) who, after receiving successful treatment for Helicobacter pylori (HP) infection, was found to have significant worsening of RA signs and symptoms. These authors conclude that RA patients may experience disease worsening with HP eradication treatment and surmise that it may be due to, “…disruption of the established oral tolerance against stress protein such as mycobacterial heat shock protein 65.”
[Seroprevalence of Helicobacter pylori in rheumatoid arthritis and its relationship to pharmacotherapy]. Vnitr Lek. 2004 Dec;50(12):911-6.
A study was conducted in the Slovak Republic of 137 hospitalized rheumatoid arthritis (RA) patients to determine the seroprevalence of Helicobacter pylori (HP) infection and if there was any relationship to the modes of treatment used to control the disease symptoms of these patients. Of all the RA patients tested for HP by ELISA, 57% were positive by IgG, 60% by IgA, and 51% were both IgG- and IGA-positive. In patients who were both HP IgG- and IGA-positive, a greater frequency of extra-articular signs were found. Also, RA patients who used anticoagulation drugs had a higher frequency of HP IgG antibodies, whereas those being treated with methotrexate had an increased rate of HP IgA antibodies.
Nonsteroidal anti-inflammatory drug-associated upper gastrointestinal lesions in rheumatoid arthritis patients. Relationships to gastric histology, Helicobacter pylori infection, and other risk factors for peptic ulcer. Scand J Gastroenterol. 1998 Aug;33(8):811-6.
It is generally accepted that non-steroidal anti-inflammatory drugs (NSAIDs) may increase the risk for upper gastrointestinal lesions (peptic ulcers) in rheumatoid arthritis (RA) patients who consistently use this class of drugs for pain relief. In this study, Finish researchers set out to determine if there was any increased risk in NSAID-using RA patients with concomitant Helicobacter pylori (HP) infection. The findings were that both patients groups, with or without this infection, were at greatly increased risk of ulcers with NSAID use and that corticosteroids also increased this risk.
RBF Commentary: It is of note that many RA patients commonly use NSAIDs to control inflammatory symptoms and that stomach ulcers and gastritis may be solely attributed to their chronic use. In these cases, infection with HP may be overlooked or underestimated, thereby missing an opportunity for appropriate diagnosis and eradication therapy to ease RA symptoms and progression.