Dr.  Teitelbaum's comments: The article below shows antibiotic eradication of H pylori, the infection that causes stomach ulcers, markedly improves rheumatoid arthritis with persistent benefits that last years after even just 1 week of antibiotics.

Excellent article, but it says nothing about H pylori really causing the arthritis, as the antibiotics could have helped by treating dozens of other infections. The key finding is that antibiotics help rheumatoid arthritis, and the effect is likely secondary to killing an infection and NOT a direct anti-inflammatory effect of the antibiotic-as several different antibiotics have now been shown to be effective and the benefits persist even after the antibiotics are stopped. In the repeated studies showing that minocycline (tetracycline) helps rheumatoid arthritis, skeptics attributed this to tetracycline being anti-inflammatory.

Either way though, as we are using very expensive and toxic treatments for rheumatoid arthritis, the question is why most rheumatologists are still not using antibiotics and fish oil along with the other VERY expensive treatments they are constantly being bombarded with? The answer is , simply and sadly, that these treatments are too cheap to warrant advertising them(and paying for FDA approval) to promote them for this use.

P. Zentilin, B. Seriolo, P. Dulbecco, E. Caratto, E. Iiritano, D. Fasciolo, C. Bilardi, C. Mansi, E. Testa, V. Savarino (2002)
Eradication of Helicobacter pylori may reduce disease severity in rheumatoid arthritis Alimentary Pharmacology & Therapeutics 16 (7), 1291-1299.July 2002.
doi:10.1046/j.1365-2036.2002.01284.x

Background: A triggering infectious agent has long been postulated in rheumatoid arthritis. Data on the possible role of Helicobacter pylori infection are lacking.

Aim: To assess the effect of H. pylori eradication in patients with rheumatoid arthritis.

Results: H. pylori-eradicated rheumatoid arthritis patients showed progressive improvement over time (P < 0.0001) of all clinical indices compared with baseline, whereas H. pylori-negative rheumatoid arthritis patients remained substantially unchanged. After 2 years, H. pylori-eradicated rheumatoid arthritis patients differed significantly (P < 0.04-0.0001) from patients without H. pylori infection in terms of improvement of all clinical parameters. At the same time point, several laboratory indices (erythrocyte sedimentation rate, fibrinogen, alpha-2-globulins and antinuclear antibody) showed significantly lower values (P < 0.02-0.0003) in the H. pylori-eradicated subgroup compared to the H. pylori-negative subgroup.

Conclusions: Our data suggest that H. pylori infection is implicated in the pathogenesis of rheumatoid arthritis, in that its eradication may induce a significant improvement of disease activity over 24 months. H. pylori eradication seems to be advantageous in infected rheumatoid arthritis patients, but controlled studies are needed.

The infected subgroup was treated with 1-week eradication therapy consisting of omeprazole, 20 mg 2x day Amoxicillin 1000 mg 2x day and clarithromycin, 250 mg 3x day.