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1 September 1995 | Volume 123 Issue 5 | Pages 392-393
In his editorial on minocycline treatment of rheumatoid arthritis, Dr. Paulus compares the favorable outcome to the outcome seen with treatment of a smoldering chronic infection [1]. The partial remission induced by minocycline therapy and relapse following its discontinuation suggest that antibiotic responsiveness may actually address a secondary "infection" induced by nonsteroidal anti-inflammatory drugs (NSAIDs) taken by all patients throughout the Monocycline in Rheumatoid Arthritis (MIRA) clinical trial [2]. Long-term NSAID exposure produces intestinal hyperpermeability and inflammation, which cannot be reversed by misoprostol but which is both prevented and reversed by the administration of metronidazole [3]. Therapy with NSAIDs to treat rheumatoid arthritis increases patients' antibody levels to Clostridium perfringens and its
1. Paulus HE. Minocycline treatment of rheumatoid arthritis [Editorial]. Ann Intern Med. 1995; 122:147-8.
2. Tilley BC, Alarcon GS, Heyse SP, Trentham DE, Neuner R, Kaplan DA, et al. Minocycline in rheumatoid arthritis. A 48-week, double-blind, placebo-controlled trial. Ann Intern Med. 1995; 122:81-9.
3. Davies GR, Wilkie ME, Rampton DS. Effects of metronidazole and misoprostol on indomethacin-induced changes in intestinal permeability. Dig Dis Sci. 1993; 38:417-25.
4. Dearlove M, Barr K, Neuman V, Bird HA, Gool HC, Wright V. The effect of non-steroidal anti-inflammatory drugs of faecal flora nd bacterial antibody levels in rheumatoid arthritis. Br J Rheumatol. 1992; 31:443-7.
5. Severijnen AJ, Kool J, Swack AJ, Hazenberg MP. Intestinal flora of patients with rheumatoid arthritis: induction of chronic arthritis in rats by cell wall fragments of Eubacterium aerofaciens strain. Br J Rheumatol. 1990; 29:433-9. About Letters
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
LETTER
Minocycline and Rheumatoid Arthritis Revisited
TO THE EDITOR: 
toxin [4]. Bacterial cell-wall polymers isolated from normal enteric anaerobes can induce chronic arthritis in experimental animals [5]. Therapy with NSAIDs increases intestinal permeability and allows sensitization to components of the indigenous flora of the gut; these actions may not only cause an inflammatory enteritis, reversible by antibiotic agents but may aggravate inflammatory arthritis, a condition also reversible by antibiotic agents. This theory can be readily tested by comparing changes in intestinal lactulose permeability and stool leukocyte counts with changes in clinical variables.
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