Researchers at the University of Toronto reviewed the scientific literature on the treatment of rheumatoid arthritis with the antibiotic minocycline, and found that minocycline is an effective treatment for rheumatoid arthritis. They found that those who benefitted the most from minocycline had the disease for more than one year and had a high rheumatoid factor blood test. There were no increased risks of adverse events. Minocycline had a greater effect on reduction of disease activity than doxycycline.
Should tetracycline treatment be used more extensively for rheumatoid arthritis? Metaanalysis demonstrates clinical benefit with reduction in disease activity. Journal of Rheumatology, 2003, Vol 30, Iss 10, pp 2112-2122. M Stone, PR Fortin, C PachecoTena, RD Inman. Inman RD, Univ Toronto, Toronto Western Hosp, Arthrit Ctr Excellence, Hlth Network, Div Rheumatol, Dept Med, 399 Bathurst St, Toronto, ON M5T 2S8, CANADA
Abstract: The tetracyclines are antimicrobials that also inhibit expression of certain matrix metalloproteinases (MMPs). We conducted a series of experiments to determine if minocycline could inhibit MMP expression and limit human aortic smooth muscle cell (SMC) proliferation and migration. Analysis of SMC proliferation was performed after cells were grown in minocycline-incubated media. SMC migration activity was assayed in a micro-Boyden chamber. Western blotting revealed that minocycline reduced SMC production of MMP-2 in a dose dependent manner. Increasing doses of minocycline progressively reduced SMC proliferation to 49% of control values and limited SMC migration to 15% of control. When administered to rats with balloon injured carotid arteries, intraperitoneal doses of minocycline (70-100 mg/kg) reduced neointima formation by 76%, but were associated with liver toxicity. Higher doses were lethal and lower doses were ineffective. Minocycline, applied to injured arteries in a pluronic gel with a low pH, was also ineffective. In summary, minocycline lowers MMP-2 expression, reduces SMC proliferation and migration, and inhibits neointimal hyperplasia, but its efficacy is limited by systemic toxicity. See reports #J106 and #J159.
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