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Tiny Markers May Point to Arthritis Progression

May help doctors find who needs aggressive treatment for rheumatoid form

FRIDAY, Jan. 9, 2004 (HealthDayNews) -- Finding biomedical markers that indicate progressive arthritis is key to determining which patients need aggressive therapy and which ones don't, says a new study.

"We still are very poor at profiling who needs aggressive therapy and who is going to have progressive disease and who is not," says Dr. Eric L. Matteson, a professor of medicine at the Mayo Clinic College of Medicine.

To try to find markers that might indicate progressive arthritis, Matteson's group studied 111 patients who had early-stage rheumatoid arthritis, according to their report in the January issue of Arthritis and Rheumatism.

All the patients were started on hydroxychloroquine, a mild treatment, and progressed to more dramatic treatment with methotrexate or other drugs, depending on how their symptoms improved, Matteson notes.

The researchers took blood tests and X-rays and looked at clinical symptoms to find markers that might indicate the odds for disease progression.

The patients were followed for two years. Matteson's team found 52 percent of the patients had their symptoms controlled by methotrexate and NSAIDs and did not need more aggressive therapy. In addition, 48 percent of the patients did not develop progressive disease.

Matteson says that clinical markers, such as functional status, the number of joints involved, joint pain and swelling were not helpful in determining disease progression.

The things that predicted progression were positive rheumatoid factor -- an antibody found in a blood test -- and some genetic variations, particularly one called HLADRB1*04, he says.

They also found some novel markers that were promising in predicting disease progression. These are high levels of CD4 and CD28 null T-cells, which are indicators of premature aging of the immune system, Matteson notes.

In addition, Matteson's team discovered a different form of a gene of uteroglobin, a protein, appears to protect against joint damage.

"There are a lot of people who have mild disease and do well with mild therapy," Matteson says. "There are some genetic markers that are predictive of progressive disease, and maybe we should think about using these markers in clinical practice for guiding our therapy."

Right now treatment is guided by clinical presentation, Matteson says. But in the future these markers might be used to identify people who will have good and bad treatment outcomes. "If we knew early which patients were going to have more severe disease, we could treat them more aggressively at the outset."

Dr. John Klippel, president and chief executive officer of the Arthritis Foundation, says that "trying to improve our ability to predict the outcome of rheumatoid arthritis is important and the findings of this study are an important step."

Klippel says these findings add to the understanding of the basic mechanisms of arthritis. For example, the findings raise the knowledge of the influence of genetics and the aging of the immune system on arthritis.

"In addition, the understanding of the importance of uteroglobin as a protective pathway in rheumatoid arthritis has the potential for developing therapies," Klippel says.

"These findings will allow rheumatologists to be more accurate in predicting joint damage, and as a consequence it will help in making decisions about appropriate therapy," he says.

More information

To learn more about arthritis, visit the Arthritis Foundation or the National Institute of Arthritis and Musculoskeletal and Skin Diseases.

SOURCES: Eric L. Matteson, M.D., professor, medicine, Mayo Clinic College of Medicine, Rochester, Minn.; John Klippel, M.D., president and chief executive officer, Arthritis Foundation, Atlanta; January 2004 Arthritis and Rheumatism
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