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The researchers found people who were osteoarthritis-free for two years and then were diagnosed with asthma or eczema, then followed them up. For a control group, they followed patients who were also two years old without osteoarthritis but had no subsequent diagnosis of asthma or eczema. The researchers then matched each diagnosed person to someone in the control group with similar demographic characteristics, frequency of outpatient visits, presence of other diseases, and several additional factors, to see who developed osteoarthritis. In the primary cohort, each group had approximately 110,000 patients.
Paving the way to successful treatment
The authors found that if a patient had asthma or eczema, there was a 58% increased risk of developing osteoarthritis over about 10 years. If they had both asthma and eczema, the risk increased to 115%.
To see the effect of another lung disease, which is not mediated by allergens, the researchers compared chronic obstructive pulmonary disease – in which airflow from the lungs is constricted – with asthma. They found that asthma patients had an 83% increased risk of developing osteoarthritis compared to COPD patients. They concluded that lung disease without an allergic reaction does not predispose to osteoarthritis, again suggesting that activation of allergic pathways is the critical factor.
Claims data from the primary analysis did not include body mass index, a risk factor for osteoarthritis, so the researchers validated their findings in an independent dataset using the Stanford Research Repository. The results were similar, showing that allergic diseases increase the risk of developing osteoarthritis, even after taking into account the key variable of body mass index.
According to Baker, existing drugs for asthma attacks and for mast cell activation syndrome — a condition in which a patient experiences repeated bouts of anaphylaxis symptoms — could be candidates for the treatment of osteoarthritis. These drugs inhibit mast cells and allergic cytokines (by-products of mast cells that cause inflammation).
“We now have a strong basis to study this as an intervention, to see if targeting pathways such as inhibiting mast cells or allergic cytokines can actually reduce the development and/or progression of osteoarthritis,” Baker said.
Researchers from Chinook Therapeutics in Seattle, Boston University School of Medicine and the VA Palo Alto Health Care System contributed to the work.
The study was funded by the National Institutes of Health (grants R25 AI 147369 and P30 072571), the Department of Veterans Affairs, the Department of Defense, and the Stanford Center for Clinical and Translational Research and Education.
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