Vanessa Kronzer, MD, on Asthma and Rheumatoid Arthritis

It has been thought that rheumatoid arthritis (RA) originates at mucosal surfaces, particularly in the airway mucosa. To determine whether this hypothesis is correct, researchers led by Vanessa Kronzer, MD, who is a resident in the Department of Employee and Community Health at the Mayo Clinic, studied exposure data from 1023 patients with RA from a single-center biobank.

Results of the case-control study1 showed that while asthma and allergies may be associated with an increased risk for RA, passive smoke exposure and earlier age of starting smoking did not influence risk.

Consultant360 caught up with Dr Kronzer about her study and its findings.

CONSULTANT360: What prompted you to conduct your study?

Vanessa Kronzer: I am interested in understanding where autoimmune disease comes from. RA is an important disease to study, since it is one of the most common rheumatologic autoimmune diseases. In particular, we think that RA originates in the lungs. 

Mayo Clinic has a great resource called the biobank available, which nobody had ever used to study RA, despite the fact that there are approximately 1000 patients with RA in it. The questionnaire used for this biobank has very detailed questions about some respiratory-related conditions such as smoking history, and comorbidities such as asthma. It also has important control variables like educational history and allergy status. Allergy was originally included to control for the association between RA and asthma, and we discovered it was a profound predictor of RA itself.

CON360: Were you surprised by the findings?

VK: We were surprised about the association with RA and asthma since the classic thinking was that RA and allergy occupy distinct and separate immunological pathways. In particular, the strong association with food allergy we found is also intriguing and does fit with clinical experience that some of our rheumatologists have had. The findings also showed that asthma was associated with RA in the full cohort but not an incident cohort. One reason is that the incident cohort is smaller, so it had less power to find statistically significant findings even though it trended the same way. Another possibility is that people who develop RA earlier and later are different in some way. For example, perhaps the people who develop RA earlier in life have more immunologic dysfunction, which also predisposes them to allergies.

CON360: What do you think is the connection between food allergies and RA?

VK: People with autoimmune diseases, including RA, have altered immune systems that predispose them to immunological diseases of all kinds, including allergies. Digging through the literature on food allergy in particular, I was intrigued to find that this association was a “hot topic” even in the 1960s. In fact, some rheumatologists at that time believed RA might have resulted from food allergies and recommended their patients avoid certain food allergens. This concept of foods triggering or exacerbating autoimmune diseases seems to have resurfaced again lately. It is certainly possible that exposure to certain foods, especially allergenic ones, could predispose to autoimmune conditions like RA.

CON360: How can a rheumatologist apply these findings to clinical practice?

VK: These findings suggest that we should have a heightened clinical suspicion of RA, or potentially even other autoimmune diseases, in anyone who has evidence of other immune dysfunction such as asthma or allergy.

CON360: What are the next steps of your research?

VK: I plan to explore these associations in another cohort with some colleagues in Sweden and am also looking into studying the association between RA and allergy with some immunology colleagues here on a cellular level. And of course, I will also be looking into other interesting associations that the biobank data holds because it is an amazing resource.


For more on the study, click here.

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