Ms. P, Hispanic and now 39 years old, first presented with nonspecific arthritis diagnosed at age 20. She also noted a chronic, watery nasal secretion, which she attributed to a facial injury suffered when she was 7. Her medical history included onychomycosis, gastritis (with positive test for Helicobacter pylori), migraine, and anxiety. Treatment resolved the first two conditions; she still occasionally needs therapy for migraine and anxiety.


Ms. P’s arthritis was characterized by joint pains in her hands and years of stiffness. Her metacarpophalangeal joints were symmetrically tender to palpation and exhibited very mild inflammation. An arthritis profile was positive for rheumatoid arthritis (RA).

I started valdecoxib (Bextra), then oral methotrexate. Later, fluid retention prompted a switch from valdecoxib to celecoxib (Celebrex). And because of an incomplete response, oral methotrexate was replaced with an injectable form. She was unable to tolerate chloroquine. This regimen controlled her arthritis symptoms until she was able to discontinue it completely.

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I began my evaluation of Ms. P’s nasal secretion by ordering radioallergosorbent testing (RAST) for respiratory allergens. The results indicated allergies to pollens, grass, and weeds. I started Ms. P on oral antihistaminics, decongestants, azelastine (ophthalmic and nasal formulations), steroids, ipratropium, and saline irrigation. Later, I added immunotherapy for two years, but this proved unsuccessful and was discontinued. In 2003, ImmunoCAP testing confirmed the allergies to pollens, grass, and weeds and detected allergies to corn, garlic, orange, peanuts, potato, rice, soybean, tomato, and wheat. There were no indications of allergy to dairy products.


Ms. P began avoiding foods to which she was allergic, as well as dairy products and meat. The diet alleviated her nasal secretion (she still takes nasal azelastine) and completely resolved her RA. This finding is supported by the fact that the opposite is also true—she can trigger an attack of arthritis in her hands by eating the suspect foods.

Three years after detection of her food allergies, she continues on a diet based mainly on fruits and vegetables, cereals, and little meat. She also takes vitamins and other natural supplements, such as flax seeds. This diet is the only treatment she uses for her RA. She is able to work cleaning houses without restrictions and has not developed any joint deformity or other extra-articular manifestations or complications. Retesting with both RAST and ImmunoCAP in 2005 found respiratory but no food allergies.


RA was initially considered a single disease, but there is controversy over whether it is a syndrome with multiple etiologies. Allergy has not been reported as a risk factor for RA.

The various factors described as having a role in the development of RA include (1) immune and inflammatory responses to infection (bacterial or viral); (2) genetics; (3) autoimmunity mediated by humoral and cellular mechanisms that affect the components of synovium and cartilage; (4) cytokines that induce inflammation and tissue destruction; and (5) autonomous tissue-invading cells generated by transformation of cellular constitutents of the synovial lining.1-8 RA is a “young disease,” i.e., it was not described until fairly recently, suggesting that a new environmental factor may play an important role in RA pathogenesis. The disease affects 0.5%-1% of people worldwide, an indication that genetics is not a major factor.


Using allergen avoidance and nasal azelastine as her only medical treatment, Ms. P has achieved almost complete clinical control of her allergies. Tests for immunoglobulin E antibodies remain positive only in the respiratory profile and negative for food allergens. Her RA is in remission clinically, and a plain x-ray was negative.

Is this patient in spontaneous remission? Or could it be that the antibodies formed against the food allergens were attacking a component in Ms. P’s joints? It’s food for thought and fodder for additional research.

Dr. Martinez is an internist and geriatrician in Yakima, Wash.


1. Albert LJ. Infection and rheumatoid arthritis: guilt by association? J Rheumatol. 2000;27:564-566.

2. Takeda T, Mizugaki Y, Masubara L, et al. Lytic Epstein-Barr virus infection in the synovial tissue of patients with rheumatoid arthritis. Arthritis Rheum. 2000;43:1218-1225.

3. Zhang Z, Wu X, Limbaugh BH, Bridges SL Jr. Expression of recombination-activating genes and terminal deoxynucleotidyl transferase and secondary rearrangement of immunoglobulin kappa light chains in rheumatoid arthritis synovial tissue. Arthritis Rheum. 2001;44:2275-2284.

4. Dong H, Strome SE, Matteson EL, et al. Costimulating aberrant T cell responses by B7-H1 autoantibodies in rheumatoid arthritis. J Clin Invest. 2003;111:363-370.

5. Tan SM, Xu D, Roschke V, et al. Local production of B lymphocyte stimulator protein and APRIL in arthritic joints of patients with inflammatory arthritis. Arthritis Rheum. 2003;48:982-992.

6. Ji H, Ohmura K, Mahmood U, et al. Arthritis critically dependent on innate immune system players. Immunity. 2002;16:157-168.

7. Meyer JM, Han J, Moxley G. Tumor necrosis factor markers show sex-influenced association with rheumatoid arthritis. Arthritis Rheum. 2001;44: 286-295.

8. Orozco-Alcala JJ, Medina GB. Artritis Reumatoide. Mexico City, Mex.: Nieto Editores, SA de CV; 2002.