Posted by: Indonesian Children | May 11, 2010

Rheumatoid Arthritis, Food Allergy and Adverse Food Reaction

Rheumatoid Arthritis, Food Allergy and Adverse Food Reaction

Widodo Judarwanto
Children Allergy Center – Bunda Jakarta Hospital, Indonesia
 
Patients with rheumatoid arthritis (RA) often feel that there is an association between food intake and their disease activity, but evidence to support such a connection has been contradictory. Reports are usually based on diet experiments with quite different protocols, followed by some sort of food challenge.
The hypothetically negative influence of food on the clinical activity of seropositive rheumatoid arthritis was studied using two types of artificial elementary food. One diet was allergen free, the other allergen restricted, containing only lactoproteins and yellow dyes. Ninety four patients entered the study, which lasted 12 weeks. During the second four week period they were randomly assigned to one of the two artificial foods. Comparison between baseline and subsequent periods showed only subjective improvements. No differences were seen between the clinical effects of the two tested diets. Nine patients (three in the allergen restricted group, six in the allergen free group) showed favourable responses, followed by marked disease exacerbation during rechallenge. Dietary manipulation also brought about changes in objective disease activity parameters in these patients. The existence of a subgroup of patients in whom food intolerance influences the activity of rheumatoid factor seropositive rheumatoid arthritis deserves serious consideration.
Food allergy is a complex immune mechanism that occurs in many parts of the body with diverse results . It is extremely important to identify people who have food allergy because of the association of allergy with chronic disorders. The diagnosis of food allergy is based upon a careful history, physical examination, specific tests for immunoglobulin E (IgE), such as the skin prick test (SPT), the radioallergosorbent test and oral food challenges . Food allergies can be determined with the SPT, which is an easy and cheap method. However, a food elimination/challenge trial is a good and reliable way to confirm a food allergy suggested by the SPT . Food allergy was recorded in 1953 as a causative factor in some cases of arthritis . Recent studies have reported that many of the signs and symptoms of rheumatoid arthritis (RA) may be linked to food allergies . In many studies, several allergen-free or hypoallergenic dietary manipulations have been shown to ameliorate clinical manifestations of RA , but the mechanisms by which this occurs are unknown.

On the other hand, recent research has uncovered the important role of cytokines which promote inflammation, such as tumour necrosis factor-{alpha} (TNF-{alpha}) and interleukin-1ß (IL-1ß). Also, TNF-{alpha} and IL-1 are considered to be the key cytokines in the development of RA . Evidence supports the correlation of levels of disease activity in RA and the progression of joint damage with levels of TNF-{alpha} and IL-1. In RA, TNF-{alpha} appears to be primarily responsible for driving inflammation, while IL-1 plays a critical role in destruction of cartilage and bone. IL-1 exists in two forms, IL-1{alpha} and IL-1ß, which are transcribed from closely related but distinct genes. IL-1{alpha} is primarily bound to the cell membrane while IL-1ß is the predominant extracellular form of IL-1.

In reviewing the literature, it becomes clear that there are few studies investigating the mechanisms of the relationship between diet and TNF-{alpha} and IL-1ß. It was reported that fish oil can suppress proinflammatory cytokine production in RA patients . Several studies have shown that n-3 fatty acid supplementation can reduce the production of IL-1 and TNF-{alpha}, and results in an important reduction in morning stiffness duration and tender joint count in patients with RA .

However, the relationship between food allergy and proinflammatory cytokines in RA is still unknown. Therefore, we investigated the effect of individualized diet challenges consisting of allergenic foods on TNF-{alpha} and IL-1ß levels in patients with RA.

Food hypersensitivity in RA does not reflect IgE mediated allergy, and most studies have concluded that food is unlikely to have a pathogenic effect in RA. Thus, Panush carried out blinded encapsulated challenges, and no more than 5% of the RA patients were deemed to show immunological food sensitivity. Nevertheless, a recent large European epidemiological study, determining odds ratios (ORs) after adjusting for possible confounding variables, suggested that there is a significant association between inflammatory polyarthritis and a high intake of red meat (OR = 1.9), meat and meat products combined (OR = 2.3), and total proteins (OR = 2.9).
Few previous reports have considered that a pathogenic dietary effect on RA could depend on a persistent intake of food; a brief test challenge with a relatively small dose might not precipitate clinical symptoms. Studies considering the quantitative variable have in fact tended to suggest that food does have pathogenic importance, at least in a significant fraction (20–40%) of the patients.
Attempts to identify food sensitive RA patients by measuring food specific antibodies or immune complexes in serum have failed. Our previous investigation likewise concluded that serum antibody measurements seldom predict or confirm food hypersensitivity in RA patients. Although increased IgM activities were found, there was no convincing association with clinical variables or dietetic benefits. Raised serum IgA activity to gliadin has been reported in RA patients, but the levels were low compared with IgG and IgM directed against the same antigen in patients as well as controls.Raised IgG activity to gliadin was found in 47% of 93 RA patients, and 41% concurrently had IgA rheumatoid factor (RF) and there was some association with duodenal villous atrophy.However, a subsequent study was contradictory.
Overall, serum antibodies do not appear to provide an immunological link between diet and RA. The reason might be that activation of the intestinal immune system is not reliably reflected in the serum, and the fact that circulating IgA RF is predominantly polymeric supports a mucosal origin.Moreover, RA patients may have occult small intestinal inflammation and increased mucosal permeability independent of the use of non‐steroidal anti‐inflammatory drugs (NSAIDs).

 

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