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Psoriatic Arthritics Have Increased Antibodies To Gliadin, Coeliac Disease

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Psoriatic Arthritics Have Increased Antibodies To Gliadin, Coeliac Disease

A DGReview of : " IgA antibodies to gliadin and coeliac disease in psoriatic

arthritis "

Rheumatology Online

01/22/2002

By Anne MacLennan

Patients with psoriatic arthritis have an increased prevalence of serum

antibodies to gliadin and of coeliac disease.

Moreover, patients with raised IgA to gliadin (AGA) appear to have more

pronounced inflammation than those with a low IgA AGA concentration. These are

the conclusions of a study of IgA antibodies to gliadin and coeliac disease in

psoriatic arthritis (PsoA).

Study participants were 114 PsoA patients with skin disease of 20-year (±13)

duration and joint disease of 11-year (±10) duration.

All subjects completed a medical history questionnaire and underwent clinical

examination, including radiology.

Researchers determined the patients' serum IgA AGA and IgG AGA, IgA antibodies

to endomysium and immunoglobulins, erythrocyte sedimentation rate (ESR) and

C-reactive protein (CRP) concentration.

Of the 114 patients, five (4.4 percent) had coeliac disease.

After the researchers excluded these five patients, the mean IgA AGA

concentration was significantly higher than that in a reference group.

None of the patients had IgA antibodies to endomysium.

Mean serum IgA concentration was significantly increased and IgM decreased.

Patients with a high concentration of IgA AGA had significantly higher ESR and

CRP and a longer duration of morning stiffness than those with a low AGA

concentration.

Thus, PsoA patients have an increased prevalence of raised serum IgA AGA and of

coeliac disease, and a raised versus a low IgA AGA concentration appears to be

linked with more pronounced inflammation, these researchers conclude.

This work was done by U. Lindqvist and colleagues from Medicine, Dermatology and

Venereology and Clinical Immunology, Department of Medical Sciences, University

Hospital, Uppsala, Sweden.

Rheumatology 2002; 41: 31-37

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