Association of inflammation with raised serum IgA in ankylosing spondylitis

Table of Contents

Patients and methods

Results

Discussion

References

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Paper 9

Annals of the Rheumatic Diseases, 1980, 39, 545-549

P. COWLING,1 R. EBRINGER,2 AND A. EBRINGER1

From the * Immunology Unit, Department of Biochemistry, Queen Elizabeth College, London W8, and the 2Department of Rheumatology, Middlesex Hospital, Arthur Stanley House, Tottenham Street, London W1P 9PG

SUMMARY
Serum immunoglobulins were measured in 122 patients with ankylosing spondylitis (AS) during various phases of disease activity and compared to those in 58 healthy subjects. The mean serum IgA was 38 % higher in patients (306 -9 mg.'dl) than in controls (222 · 7 mg/dl) (P<0 -005), but there was no significant difference in IgG and IgM levels. Increased IgA was associated with laboratory parameters of active inflammatory disease. The mean IgA in patients having an ery-throcyte sedimentation rate (ESR) equal to or greater than 15 mm/h was 369 mg/dl, 65% higher than in controls (P<0-001), whereas there was no significant difference between controls and patients with an ESR of less than 15 mm/h. The mean IgA in patients having a C-reactive protein (CRP) level equal to or greater than 15 ug'ml (15 mg/1) was 387-8 mg.'dl, 74% higher than in controls (P<0-001), and again there was no significant difference between controls and patients with CRP levels less than 15 ug/ml. (SI conversion: g'l=mg'dl X 0 -01). It is suggested that selective increase of serum IgA occurs predominantly during phases of active inflammatory disease in AS, and this finding is compatible with the concept of a microbial triggering agent acting across an IgA secreting organ such as the gut.

There is evidence that gastrointestinal infection may be an important aetiological factor in ankylosing spondylitis (AS). Sacroiliitis and AS are common sequelae in persons who develop arthritis or Reiter's disease after dysenteric infection with salmonella, shigella, or Yersinia enterocolitica.1 We have reported an increased isolation of Klebsiella pneumoniae from the faeces of AS patients before and during active phases of the disease2 or during episodes of acute anterior uveitis.3 Investigation by lymphangio-graphy has shown that pelvic and paraspinal lymphadenopathy precedes the radiological changes in AS4. Raised levels of serum IgA in patients with AS have been reported5"8. Plasma cells in the gut associated lymphoid tissue are the major source of serum IgA,9 and investigations in animals raised in germ-free conditions have shown that after oral immunisation the main specific plasma cell response is IgA in character and nearly all the circulating specific antibody is IgA.10

We report here our studies on serum immuno-globulin levels in AS.

Accepted for publication 4 December 1979 Correspondence to Dr R. Ebringer.