Association of gut inflammation with increased serum IgA class Klebsiella antibody concentrations in patients with axial ankylosing spondylitis (AS): implication for different aetiopathogenetic mechanisms for axial and peripheral AS?

doi:10.1136/ard.56.3.180

Annals of the Rheumatic Diseases 1997;56:180-183; doi:10.1136/ard.56.3.180

Ann Rheum Dis 1997;56:180-183 ( March )

Concise reports

Association of gut inflammation with increased serum IgA class Klebsiella antibody concentrations in patients with axial ankylosing spondylitis (AS): implication for different aetiopathogenetic mechanisms for axial and peripheral AS? Outi Mäki-Ikola,^a Marjatta Leirisalo-Repo,^b Ulla Turunen,^b Kaisa Granfors^a

^a National Public Health Institute, Department in Turku, Turku, Finland , ^b Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland

Correspondence to: Dr O Mäki-Ikola, National Public Health Institute, Department in Turku, Kiinamyllynkatu 13, FIN-20520 Turku, Finland.

Accepted for publication 9 December 1996

OBJECTIVES $---$ A role for Klebsiella pneumoniae in ankylosing spondylitis (AS) has been suggested because faecal carriage of Klebsiella andserum Klebsiella specific antibodies may be increased in thisdisease. This study has extended the earlier findings by comparingKlebsiella specific serum IgA class antibodies with inflammatorychanges in thegut.
METHODS $---$ IgA antibodies to K pneumoniae, Escherichia coli, and Proteus mirabilis in serum samples of 25 patients with AS, of eightcontrol patients, and of 100 healthy blood donors were measuredby enzyme immunoassay. Gut inflammation of the patients was studiedbyileocolonoscopy.
RESULTS $---$ Increased IgA antibody concentrations to K pneumoniae associated with gut inflammation in patients with axial form of AS.Such association was not seen in patients with peripheral formofAS.
CONCLUSIONS $---$ These findings may provide further evidence for the role of K pneumoniae in the pathogenesis of AS. However, at least someof the patients with axial AS without gut inflammation, as wellas patients with peripheral AS did not have increased K pneumoniaeantibody concentrations, which may be regarded as evidence againstthe direct role of K pneumoniae in the pathogenesis. The aetiopathogeneticmechanisms in the axial and peripheral form of AS may bedifferent.

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