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2001 National Guideline on the Management of Sexually Acquired Reactive Arthritis

Author(s)BASHH; Clinical Effectiveness Group (Association for Genitourinary Medicine and the
Medical Society for the Study of Venereal Diseases)
AbstractReactive arthritis (ReA) is a sterile inflammation of the synovial membrane, tendons
and fascia triggered by an infection at a distant site, usually gastro-intestinal or genital.
ReA triggered by a sexually transmitted infection (STI) is referred to as sexually
acquired reactive arthritis (SARA). This includes sexually acquired Reiter’s syndrome,
described as the triad of urethritis, arthritis and conjunctivitis, with or without other
cutaneous or mucous membrane lesions such as, keratoderma blennorrhagica, circinate
balanitis/vulvitis, uveitis, oral ulceration, cardiac or neurological involvement.

Most commonly lower genital tract infections, either urethritis or cervicitis, are
associated with SARA with objective features of SARA being present in 0.8-4% of
cases. The place of upper genital tract infection, such as prostatitis and salpingitis, is
unresolved. Previously, it was suggested that infection with the human immune
deficiency virus (HIV) was directly associated with SARA but current evidence
suggests this is not so.

The precise mechanisms linking infective agents with SARA are not clearly understood
so links with specific micro-organisms are partly speculative.
Chlamydia trachomatis, the commonest identifiable cause of non-gonococcal
urethritis (NGU), has been the micro-organism most strongly linked to SARA being
identified in 35-69% of cases, using non-nucleic acid amplification techniques.
Neisseria gonorrhoeae has been linked with up to 16% of cases, as distinct from its
role in septic, gonococcal arthritis. The precise role of this micro-organism in
relation to SARA remains unknown.
Ureaplasma urealyticum has been linked with a few cases and may be a cause of
SARA in a minority.
A causal role for other genital tract pathogens and commensals is possible but there
is currently insufficient evidence for evaluation.
Date of publishing08/01/2001
Date of last review by us08/15/2007
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