title: Serum amyloid A in the assessment of early inflammatory arthritis.
abstract: OBJECTIVE
  Acute phase serum amyloid A (A-SAA) has been reported to be more sensitive than C-reactive protein (CRP) as a marker of disease activity. It may function in immune regulation and is linked to the development of secondary amyloidosis. We investigated the profile of A-SAA in early inflammatory arthritis and compared A-SAA with CRP and erythrocyte sedimentation rate (ESR) in relation to diagnosis and disease activity.
  
  
  METHODS
  Using a sensitive and specific ELISA, A-SAA was measured in the serum of 140 patients with early arthritis (disease duration 2 weeks to 24 mo, mean 6 mo). CRP was determined using a standard ELISA; ESR and clinical disease activity variables were also recorded.
  
  
  RESULTS
  Sixty-four patients had rheumatoid arthritis (RA), 19 psoriatic arthritis (PsA), 28 undifferentiated arthritis (UA), and 29 other forms of arthritis. A-SAA levels correlated with both CRP (r = 0.73, p = 0.0001) and ESR (r = 0.6, p = 0.0001). The magnitude of the A-SAA response was greater than either the CRP or ESR, and very high A-SAA levels were observed in disease as early as 2 weeks. Highest A-SAA concentrations occurred in RA (median 70.3 mg/l, maximum 1542) compared with the other groups (medians, PsA: 33 mg/l; UA: 12.3 mg/l; other arthritis: 11.2 mg/l), with values > 520 mg/l observed exclusively in RA. A-SAA, unlike CRP or ESR, could distinguish patients with a final diagnosis of RA from those who had persistent UA. In RA, A-SAA provided the strongest correlations with clinical measurements of disease activity. Clinical improvement was also best represented by A-SAA, while disease deterioration was associated with a significant increase in A-SAA values, but not CRP or ESR.
  
  
  CONCLUSIONS
  Compared with ESR or CRP, A-SAA correlates best with markers of disease activity, and in patients with recent onset arthritis, very high levels of SAA occur exclusively in RA. As A-SAA is sensitive to change and accurately reflects alterations in disease status, it is the best marker available for the assessment of inflammatory joint disease.
authors.affiliation: Department of Rheumatology, St. Vincent's University Hospital, Dublin, Ireland.
authors.forename: G
authors.initials: G
authors.lastname: Cunnane
authors.forename: S
authors.initials: S
authors.lastname: Grehan
authors.forename: S
authors.initials: S
authors.lastname: Geoghegan
authors.forename: C
authors.initials: C
authors.lastname: McCormack
authors.forename: D
authors.initials: D
authors.lastname: Shields
authors.forename: A S
authors.initials: AS
authors.lastname: Whitehead
authors.forename: B
authors.initials: B
authors.lastname: Bresnihan
authors.forename: O
authors.initials: O
authors.lastname: Fitzgerald
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001168:Arthritis / Q000097:blood* / Q000175:diagnosis*; D001799:Blood Sedimentation; D002097:C-Reactive Protein / Q000032:analysis*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D000685:Serum Amyloid A Protein / Q000032:analysis*; D012720:Severity of Illness Index; D013997:Time Factors
chemical_list: D000685:Serum Amyloid A Protein; D002097:C-Reactive Protein