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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: J Rheumatol. 2015 Dec 15;43(2):273–281. doi: 10.3899/jrheum.150179

Table 1.

Features of patients from both RA cohorts

Dartmouth Established RA Cohort Lebanon, NH, USA Sherbrooke Early RA Cohort Sherbrooke, QC, Canada
Seronegative Seropositive Seronegative Seropositive
Patients, % of cohort (n) 21% (45) 79% (167) 49% (165) 51% (171)
Age, mean ± SD years (range) 57 ± 12 (29-74) 58 ± 11 (19-91) 62 ± 16 (19-89) 57 ± 13 (19-89)
Women, % (n) 67% (30) 71% (119) 64% (106) 60% (103)
Years of symptoms, mean ± SD (unavailable for much of Dartmouth cohort) 9% with <1 year from disease onset 14% with <1 year from disease onset 0.44 ± 0.43 0.45 ± 0.33
Range of disease duration From new onset to >20 years From new onset to >20 years 0-12 months from disease onset 0-12 months from disease onset
Anti-CarP level, mean ± SD 15.5 ± 54.1 70.2 ± 184.1 5.8 ± 12.6 34.9 ± 88.0
DAS28-CRP, mean ± SD Unavailable Unavailable 5.1 ± 1.5 5.0 ± 1.4
CRP mg/L, mean ± SD Unavailable Unavailable 24.4 ± 33.9 26.5 ± 35.7
Anti-CCP units/ml, mean ± SD N/A 419 ±337 N/A 200 ± 136
IgM RF IU/ml, mean ± SD N/A 135 ± 76 N/A 170 ± 79
Anti-Sa status, % positive (n) N/A 57% (90/158) 2% (3/134) 51% (72/142)
Total IgG mg/ml, mean ± SD 16 ± 11.6 17.6 ± 10.0 9.2 ± 2.5 21.1 ± 7.6
CXCL13 pg/ml, mean ± SD 116 ±76 1938 ± 6154 313 ± 1460 1490 ± 2460
CXCL10 pg/ml, mean ± SD 164 ± 207 392 ± 1121 118 ± 308 168 ± 307
Shared epitope % positive (n) 46% (6/13) 83% (89/107) 26% (33/128) 50% (70/141)
RA treatment Wide range from none to biologic therapy Wide range from none to biologic therapy Predominantly DMARD and corticosteroid naive Predominantly DMARD and corticosteroid naive

In the Dartmouth seronegative patients, only 28 of 45 patients had measured values for total IgG, CXCL13, and CXCL10. When percentages are given but not all patients in that group were tested (i.e. Shared epitope), the “n” is displayed as a fraction representing number of positive over number of those tested. Classification by serostatus and Anti-Sa reactivity was determined using different methods for the two cohorts (see Materials and Methods section).