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. 2015 Jan 8;11(1):e1004005. doi: 10.1371/journal.pcbi.1004005

Table 1. Composition of study cohorts.

Data Set Pendergrass Milano Hinchcliff
SSc Control SSc Control Morphea SSc Control Morphea
All subjects N = 22 N = 9 N = 24 N = 6 N = 3 N = 34 N = 11 N = 1
Age*, mean (SD) 46.1 (9.1) NA 51.8 (10.4) 40.2 (10.6) 50.7 (2.9) 47.7 (11.7) 41.2 (11.8) 47
Sex, n (% women) 17 (77.3) NA 21 (87.5) 5 (83.3) 3 (100.0) 32 (94.1) 7 (63.6) 1 (100.0)
SSc patients only N = 22 N = 24 N = 34
SSc subtype, n (% diffuse) 22 (100.0) 17 (70.8) 31 (91.2)
SSc disease duration*, mean (SD) 18.4 (13.1) mos 7.7 (7.2) yrs 52.7 (67.4) mos
SSc autoantibody, n (% positive)
Scl-70 3 (13.6) 5 (20.8) 9 (26.5)
RNA Pol III 3 (13.6) NA 9 (26.5)
ACA 1 (4.5) 2 (8.3) 2 (5.9)
SSc intrinsic subset, n (%)
Inflammatory 9 (40.9) 5 (20.8) 17 (50.0)
Proliferative 8 (36.4) 11 (45.8) 7 (20.6)
Normal-like 2 (9.1) 4 (16.7) 7 (20.6)
Limited NA 3 (12.5) 2 (5.9)

*At base biopsy.

The three cohorts of patients with SSc analyzed in this study: Milano et al. [1], Pendergrass et al. [11], and an expanded version of Hinchcliff et al. [4].