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. Author manuscript; available in PMC: 2017 Dec 7.
Published in final edited form as: Lancet. 2017 Mar 2;389(10080):1710–1718. doi: 10.1016/S0140-6736(17)30317-3

Table 3.

Competing-risk model including extracellular matrix gene signature

Stricturing behaviour (B2) Penetrating behaviour (B3)


HR (95% CI) p value HR (95% CI) p value
Age at diagnosis 1·07 (0·91–1·27) 0·42 1·45 (0·98–2·14) 0·0606

African American race 0·30 (0·04–2·47) 0·27 2·31 (0·4–13·27) 0·35

Isolated ileal location (L1) 1·09 (0·39–2·99) 0·87 1·36 (0·37–4·93) 0·64

ASCA IgA positive 1·48 (0·58–3·75) 0·41 2·92 (0·81–10·48) 0·10

CBir1 positive 2·14 (0·84–5·44) 0·11 7·99 (1·89–33·77) 0·0047

Extracellular matrix gene signature 1·70 (1·12–2·57) 0·0120 1·21 (0·53–2·73) 0·65

This table includes data for a sub-cohort of 243 patients for whom ileal gene expression data were available. When the extracellular matrix gene signature was excluded, AUROC was 0·66, sensitivity 69%, specificity 66%, positive predictive value 22%, negative predictive value 94%, and prevalence of complications 11·9% (7·4% for B2 and 4·5% for B3). With the addition of the extracellular matrix gene signature, AUROC was 0·72, sensitivity 69%, specificity 71%, positive predictive value 24%, and negative predictive value 94%. The discriminant power was computed via leave-one-out cross-validation.

HR=hazard ratio. ASCA=anti-Saccharomyces cerevisiae antibodies. AUROC=area under the receiver operator characteristic curve.