Table 2.
Anti-KIF20B positivity and OR between patients with and without NPSLE manifestations* within 5 years of follow-up using attribution model B
| Any NPSLE manifestation (n=153) | No NPSLE manifestations (n=642) | OR (95% CI) | |
| Anti-KIF20B+, n (%) | 42 (27.5) | 195 (30.4) | 0.9 (0.6 to 1.3) |
| Any CNS manifestation (n=127) | No CNS manifestations (n=668) | ||
| Anti-KIF20B+, n (%) | 34 (26.8) | 203 (30.4) | 0.9 (0.6 to 1.3) |
| Any PNS manifestation (n=34) | No PNS manifestations (n=761) | ||
| Anti-KIF20B+, n (%) | 11 (32.4) | 226 (29.7) | 1.1 (0.5 to 2.4) |
| Any CN† (n=10) | No CN (n=785) | ||
| Anti-KIF20B+, n (%) | 7 (70.0) | 230 (29.3) | 5.2 (1.4 to 18.5) |
Bold indicates statistically significant results.
*ACR NPSLE manifestations with onset within 10 years of SLE diagnosis and still present within the enrolment window or occurred subsequently; no ‘exclusions’; not one of the NPSLE manifestations with high prevalence in the general population identified by Ainiala et al.23 Only the significant CNS and PNS subtypes are shown.
†Individual CN manifestations were trochlear, abducens, vestibulocochlear, facial, glossopharyngeal, optic and trigeminal.
ACR, American College of Rheumatology; CN, cranial neuropathy; CNS, central nervous system; KIF20B, kinesin family member 20B; NPSLE, neuropsychiatric SLE; PNS, peripheral nervous system.