The considerable difficulties in making sense of the literature on patients with lupus involving the central nervous system are re-emphasised in the paper by Rood et al.1 The authors, who to be fair take a sensibly cautious approach to their results, nevertheless seek to persuade us that the IL10 locus is associated with neuropsychiatric lupus on the basis of a historical case notes review of 42 lupus patients with neuropsychiatric disease, compared with 50 who lack such involvement.

Their conclusion needs to be treated with caution. Does it make sense to lump together 42 highly diverse patients and make the kind of claim they have made? The authors suggest that CNS lupus is attributable to either antiphospholipid antibody related thrombotic events, or “immune mediated” disease. This division is artificial. There is a considerable literature on CNS lupus that proposes that a wide variety of immunopathogenic mechanisms may be responsible in individual cases. These mechanisms include thrombotic effects, which may be linked to antiphospholipid antibodies, a true vasculitis, a cross reaction between antibodies that recognise the lymphocyte surface targets and neurological antigens, and antibodies to a wide variety of neurological targets. A considerably larger number of patients will have to be studied before any claims of links to an IL10 promoter haplotype can be truly convincing.

We agree with the authors that patients with SLE have …