Clinical challenges abound in cutaneous lupus erythematosus (CLE). Diagnosis of CLE is not straightforward because of its varied presentations and mimicry of other skin diseases. Up to half of CLE patients are recalcitrant to first-line treatments such as antimalarials. CLE patients who do not have SLE can later progress to SLE, but it is not evident which ones are at higher risk. Identification of key biomarkers in CLE can help address these conundrums. For instance, the anti-SS-A antibody has been associated with subacute CLE patients, which was first observed by Drs. James Gilliam and Richard Sontheimer in our institution. Type I interferon- inducible proteins such as MxA and guanylate binding protein-1 and the chemokines CXCL9 and CXCL10 have been proposed as biomarkers that may support diagnosis and track disease activity. Recently, biomarker candidates have emerged that may assist in determining treatment response to oral antimalarials. For example, an increased myeloid dendritic cell population with higher TNF-α expression may be predictive of poor treatment response to hydroxychloroquine in CLE patients. Finally, biomarkers can carry key prognostic information for CLE patients.

Autoantibodies against nuclear antigens (e.g. anti-double-stranded DNA and anti-Smith antibodies) and elevated erythrocyte sedimentation rate and low complement have been more often identified in CLE patients who develop SLE. Further studies are needed to confirm roles of these various candidate biomarkers and their involvement in CLE pathogenesis.