• autoantibodies
• systemic lupus erythematosus
• polymyositis

We thank the authors1 for their interest in our paper2 and are grateful for the opportunity to respond to the points raised. We agree with the opinion of Mahler et al that ‘SLE frequently express many autoantibodies and sera accompanied by mixed HEp-2 IIF pattern were very common’. We adopted the same methods for anti-Ku screening that Spielmann et al 3 used in their study to avoid missing multiple autoantibody-positive cases. The Spielmann group included ANA-positive sera showing several ANA patterns (ICAP nomenclature: AC-1, AC-4 or AC-5) for ELISA analysis.

Although Mahler et al noted that ‘In our experience, anti-Ku antibodies are frequently found in SLE patients potentially associated with overlap features of a myopathy’, of the four anti-Ku antibody-positive myositis patients in their referenced study, only two patients had systemic lupus erythematosus (SLE) overlapping with myositis.3 Given that 33 anti-Ku-positive SLE patients in their study4 did not have myositis, it seems that SLE and myositis are less likely to overlap. We need to be careful in discussing the frequency of anti-Ku-associated clinical phenotypes.

We detected anti-dsDNA and anti-ssDNA antibodies by using two commercial ELISA kits (MBL, Nagoya, Japan). These kits are commonly used in Japan and are covered by health insurance for clinical laboratory tests. As Mahler et al noted that there is variability between anti-dsDNA assays,1 we need to use immunofluorescence tests with Crithidia luciliae as a substrate for confirmation.