Comment on: Successful treatment of rapid progressive interstitial lung disease in a case of anti-Zo antibody positive anti-synthetase syndrome.

Abstract

We read with great interest the case report by Yongxia Li et al1 entitled “Successful treatment of rapid progressive interstitial lung disease in a case of anti-Zo antibody positive anti-synthetase syndrome.” We appreciate the efforts of the authors to summarize the clinical features of patients with the anti-Zo antibody, which is uncommon and is an anti-tRNA synthetase antibody. The report provided insights into treatment strategies for anti-synthetase syndrome (ASS). Since anti-Zo antibody-positive ASS with rapidly progressive interstitial lung disease (RP-ILD) has been rarely reported, this case report is very valuable. However, we would like to bring to the attention of the authors and the readers 2 points that would increase the significance of the report. First, the report by Li et al1 summarized 13 previously reported anti-Zo antibody-positive cases in Table 1. We noticed that Cases 1 and 12 may be duplicates. We believe that Case 12 of Li et al1 corresponds to Case 1 in a case series that was reported by Tansley et al2 based on the original case report by Betteridge et al.3 However, Li et al1 report the ages of Cases 1 and 12 differently, as 46 and 49 years old, respectively. If these are indeed 2 separate cases, we would appreciate clarification on the source of Case 12 in Table 1. Second, Li et al1 focus on the clinical features of anti-Zo antibody-positive RP-ILD and on strategies for treating it, but the detection method for the anti-Zo antibody was not described. We would like to inquire about the measurement method used to detect the anti-Zo antibodies. Hamguchi et al4 evaluated the performance of a commercial line-blot (LB) assay system for autoantibody detection in myositis and systemic sclerosis and warned against false positives and false negatives, except for anti-centromere antibody and anti-Jo-1 antibodies. Tansley et al5 compared the accuracy of LB, dot-blot (DB), and enzyme-linked immunosorbent assay (ELISA) to that of immunoprecipitation (IP), which is the gold standard for assaying myositis-specific/-associated autoantibodies (MSA/MAA), and noted that using only a single assay, other than IP, still has limitations in detecting MSA/MAA. Infantino et al6 emphasized the importance of combining multiple assays, such as indirect immunofluorescent antibody (IIF) test and LB, to detect MSA/MAA accurately. They noted the significance of cytoplasmic patterns in IIF staining for diagnosing ASS. Tansley et al2 also noticed that a cytoplasmic speckle on IIF of HEp-2 cells could provide useful clues when anti-Zo antibody testing is unavailable. It would be beneficial to mention IIF staining patterns in the case of Li et al1 as in our previous report.7 Given that the diagnosis of ASS is based on the detection of anti-tRNA synthetase antibodies and that each autoantibody has unique clinical characteristics,8 the description of the detection methods seems essential. In conclusion, we believe that clarifying the points mentioned above would increase the significance of the case report and provide greater benefit to clinicians. We look forward to hearing from the authors. HK and YM were involved in the conception of the work and manuscript drafting. SK, NA, SI, and YY contributed to the analysis and interpretation of the underlying article. MM and TT contributed to the revision of the manuscript drafts. MA supervised the study and contributed to manuscript drafting. None. No funding. None to declare.