A case of antisynthetase syndrome in a rheumatoid arthritis patient with anti-PL-12 antibody following treatment with etanercept

Abstract

In our earlier study, we had reported the case of a patient with rheumatoid arthritis (RA), who had anti-Jo-1 antibodies. This patient had received etanercept (ETN) therapy for RA, after which she had developed overt polymyositis (PM). Although various autoimmune phenomena, including lupus-like diseases, vasculitides, or psoriatic skin lesions, are associated with antitumor necrosis factor (TNF) therapy, the development of PM/dermatomyositis (DM) or antisynthetase syndrome following anti-TNF therapy is extremely rare. Here, we report a case of an RA patient with anti-PL-12 antibodies, who received ETN therapy and subsequently developed the antisynthetase syndrome. She recovered when ETN therapy was withdrawn and high-dose corticosteroid was administered. To date, there have been only five reported cases of RA patients with anti-Jo-1 antibodies who developed overt PM/DM following anti-TNF therapy and only one case of antisynthetase syndrome in an RA patient with anti-PL-7 antibodies. Our patients and the abovementioned reports strongly suggest that onset of overt PM/DM or antisynthetase syndrome in RA patients with anti-aminoacyl tRNA synthetase antibodies is associated with anti-TNF therapy.

The Association of Anti-Aminoacyl-Transfer Ribonucleic Acid Synthetase Antibodies in Patients With Rheumatoid Arthritis and Interstitial Lung Disease

“…28 Recent reports suggest that anti-tumor necrosis factor-alpha treatment of patients with elevated anti-ARS antibody levels may trigger myositis. 29 However, our results show that even in RA patients testing positive for anti-ARS antibodies and who were administered bDMARDs, connective tissue disorder complications such as PM/DM or transition/progression were absent. Although ILD complication was observed in 57% of RA patients who had autoantibodies against ARS, treatment with MTX and bDMARDs could be safely and effectively administered.…”

A case of interstitial pneumonia associated with anti‐PL‐7 antibody in a patient with rheumatoid arthritis

“…Currently, it is not known why anti-ARS antibodies become positive in RA patients. Ishikawa et al reported the case that the treatment with TNF-α inhibitor was possibly the trigger to develop ASS in an RA patient (15). Because the positive rate of anti-ARS antibody in RA patients is low, more clinical experiences are needed to elucidate the etiology of anti-ARS antibodies in RA patients.…”

Dermatomyositis/polymyositis and anti-TNF-α therapies: a literature review

“…As suggested by Hengstman in 2004, the use of anti-TNF-a blocking agents, in particular infliximab, appears in some cases very effective as induction therapy for a limited time only, because of the onset in the long-time period of severe adverse events that justified the withdrawal of the drug [35]. Another interesting fact regards the paradoxical onset of DM or PM in patients treated with TNF-a antagonists mainly for rheumatoid arthritis (15 cases) [35][36][37][38][39][40][41][42][43][44][45][46][47]. In total 18 reports of induction of DM/PM under adalimumab, etanercept, infliximab and lenercept can be retrievable (TABLE 5) [36][37][38][39][40][41][42][43][44][45][46][47].…”

“…Another interesting fact regards the paradoxical onset of DM or PM in patients treated with TNF-a antagonists mainly for rheumatoid arthritis (15 cases) [35][36][37][38][39][40][41][42][43][44][45][46][47]. In total 18 reports of induction of DM/PM under adalimumab, etanercept, infliximab and lenercept can be retrievable (TABLE 5) [36][37][38][39][40][41][42][43][44][45][46][47]. In three of such cases (two of PM and one of DM) the patients after the introduction of the anti-TNF-a therapy fulfilled the criteria for the diagnosis of antisynthetase syndrome (antisynthetase positive antibodies, mainly Jo-1; myositis, arthritis and interstitial lung disease) [38,40,41].…”