Anti‐Mi‐2 antibody‐positive inflammatory myopathy during treatment with golimumab

Abstract

A 56‐year‐old woman, who was treated with golimumab for rheumatoid arthritis, presented with myalgia and rash. She had proximal limbs weakness, and erythematous papules were evident on her hands and face. Her serum creatine kinase levels were elevated, and anti‐Mi‐2 antibody was detected. Magnetic resonance imaging of muscles revealed inflammatory lesions in muscles and soft tissues. She was diagnosed with inflammatory myopathy. A drug‐induced mechanism was suspected; therefore, we stopped treating her with golimumab and instead treated her with prednisolone. Subsequently, her symptoms gradually improved. This case suggests that tumor necrosis factor‐alpha inhibitors may induce anti‐Mi‐2 antibody‐positive inflammatory myopathies.

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“…The DMARDs can be of biologic origin (bDMARDs) that are peptide in nature and mostly immunoglobulins obtained from living cells [80]. The bDMARDs include bio-original (boDMARDs) and biosimilar (bsDMARDs) for example anti-TNF proteins and chimeric MCABs containing infliximab that inhibit TNF-α by binding to TNF-receptor (TNFR), chimeric MCABs rituximab that target B-cell surface CD20 proteins to suppress inflammation while humanized MCABs golimumab and adalimumab that target TNF-α and also cause apoptosis of macrophages (Figure 3) [81][82][83][84]. The artificially synthesized DMARDs include conventional synthetic csDMARDs for example methotrexate that inhibits the JAK-STAT pathway and also inhibits the IL-22, helper T-cells, and purine biosynthesis by blocking 5-aminoimidazole-4-carboxamide ribonucleotide transferase (AICART) that in turn inhibits adenosine deaminase (ADA), hydroxychloroquine that induces apoptosis of lymphocytes, inhibit TNF-α and prevents chemotaxis of macrophages to the synovium, leflunomide that inhibits proliferation of lymphocytes and suppresses of pyrimidine synthesis by inhibition of tyrosine kinase and dihydroorotate dehydrogenase, and sulfasalazine that inhibits IL-1, TNF-α, and induces apoptosis of lymphocytes while the targeted synthetic tsDMARDs for example tofacitinib and ruxolitinib act as Jak-1, Jak-2 and Jak-3 inhibitors that in turn suppress the formation of PICs including IL-6, IL-8 and IFN-γ (Figure 4) [85][86][87][88][89][90][91][92][93][94].…”