Case Presentation: Rheumatoid myositis is often underdiagnosed due to its variable laboratory, MRI, and biopsy findings and often misdiagnosed as idiopathic polymyositis.50-year-old female with seronegative RA and vocal cord dysfunction after COVID-19 infection presented with worsening proximal muscle weakness, dysphagia, and arthritis. A few years back she had multiple episodes of bilateral MCP swelling and diagnosed with seronegative RA when MRI showed erosive arthritis. She was started on methotrexate with improvement.Three weeks prior to her presentation, she experience generalized muscle pain, proximal weakness, bilaterally MCPs redness and inflammation with CK of 873 U/L. Based on these findings with high suspicion of dermatomyositis, she was started on systemic steroids and she was discharged on Prednisone 40mg daily. However, patient had worsening symptoms and presented to our hospital. MRI of right lower extremity showed diffuse muscle atrophy without T2 enhancement or hyperintensity concerning for myositis. She denies any statin use. Muscle biopsy showed few atrophic fibers that could suggest early denervation without clear pathologic abnormality. Extended myositis panel sent to Mayo Clinic was negative for anti-Jo 1, anti-PL 7, anti-PL 12, anti-EJ antibody, anti-OJ anti-MI 2 antibody, anti-TIF gamma antibody, anti-NXP-2, anti-SAE 1 antibody, anti-PML-SCL 100 antibody, anti-ku antibody, anti-SSA 52, anti-U 1 RNP antibody. Labs including inflammatory markers, CK, aldolase were within normal limits. CK on this admission was 178 U/L. She had negative rheumatoid factor, ANA, ANCA, anti-CCP, HMG Co. a antibody negative. CT head, chest, abdomen and pelvis did not level any malignancy. She was started on Solu-Medrol 80 mg IV for 3 days with some improvement in the dysphagia and muscle strength and transitioned to prednisone 60 mg daily. Methotrexate was continued and dose increased from 15 mg to 20 mg weekly. Her daily hydroxychloroquine 200mg twice daily was continued. Given the clinical picture and after exclusion the diagnosis of rheumatoid arthritis associated myositis was made.

Discussion: Rheumatoid myositis is typically described as immune inflammatory infiltrates with laboratory features of polymyositis, but there is great variability in degrees of skeletal muscle involvement that caused it to remain poorly characterized, under-diagnosed, and under-treated. Typical signs and symptoms are symmetric muscle pain with proximal weakness which prompts a broad differential. Miro et al studied the frequency and characteristics of symptomatic muscle disease (defined as weakness and muscle wasting) in patients with RA. The diagnosis was varied, including classic poly/dermatomyositis, polyarteritis nodosa, drug-induced myopathy, and muscular mononuclear cell infiltration. Serum CK was elevated in only 1 of 3 cases of mononuclear cell infiltration. It was inferred that CK is not a sensitive marker of inflammatory muscle disease in RA. This suggestion was supported in our patient who had a normal CK level despite histologic evidence of myofiber atrophy and necrosis. Hence, serum CK activity could be spuriously normal in patients affected by rheumatoid myositis. Our diagnosis for her was Rheumatoid associated myositis given broad negative workup and evidence of muscle atrophy on biopsy.

Conclusions: Our case suggests that in RA myositis may be more common than appreciated. We want to emphasize the relevance of muscle involvement as a potential manifestation of rheumatoid arthritis.