tetano
Editor, Senior Moderator
Am J Case Rep
. 2025 Dec 17:26:e949788.
doi: 10.12659/AJCR.949788. COVID-19-Associated MDA5-Mediated Necrotizing Myositis
Sarah Steadman[SUP] 1 [/SUP], Amit Sikder[SUP] 2 [/SUP], Harsh R Desai[SUP] 3 [/SUP], Bradley Collins[SUP] 4 [/SUP], Tiffany Baker[SUP] 5 [/SUP], Julie Worthington[SUP] 6 [/SUP]
Affiliations
BACKGROUND Rhabdomyolysis and autoimmune myopathies often present with similar clinical features, including myalgias, muscle weakness, and elevated serum creatine kinase (CK) levels. This overlap can make early diagnosis challenging and delay appropriate management. The recent rise in SARS-CoV-2 infections has led to an increasing number of reports of autoimmune myositis associated with the virus. CASE REPORT Here, we present a unique case of a young African American male who developed myalgias and bilateral upper and lower extremity weakness without any skin changes following a recent SARS-CoV-2 infection. His CK level exceeded 300 000 U/L; however, he had normal inflammatory markers and a basic autoimmune panel, and a chest computed tomography scan did not demonstrate interstitial lung disease. Initial treatment with intravenous fluids for presumed viral-induced rhabdomyolysis showed minimal clinical improvement. Surprisingly, empiric steroid therapy led to a rapid recovery in both CK levels and symptoms. A subsequent muscle biopsy revealed necrotizing myositis, and an autoimmune myositis panel showed elevated melanoma differentiation-associated gene 5 (MDA5) antibodies. CONCLUSIONS To the best of our knowledge, this is the first reported case of MDA5-associated necrotizing myositis following SARS-CoV-2 infection. Most patients with MDA5-related disease develop skin changes and underlying interstitial lung disease; however, our patient lacked these findings. At an 8-month outpatient follow-up, the patient had residual proximal muscle weakness and remained on immunosuppressive therapy. Further research is needed to better understand the pathophysiology of COVID-19-mediated autoimmune myopathies and to develop targeted therapies for these patients.
. 2025 Dec 17:26:e949788.
doi: 10.12659/AJCR.949788. COVID-19-Associated MDA5-Mediated Necrotizing Myositis
Sarah Steadman[SUP] 1 [/SUP], Amit Sikder[SUP] 2 [/SUP], Harsh R Desai[SUP] 3 [/SUP], Bradley Collins[SUP] 4 [/SUP], Tiffany Baker[SUP] 5 [/SUP], Julie Worthington[SUP] 6 [/SUP]
Affiliations
- PMID: 41406062
- DOI: 10.12659/AJCR.949788
BACKGROUND Rhabdomyolysis and autoimmune myopathies often present with similar clinical features, including myalgias, muscle weakness, and elevated serum creatine kinase (CK) levels. This overlap can make early diagnosis challenging and delay appropriate management. The recent rise in SARS-CoV-2 infections has led to an increasing number of reports of autoimmune myositis associated with the virus. CASE REPORT Here, we present a unique case of a young African American male who developed myalgias and bilateral upper and lower extremity weakness without any skin changes following a recent SARS-CoV-2 infection. His CK level exceeded 300 000 U/L; however, he had normal inflammatory markers and a basic autoimmune panel, and a chest computed tomography scan did not demonstrate interstitial lung disease. Initial treatment with intravenous fluids for presumed viral-induced rhabdomyolysis showed minimal clinical improvement. Surprisingly, empiric steroid therapy led to a rapid recovery in both CK levels and symptoms. A subsequent muscle biopsy revealed necrotizing myositis, and an autoimmune myositis panel showed elevated melanoma differentiation-associated gene 5 (MDA5) antibodies. CONCLUSIONS To the best of our knowledge, this is the first reported case of MDA5-associated necrotizing myositis following SARS-CoV-2 infection. Most patients with MDA5-related disease develop skin changes and underlying interstitial lung disease; however, our patient lacked these findings. At an 8-month outpatient follow-up, the patient had residual proximal muscle weakness and remained on immunosuppressive therapy. Further research is needed to better understand the pathophysiology of COVID-19-mediated autoimmune myopathies and to develop targeted therapies for these patients.