Discussion

This case illustrates the diagnostic challenges of autoimmune-mediated rhabdomyolysis in the absence of confirmatory serologies. Statin-associated IMNM is often antibody-positive; however, approximately two-thirds of cases may lack detectable anti-HMGCR antibodies [3]. Diagnosis must therefore integrate clinical presentation, imaging, and exclusion of alternative etiologies. Along with cessation of any offending agents and supportive care, treatment for IMNM typically consists of immunosuppressive therapy, often high-dose glucocorticoids in combination with steroid-sparing immunosuppressive agents. Statin-induced IMNM treatment can include adjunctive intravenous immunoglobulins (IVIG) as well.

Concomitant use of statin and ticagrelor has been shown to induce rhabdomyolysis and therefore remains a likely differential for our patient's presentation [4]. However, the patient was maintained on DAPT therapy throughout his hospitalization. While this does not necessarily exclude the statin-tigacrelor combination as a rhabdo etiology, the continuation of one of the proposed offending agents does not correlate with the patient's rapid clinical improvement.

While statins are a well-recognized cause of both toxic and immune-mediated myopathies, long-term therapy does not preclude the development of late autoimmune complications [5,6]. Furthermore, clinical features of toxic statin myopathy involve a rapid resolution of elevated CK once statins are held. However, in our patient, his persistent initial elevation and eventual slow resolution of CK levels increase the likelihood of immune-mediated myopathy. This is further supported by MRI findings showing asymmetric edema of the semimembranosus and rectus femoris muscles, which is more consistent with IMNM compared to the symmetrical, pan-compartmental edema associated with statin toxicity [7].