S5831 First Reported Case of Immune-Mediated Necrotizing Myopathy as a Paraneoplastic Manifestation of Hepatocellular Carcinoma

Introduction: Immune-mediated necrotizing myopathy (IMNM) is a rare, aggressive inflammatory myopathy characterized by subacute proximal muscle weakness, markedly elevated creatine phosphokinase (CPK), and myofiber necrosis on biopsy. It is often associated with anti-HMG-CoA reductase or anti-SRP antibodies, especially in statin users, but can also present as a paraneoplastic syndrome. While IMNM has been reported in association with several malignancies—including gastrointestinal, lung, prostate, uterine, and hematologic cancers—there are no previously published cases linking IMNM to HCC. Case Description/Methods: A 73-year-old man with diabetes, hypertension, and a stable hepatic mass presented with 3 months of progressive bilateral lower extremity weakness, frequent falls, and new urinary and fecal incontinence. He also had chronic neck and back pain. On admission, he had elevated creatinine, CPK, and troponin. Neurological exam revealed symmetric proximal and distal weakness in the lower extremities with reduced reflexes. Imaging ruled out acute intracranial pathology; cervical spine MRI showed degenerative changes with canal stenosis, but these did not fully explain his clinical picture. Anti-HMG-CoA reductase antibodies were negative despite statin use. Muscle biopsy confirmed immune-mediated necrotizing myopathy. Given the absence myositis-specific antibodies, a paraneoplastic etiology was pursued. Abdominal MRI revealed marked progression of a previously stable hepatic lesion, now an exophytic right lobe mass consistent with LI-RADS 5 HCC. The patient was deemed not a surgical candidate. He was initially treated with a 5-day IVIG course, leading to substantial improvement in strength. Interventional radiology performed Y90 radioembolization. However, the tumor persisted. Recently, he underwent aggressive locoregional therapy with transarterial chemoembolization (TACE) for more effective tumor control. Discussion: While IMNM is an established paraneoplastic entity, its occurrence secondary to HCC has not been previously reported. This case underscores the importance of considering malignancy in the differential diagnosis of seronegative necrotizing myopathy. Although IVIG provided initial neurologic improvement, the patient’s myopathy worsened over time, likely due to ongoing tumor burden and lack of definitive oncologic control. He ultimately became wheelchair-bound pending more effective HCC-directed therapy. This case aims to expand the spectrum of HCC-associated paraneoplastic syndromes.