Case Presentation: A 54 year-old Caucasian male presented with 1 week of progressively worsening bilateral lower extremity weakness. This was preceded by 1 month of nausea, vomiting, and right upper quadrant pain. On evaluation, his vitals were within normal limits and his physical examination was significant for bilateral proximal lower extremity weakness with normal distal strength, normal reflexes, and normal sensation. Due to GI symptoms followed by lower extremity weakness, lumbar puncture was done that revealed normal protein, glucose, and cytology. He had an elevated CK of 8245, with peak 107,000, and myoglobinuria. Liver function tests revealed an elevated AST and ALT of 724 and 440 respectively and subsequent viral hepatitis panel revealed acute hepatitis B. EMG confirmed a myopathic process rather than neuropathic. Muscle biopsy showed a necrotizing myositis. An extensive diagnostic evaluation was negative, including ANA, ANCA, Anti HMG-CoA reductase, complements, Anti SSA and SSB, Anti Sm, Anti RNP, RF, Anti CCP, TSH, and HIV testing. He was diagnosed with Hep B associated necrotizing myositis. Treatment was initiated with high dose glucocorticoids, IVIG, and tenofovir leading to gradual improvement in muscle strength and mobility.
Discussion: In symptomatic patients, acute hepatitis B typically presents with constitutional symptoms, nausea, jaundice, and RUQ pain. In our patient’s case, these symptoms were more indolent and he did not present until disease had progressed to significant lose of muscle strength. In the US, the most common viruses associated with myositis are influenza A and B, and enterovirus. There have been a few case reports of Hepatitis B associated myositis. Our patient’s muscle biopsy was consistent with necrotizing autoimmune myositis (NAM), which is a subtype of inflammatory myopathy that accounts for 19% of all inflammatory myopathies. It can occur idiopathically, after viral infections, with malignancy, with connective tissue disorders, or with statin use. NAM typically presents as subacute onset of proximal muscle weakness and can have CK levels up to 50 times the upper limit of normal. Muscle biopsy can help to distinguish the various inflammatory myopathies from one another, with NAM characterized by multiple necrotic fibers seen with surrounding macrophages. Treatment consists mainly of steroids, with IVIG and rituximab as additional options if no significant improvement is made.
Conclusions: In patients presenting with proximal muscle weakness and significantly elevated CK, the differential is broad and muscle biopsy can help determine the subtype of myositis. Hepatitis B has been associated with NAM in a few case reports, and our case is another example. Although not common, it is important to keep viral etiologies in mind when seeing these patients, as they may benefit from antiviral treatment, but more research is still needed.