Longitudinally extensive transverse myelitis with concurrent acute sensorimotor polyneuropathy secondary to hepatitis B virus reactivation: a case report

Abstract Background Hepatitis B virus (HBV) reactivation is a well-recognised complication of immunosuppressive therapy, particularly following B-cell-depleting agents such as rituximab. Although several extrahepatic neurological manifestations of HBV have been described, concurrent transverse myelitis and Guillain Barre syndrome (GBS) associated with HBV reactivation has not previously been reported. Case Presentation A 58-year-old man with a history of transformed diffuse large B-cell lymphoma developed HBV reactivation eight months after completing rituximab-based chemotherapy (R-CHOP) following premature cessation of antiviral prophylaxis. He presented with severe acute hepatitis, characterised by alanine aminotransferase 2,974 U/L, hepatitis B surface antigen seroreversion, hepatitis B e antigen positivity and detectable HBV DNA. Despite prompt recommencement of entecavir, he developed rapidly progressive lower limb weakness, paraesthesia, a T4 sensory level, neurogenic bladder and bowel dysfunction and absent lower limb reflexes. Magnetic resonance imaging demonstrated longitudinally extensive T2 hyperintensity extending from C4 to T10, consistent with transverse myelitis. Nerve conduction studies demonstrated a mixed axonal and demyelinating sensorimotor polyneuropathy consistent with Guillain Barre syndrome. Cerebrospinal fluid analysis excluded infectious, autoimmune and other inflammatory causes, including central nervous system HBV infection. The patient was treated with a five-day course of intravenous immunoglobulin alongside continued antiviral therapy. This resulted in progressive neurological recovery, complete radiological resolution of spinal cord abnormalities within three weeks, suppression of HBV viraemia, hepatitis B surface antigen clearance and normalisation of liver biochemistry by three months. Residual neurogenic bladder dysfunction persisted at follow-up. Conclusions This case represents, to our knowledge, the first reported association of concurrent transverse myelitis and Guillain Barre syndrome occurring during HBV reactivation. It expands the recognised neurological spectrum of HBV associated immune-mediated disease and highlights the importance of considering HBV reactivation in patients presenting with acute inflammatory neurological syndromes following immunosuppressive therapy. Early recognition, prompt antiviral treatment and immunomodulatory therapy may result in favourable neurological and virological outcomes.