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Abstract Details

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) Triggered by Reactivation of Chronic Hepatitis B Infection
Autoimmune Neurology
P4 - Poster Session 4 (11:45 AM-12:45 PM)

Chronic inflammatory demyelinating polyneuropathy (CIDP) is a debilitating autoimmune neurological disorder characterized by proximal and distal weakness, sensory loss, and areflexia with insidious progression over eight weeks or more after symptom onset1. While both Guillain-Barre syndrome (GBS) and CIDP may develop after vaccination or infection, antecedent infection is more strongly linked to GBS2. Existing studies indicate rare associations between CIDP and infections with HIV, Hepatitis B and C, EBV, CMV, Bartonella henselae, Mycoplasma pneumoniae, HTLV-1, and Zika virus3. Here, we describe a patient who presented with acute-onset CIDP in association with otherwise asymptomatic reactivation of chronic Hepatitis B infection.


A 50-year-old man presented with 7-week history of progressive numbness and paresthesias of the bilateral upper and lower limbs followed by lower extremity weakness and progressive gait decline. Examination disclosed stocking-glove sensory loss to all sensory modalities, MRC grade 3/5 strength in the bilateral shoulder and pelvic girdle and intrinsic hand muscles with grade 4/5 strength in the remaining muscle groups, and diffusely absent DTRs. Laboratory studies showed elevated AST (86 U/L), ALT (152 U/L), and total bilirubin (1.7 mg/dL), positive HBc-IgG, HBsAg, and HBeAb, equivocal HBc-IgM, negative HBsAb and HBeAg, and HBV DNA of 130,207,286 IU/mL.  CSF analysis revealed albuminocytologic dissociation with 1 WBC and protein level of 50 mg/dL. NCS/EMG showed a severe, subacute to early chronic, generalized demyelinating motor greater than sensory polyneuropathy with secondary axonal loss and active denervation in the distal limb muscles, with findings meeting EAN/PNS electrodiagnostic criteria for typical CIDP4.  Tenofovir and IVIG were started with rapid improvement in the patient’s weakness and sensory deficits.

This case adds to the existing literature describing CIDP onset in the context of concurrent Hepatitis B infection.  Clinicians should consider screening for viral hepatitis in patients with new-onset CIDP and transaminitis.

Victoria Mazo, MD (USF)
Dr. Mazo has nothing to disclose.
No disclosure on file
No disclosure on file
Natasha N. Llanes, MD (VA Hospital) Dr. Llanes has nothing to disclose.
Anthony M. Bradshaw, MD (University of South Florida Department of Neurology) Dr. Bradshaw has nothing to disclose.