Acute Hepatitis B Infection Causing Guillain-Barré Syndrome (GBS): A Rare Case: 2011 ACG Presidential Poster

Abstract

Purpose: We report a rare case of Guillain-Barré syndrome (GBS) in acute hepatitis B infection. We emphasize on the awareness of this association since an early diagnosis and a timely initiation of treatment determines the neurological recovery. A 42-year-old Vietnamese female presented with a two week history of nausea, vomiting, abdominal pain, and jaundice. No clear risk factor for acute hepatitis infection was identified. Physical examination revealed icteric sclera, right upper quadrant abdominal tenderness, and jaundice. She had no neurological deficits. Laboratory data showed total serum bilirubin was 14.4, direct bilirubin 10.8, AST 850, ALT 1817, alkaline phosphatase 211, and an INR of 1.2. HBsAg, IgM anti-HBc antibody, and HBV DNA were positive. She was diagnosed with acute hepatitis B infection. On hospital day four, she developed rapidly worsening bilateral upper and lower extremity weakness. She progressed to flaccid paralysis of all extremity, and deep tendon reflexes were absent. She required intubation due to respiratory failure. The diagnosis of GBS was strongly suspected. Lumbar puncture with cerebrospinal fluid (CSF) analysis showed normal WBC of 1 and elevated total protein of 71, representing albuminocytologic dissociation as seen in GBS. Electromyography (EMG) and nerve conduction studies (NCS) confirmed the diagnosis of GBS. Treatment with intravenous immune globulin (IVIG) was started within three days after onset of neurological symptoms. She was extubated after one week of mechanical ventilation and transferred to an acute rehabilitation center. After 6 weeks, she was discharged to home with a full neurological recovery. Viral hepatitis has been implicated in acute immune-mediated polyneuropathies classified under the eponym Guillain-Barré syndrome (GBS) and accounts for ˜ 1% GBS cases. We found less than 20 reported cases of GBS complicating acute hepatitis B infections to date. Proposed mechanisms by which HBV causes GBS include molecular mimicry between HBV DNA and myelin basic protein with host immunity attacking both, HBsAg-mediated immune complex vasculitis, and direct damage by HBV. The two available treatments are IVIG and plasma exchange (PE). IVIG is as effective as PE, and no difference in measures of recovery was seen when comparing PE followed by IVIG with either treatment alone. Plasma exchange is shown to be most effective when started with in seven days of symptom onset. Acute hepatitis B infection is rarely associated with GBS. Since early diagnosis and timely administration of IVIG or plasma exchange predicts the degree of neurological recovery, gastroenterologists should be aware of this association.