Ochsner Clinic Foundation New Orleans, LA, United States
Divyesh Nemakayala, MD, Matthew Reif, MD, Andrew Welch, MD, Steven Young, MD Ochsner Clinic Foundation, New Orleans, LA
Introduction: Hepatitis A is often a self-limited illness, sometimesassociated with acute kidney injury, aplastic anemia, and acute pancreatitis. Rare case reports have observed Guillain-Barré syndrome (GBS) in Hepatitis A, with sequelae of acute respiratory failure and/or permanent extremity weakness. Our case demonstrates such an instance.
Case Description/Methods: A 65-year-old female non-drinker with no significant past medical history, and whose husband had been diagnosed with hepatitis A 14 days prior, presented with 4 days of abdominal pain, generalized weakness, nausea, vomiting, and anorexia. She was icteric and jaundiced, and initial labs showed AST 2353, ALT 3611, ALP 182, total bilirubin 9.0, INR 1.1, and positivehepatitis A IgM. On hospital day 2, she noted new weakness and sensory changes of all extremities and had dyspnea requiring bilevel positive airway pressure support; neurology was consulted. MRI of her brain and entire spine was unrevealing. A lumbar puncture showed albuminocytologic dissociation favoring atypical GBS. With 5 days of 30 mg/day IVIG, her weakness and respiratory failure resolved, her liver enzymes normalized, and was discharged to inpatient rehabilitation on hospital day 9.
Discussion: The four most common subtypes of GBS are acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy, acute motor and sensory axonalneuropathy, and Miller Fisher syndrome. Our patient’s presentation favored AIDP, most commonly seen with hepatitis A. The pathogenesis of hepatitis-A-associated-GBS remains unknown, proposed as molecular mimicry between cross-reactive Hepatitis A epitopes and the peripheral nervous system. Other authors hypothesize CSF antibody presence reflects directs central nervous sytem invasion. Ultimately, further investigation of pathogenesis is needed.
Consensus among case reports suggests that neurological dysfunction severity is independent of liver injury severity. As with most other cases, GBS onset in our patient was within 14 days of hepatitis symptoms, although the former often occurs in young males unlike in our case. Although subtype determines recovery speed, usually GBS resolves with IVIG 2-7. Early neurological consultion and close respiratory monitoring are pertinent. Given the risk of respiratory compromise and permanent neurological sequelae, one must recognize this rare, dangerous complication of hepatitis A.
Disclosures: Divyesh Nemakayala indicated no relevant financial relationships. Matthew Reif indicated no relevant financial relationships. Andrew Welch indicated no relevant financial relationships. Steven Young indicated no relevant financial relationships.
Divyesh Nemakayala, MD, Matthew Reif, MD, Andrew Welch, MD, Steven Young, MD. P0777 - Acute Hepatitis a Complicated by Guillain-Barré Syndrome, ACG 2021 Annual Scientific Meeting Abstracts. Las Vegas, Nevada: American College of Gastroenterology.
