Atypical Guillain‐Barré Syndrome Preceding Icteric Hepatitis A: A Diagnostic Challenge—A Case Report

ABSTRACT Guillain–Barré syndrome (GBS) is an acute immune‐mediated neuropathy typically triggered by infections. Rarely, it may precede acute hepatitis A (HAV), creating diagnostic challenges. We report a 32‐year‐old male presenting with ascending weakness and tingling in limbs without initial hepatic symptoms. Within 48 h, he developed jaundice and elevated liver enzymes. GBS, acute myelopathy, and metabolic and toxic neuropathies were considered. Laboratory tests confirmed acute HAV infection (anti‐HAV IgM positive). CSF showed albuminocytologic dissociation; nerve conduction studies were consistent with the AIDP subtype of GBS. The patient received intravenous immunoglobulin (2 g/kg over 5 days), supportive care, and physiotherapy. Neurological function improved progressively; full recovery was observed at 3‐month follow‐up. This case highlights the rare sequence of GBS preceding HAV, likely due to early immune‐mediated nerve injury triggered by viral infection.Clinicians should consider HAV in patients presenting with acute flaccid paralysis and concurrent or subsequent hepatic symptoms.

Publication Details

Journal
Clinical Case Reports
Published
2026-03-23
DOI
https://doi.org/10.1002/ccr3.72364
Primary Topic
Peripheral Neuropathies and Disorders
Type
article
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article

Atypical Guillain‐Barré Syndrome Preceding Icteric Hepatitis A: A Diagnostic Challenge—A Case Report

Clinical Case Reports
Peripheral Neuropathies and Disorders
article

Atypical Guillain‐Barré Syndrome Preceding Icteric Hepatitis A: A Diagnostic Challenge—A Case Report

article en

Abstract

ABSTRACT Guillain–Barré syndrome (GBS) is an acute immune‐mediated neuropathy typically triggered by infections. Rarely, it may precede acute hepatitis A (HAV), creating diagnostic challenges. We report a 32‐year‐old male presenting with ascending weakness and tingling in limbs without initial hepatic symptoms. Within 48 h, he developed jaundice and elevated liver enzymes. GBS, acute myelopathy, and metabolic and toxic neuropathies were considered. Laboratory tests confirmed acute HAV infection (anti‐HAV IgM positive). CSF showed albuminocytologic dissociation; nerve conduction studies were consistent with the AIDP subtype of GBS. The patient received intravenous immunoglobulin (2 g/kg over 5 days), supportive care, and physiotherapy. Neurological function improved progressively; full recovery was observed at 3‐month follow‐up. This case highlights the rare sequence of GBS preceding HAV, likely due to early immune‐mediated nerve injury triggered by viral infection.Clinicians should consider HAV in patients presenting with acute flaccid paralysis and concurrent or subsequent hepatic symptoms.

Clinical Case ReportsVol. 14(4)
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Peripheral Neuropathies and Disorders
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