Abstract
ABSTRACT
Background
Guillain‐Barré syndrome (GBS) is an acute, immune‐mediated polyradiculoneuropathy most often triggered by infections such as
Campylobacter jejuni
, Epstein–Barr virus (EBV), or cytomegalovirus (CMV). Although transplant‐associated GBS is recognized in adults, it remains rare in pediatric recipients, and distinguishing immune‐mediated disease from medication toxicity or critical illness can be challenging.
Methods
We describe two pediatric cases of GBS following organ transplantation, one after liver transplant and one after small bowel transplant. Clinical features, diagnostic evaluation, immunosuppression exposure, electrodiagnostic findings, imaging, and treatment outcomes were reviewed to characterize presentation patterns and diagnostic challenges.
Results
The first patient developed rapidly progressive weakness shortly after liver transplantation in the setting of organ failure, adenovirus infection, and transient supratherapeutic tacrolimus levels. She demonstrated severe motor axonal involvement on nerve conduction studies and elevated neurofilament light chains, improving after intravenous immunoglobulin (IVIG). The second patient, years after small bowel transplantation complicated by chronic immune dysregulation and EBV viremia, presented with ascending weakness, areflexia, elevated CSF protein, and MRI enhancement of cauda equina and cranial nerves. Electrodiagnostics confirmed demyelinating polyneuropathy. Symptoms improved after IVIG despite concurrent tacrolimus level elevation. Across both cases, infectious triggers, immunosuppression, and critical illness obscured early recognition.
Conclusion
GBS is an uncommon but important cause of acute weakness in pediatric transplant recipients. These cases show that GBS can occur both early and late after transplantation and may mimic medication toxicity or other complications. Early consideration of GBS, timely electrodiagnostic testing, and prompt immunotherapy are essential for optimizing outcomes in these patients.