P-110: Guillain-Barré syndrome following autologous stem cell transplantation for the treatment of multiple myeloma: a myth?

Introduction:
Guillain-Barré syndrome (GBS) is an acute autoimmune peripheral neuropathy characterized by inflammation of peripheral nerves, leading to progressive muscle weakness, paresthesia, and, in severe cases, paralysis that may require respiratory support. Although typically preceded by a viral or bacterial infection, a dysfunctional immune response triggers an inflammatory reaction directed against peripheral nerves. The exact mechanisms remain unclear, but are thought to involve a cross-reactive immune response to neural antigens shared between the exogenous agent and the nerves. Plasma cell disorders are frequently associated with neurological pathologies such as peripheral neuropathies. However, the occurrence of Guillain-Barré syndrome is rarely associated with multiple myeloma (MM), and even rarer after autologous hematopoietic stem cell transplantation.

Methods:
We present the case of a 65-year-old patient with a previous history of ischemic heart disease, treated for a lambda light chain ISS1 MM who achieved VGPR after 4 induction cycles of daratumumab-bortezomib-lenalidomide-dexamethasone, but who complained of bortezomib-induced sensory polyneuropathy. Autologous stem cell transplantation (ASCT) was complicated by Streptococcus agalactiae bacteremia, severe malnutrition, and muscle wasting, with recovery from aplasia by day 12.


On Day 20 post-transplant, the patient experienced gait disturbances and peripheral paresthesia, initially attributed to peripheral amyotrophy and post-bortezomib polyneuropathy. By Day 26, gait disturbances worsened, with distal paresis of both lower limbs and absent deep tendon reflexes. The patient was admitted to the Neurology unit, where a thorough evaluation was conducted, resulting in the diagnosis of Guillain-Barré syndrome with no specific etiology identified. The infectious workup returned negative. The patient received immunoglobulins for 5 days and underwent intensive rehabilitation, resulting in partial neurological recovery. Three months after ASCT, he began maintenance therapy with daratumumab and lenalidomide without recurrence of the neurological condition.





Results: The occurrence of GBS post-ASCT in MM consolidation treatment is very rare and poorly documented, though isolated cases in literature have noted its possible implication. The underlying mechanism may be mixed and related to immune reconstitution post-autograft. Pre-existing sensory polyneuropathy due to bortezomib poses both a risk and a confounding factor. While bacteremia with S. agalactiae is not commonly linked to GBS, it may have played a triggering role in conjunction with immune reconstitution post-ASCT

Conclusions:
This case underscores a rare autoimmune neurological complication of stem cell transplantation, prompting inquiries into diagnosis, appropriate management, especially in highly immunocompromised patients, and presenting confounding factors.