Intracranial Hypertension and Memory Loss in a Patient Treated with Ustekinumab

Abdelnabi, Mai; Short, J G; Khoromi, Suzan; Ehrlich, Alison

doi:10.1111/ajd.12248

Cited by 5 publications

(2 citation statements)

References 6 publications

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Section: Discussionmentioning

confidence: 99%

“…So far, only a few cases of ustekinumab-related neurologic adverse events have been reported, all of them with full resolution after drug discontinuation, and leukoencephalopathy was not the presenting syndrome in any of them (Table 1). 10,11,13,[15][16][17][18][19][20][21] Our patient developed rapidly progressive encephalopathy with extensive confluent supratentorial white matter lesions 12 weeks after starting treatment with ustekinumab and had a slow improvement when this drug and the background treatment with methotrexate were discontinued. The temporal association and the reasonable exclusion of alternative causes strongly suggest that the encephalopathy was an adverse effect of the therapy with ustekinumab.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Clinically reversible ustekinumab-induced encephalopathy: case report and review of the literature

Sarto

Caballol

Berenguer

et al. 2022

Ther Adv Neurol Disord

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Ustekinumab, a monoclonal antibody against interleukin (IL)-12 and IL-23 approved for the treatment of Crohn’s disease, has shown to be an effective therapy with a favourable safety profile. Clinical trials and real-world studies have reported very few neurological adverse events, including posterior reversible encephalopathy syndrome, idiopathic intracranial hypertension and headache. We describe the case of a 48-year-old man with Crohn’s disease who initiated treatment with ustekinumab on top of ongoing treatment with methotrexate 25 mg/week who presented with an acute-onset encephalopathy that rapidly evolved to severe tetraparesis and akinetic mutism, associated with extensive leukoencephalopathy and restricted diffusion on brain magnetic resonance imaging (MRI), 1 month after the second dose of ustekinumab. Comprehensive in-patient diagnostic testing ruled out vascular, demyelinating, metabolic, tumoral and infectious etiologies. Brain biopsy showed patchy infiltrates of foamy histiocytes with perivascular distribution, associated with edema, diffuse astrocytic gliosis and focal perivascular axonal destruction without demyelination, and ustekinumab-induced neurotoxicity was suspected. After drug discontinuation, the patient presented a complete clinical recovery despite the persistence of leukoencephalopathy. In conclusion, in an era in which biological therapies are continually evolving and expanding, knowledge about the potential neurotoxicity of these new therapies and their management becomes crucial. Although ustekinumab-induced encephalopathy is uncommon, the recognition of this potentially serious side effect is important because prompt withdrawal is associated with a favourable outcome. Whether methotrexate played an additional contributing role is currently unknown, but it is a factor that should be considered.

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