Neurology(R) neuroimmunology & neuroinflammation · 2025
Successful Treatment of Progressive Multifocal Leukoencephalopathy With Tenofovir Alafenamide Fumarate.
СтатьяКлинический случайНазвание и аннотация: Перевод в очереди
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Torkildsen Øivind, Bru Alla N S, Behzadi Gry Inger Nerås, Myhr Kjell-Morten
Аннотация
OBJECTIVES: Progressive multifocal leukoencephalopathy (PML) is a rare, often fatal CNS infection caused by reactivation of JC virus, typically in immunocompromised patients. No effective antiviral therapy has been established. We report a case of PML in a patient with multiple sclerosis (MS) treated with fingolimod, who received oral tenofovir alafenamide fumarate (TAF).
METHODS: This is a single-patient case report from Stavanger University Hospital, Norway. A 67-year-old woman with secondary progressive MS developed progressive neurologic symptoms during fingolimod treatment. MRI and CSF analyses confirmed PML with detectable JCV DNA. Fingolimod was discontinued, and oral TAF 50 mg/d was initiated. Clinical course, MRI changes, and CSF biomarkers were monitored over 6 months.
RESULTS: At baseline, JCV DNA was 4,940 international units [IU]/mL in CSF and the Expanded Disability Status Scale (EDSS) score was 8.5. Four days after TAF initiation, partial radiologic improvement was observed. After 3 and 6 months, JCV DNA was undetectable (<1,000 IU/mL). The patient remained clinically stable with unchanged EDSS score and tolerated TAF without adverse effects. MRI showed regression of PML lesions but development of new MS activity after fingolimod withdrawal.
DISCUSSION: This case demonstrates temporal association between TAF initiation and virologic clearance of JCV, suggesting potential antiviral activity.
CLASSIFICATION OF EVIDENCE: As a single case without controls, this report provides Class IV evidence that oral TAF might stabilize the clinical course in patients with PML.
METHODS: This is a single-patient case report from Stavanger University Hospital, Norway. A 67-year-old woman with secondary progressive MS developed progressive neurologic symptoms during fingolimod treatment. MRI and CSF analyses confirmed PML with detectable JCV DNA. Fingolimod was discontinued, and oral TAF 50 mg/d was initiated. Clinical course, MRI changes, and CSF biomarkers were monitored over 6 months.
RESULTS: At baseline, JCV DNA was 4,940 international units [IU]/mL in CSF and the Expanded Disability Status Scale (EDSS) score was 8.5. Four days after TAF initiation, partial radiologic improvement was observed. After 3 and 6 months, JCV DNA was undetectable (<1,000 IU/mL). The patient remained clinically stable with unchanged EDSS score and tolerated TAF without adverse effects. MRI showed regression of PML lesions but development of new MS activity after fingolimod withdrawal.
DISCUSSION: This case demonstrates temporal association between TAF initiation and virologic clearance of JCV, suggesting potential antiviral activity.
CLASSIFICATION OF EVIDENCE: As a single case without controls, this report provides Class IV evidence that oral TAF might stabilize the clinical course in patients with PML.