Obinutuzumab use complicated by progressive multifocal leukoencephalopathy in a patient with chronic lymphocytic leukemi
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LETTER TO THE EDITOR
Obinutuzumab use complicated by progressive multifocal leukoencephalopathy in a patient with chronic lymphocytic leukemia: a case report Gaëtane Turine1 · Frédéric London2 Received: 20 August 2020 / Accepted: 5 October 2020 © Belgian Neurological Society 2020
Keywords PML · Obinutuzumab · JC virus
Introduction Progressive multifocal leukoencephalopathy (PML) is a severe, untreatable, and often fatal brain disease caused by reactivation of the latent John Cunningham virus (JCV) [1]. The estimated prevalence of PML is 0.2 cases per 100,000 persons in the general population [1]. PML is essentially seen in immunocompromised patients, particularly those with impaired cell-mediated immunity [1]. Historically, this rare opportunistic infection was first reported in people with hematologic malignancies, namely chronic lymphocytic leukemia (CLL) and Hodgkin’s lymphoma, and later with advanced HIV infection [2, 3]. Over the past years, PML has also been associated with specific immunotherapies such as monoclonal antibodies (mAbs). Obinutuzumab is a type II humanized anti-CD20 mAb approved for use in combination with chlorambucil as treatment of CLL. Here, we present a case of PML occuring in a patient without prior exposure to immunosuppressant but recently treated with obinutuzumab in the setting of CLL.
Case presentation We present a 76-year-old, HIV-negative female with medical history significant for CLL that was diagnosed in 1996. Because she was asymptomatic, no specific treatment was * Frédéric London [email protected] 1
Department of Neurology, CHU UCL Namur, Namur, Belgium
Department of Neurology, CHU UCL Namur, 1 avenue G. Thérasse, 5530 Yvoir, Belgium
2
required. Due to disease progression, she started obinutuzumab and chlorambucil in April 2019 and received a total of six cycles ending in September 2019. In May 2020, the patient was admitted to our institution for evaluation of progressive cerebellar syndrome. Her husband reported progressive neurobehavioral symptoms and insidious onset of ataxia in the beginning of 2020. She did not go to hospital nor contact her general practitioner at that time. Neurological symptoms had significantly worsened over the weeks before admission at our facility. On examination, strength was full and symmetric. She had no sensory loss, urinary retention, or Babinski response. A prominent cerebellar syndrome with dysarthria and a marked ataxia in the four limbs, predominating on the left side, was observed. Cognitive and behavioral changes were also noticed during hospitalization. Brain magnetic resonance imaging (MRI) revealed multiple lesions highly suggestive of PML, as characterized by T2/FLAIR hyperintensities and T1 hypointensities involving both cerebellar hemispheres as well as the subcortical white matter in the right parietal region, without gadolinium enhancement and mass effect (Fig. 1a–e). Cerebrospinal fluid (CSF) analysis showed a discrete pleocytosis (8 white blood cell/mm3) but no CSF-restricted IgG oligoclonal bands. PML w
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