Contributions
Abstract: EP1530
Type: ePoster
Abstract Category: Therapy - disease modifying - Risk management for disease modifying treatments
Introduction: Clinical worsening after the first administration of natalizumab in very active relapsing-remitting multiple sclerosis (RRMS) has been seldom reported.
Case report: We present a 32 year-old man with RRMS diagnosed one year prior to the administration of natalizumab. The presenting symptoms were right optic neuritis and lower limb paresis. Brain MRI revealed multiple supra and infratentorial T2-hyperintense lesions. He was treated with high-dose methylprednisolone with partial recovery. One week later, he had a left optic neuritis. Brain MRI revealed new enhancing lesions and the diagnosis of RRMS was established. He was treated high-dose steroids and started interferon beta 1b. Six months later, he had a brainstem relapse presenting with facial paresis, limb ataxia and urinary urgency. Brain MRI showed new right pontine and bulbar T2-hyperintense lesions. He was treated with high-dose steroids. Three months later, he had another brainstem relapse presenting with internuclear ophthalmoparesis, dysarthria, left hemiparesis and ataxic gait. At this time, he was referred to our hospital center. He was treated with high-dose steroids, but severe neurological sequels persisted. Although JC serology was positive, the severity and recurrence of relapses and the increasing number of active lesions on MRI supported the decision to start natalizumab. The first natalizumab infusion was administered forty days after the last relapse. Within 36 hours, he experienced severe disease exacerbation with frontal syndrome, dysphagia to liquids, left C4 sensitive level and worsening of previous symptoms. Brain MRI showed increased number of T2-hyperintensities and enlargement of previous lesions. Anti-AQP4 and anti-natalizumab antibodies were both negative. High-dose steroids had only modest clinical benefit. Plasma exchange (5 sessions in alternate days) was performed and significant clinical and radiological improvement was observed along the treatment. At the time of discharge, only previous neurological sequels were documented.
Comments: The mechanism by which a first injection of natalizumab precipitates a clinical relapse is unknown. This case should emphasize the acknowledgment of clinical worsening as a possible early adverse effect of natalizumab, as well as the efficacy of plasma exchange on its treatment.
Disclosure: Joana Martins: nothing to disclose
Luísa Sousa: nothing to disclose
Paula Salgado: nothing to disclose
José Eduardo Alves: nothing to disclose
Ana Martins Silva: nothing to disclose
Ernestina Santos: nothing to disclose
Abstract: EP1530
Type: ePoster
Abstract Category: Therapy - disease modifying - Risk management for disease modifying treatments
Introduction: Clinical worsening after the first administration of natalizumab in very active relapsing-remitting multiple sclerosis (RRMS) has been seldom reported.
Case report: We present a 32 year-old man with RRMS diagnosed one year prior to the administration of natalizumab. The presenting symptoms were right optic neuritis and lower limb paresis. Brain MRI revealed multiple supra and infratentorial T2-hyperintense lesions. He was treated with high-dose methylprednisolone with partial recovery. One week later, he had a left optic neuritis. Brain MRI revealed new enhancing lesions and the diagnosis of RRMS was established. He was treated high-dose steroids and started interferon beta 1b. Six months later, he had a brainstem relapse presenting with facial paresis, limb ataxia and urinary urgency. Brain MRI showed new right pontine and bulbar T2-hyperintense lesions. He was treated with high-dose steroids. Three months later, he had another brainstem relapse presenting with internuclear ophthalmoparesis, dysarthria, left hemiparesis and ataxic gait. At this time, he was referred to our hospital center. He was treated with high-dose steroids, but severe neurological sequels persisted. Although JC serology was positive, the severity and recurrence of relapses and the increasing number of active lesions on MRI supported the decision to start natalizumab. The first natalizumab infusion was administered forty days after the last relapse. Within 36 hours, he experienced severe disease exacerbation with frontal syndrome, dysphagia to liquids, left C4 sensitive level and worsening of previous symptoms. Brain MRI showed increased number of T2-hyperintensities and enlargement of previous lesions. Anti-AQP4 and anti-natalizumab antibodies were both negative. High-dose steroids had only modest clinical benefit. Plasma exchange (5 sessions in alternate days) was performed and significant clinical and radiological improvement was observed along the treatment. At the time of discharge, only previous neurological sequels were documented.
Comments: The mechanism by which a first injection of natalizumab precipitates a clinical relapse is unknown. This case should emphasize the acknowledgment of clinical worsening as a possible early adverse effect of natalizumab, as well as the efficacy of plasma exchange on its treatment.
Disclosure: Joana Martins: nothing to disclose
Luísa Sousa: nothing to disclose
Paula Salgado: nothing to disclose
José Eduardo Alves: nothing to disclose
Ana Martins Silva: nothing to disclose
Ernestina Santos: nothing to disclose