ECTRIMS eLearning

Central and peripheral nervous system inflammation disease secondary to alemtuzumab therapy
ECTRIMS Learn. Jorge F. 10/25/17; 199782; EP1762
Frederico M.H. Jorge
Frederico M.H. Jorge
Contributions
Abstract

Abstract: EP1762

Type: ePoster

Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments

Alemtuzumab is a pan-lymphocyte depleting anti-CD52 antibody approved as escalation therapy for patients with multiple sclerosis (MS) with clinically or image defined active disease. It has been shown effective in reducing relapse rate and brain volume loss. However concerns have been raised due to its numerous adverse effects. We report a case of severe nervous system inflammatory response following Alemtuzumab infusion.
On March 2017 a 31-year-old woman was referred to our service due to an acute deterioration of her mental status. She had been diagnosed with multiple sclerosis in 2007 after attacks of dizziness and left hemiparesis with typically disseminated T2 lesions fulfilling diagnostic criteria on magnetic resonance imaging (MRI) and oligoclonal band (OCB) positivity on cerebrospinal fluid analysis. Despite the use of several immunomodulatory therapies - interferon beta-1a, glatiramer acetate, cyclophosphamide and natalizumab- the patient maintained frequent relapses and persistent disease activity on MRI. Alemtuzumab was first infused in January of 2017 and in March 2017 the patient presented with severe trigeminal neuralgia, marked cognitive impairment including apraxia and left-dominant tetraparesis. The MRI showed two new lesions on T1 weighted image with ring contrast enhancement in periventricular white matter, thickening and enhancement of nerve roots in bulbar (V, VII and XI nerves) and cervical segments. Infection was ruled out and the patient received 5000mg of methylprednisolone which led to marked clinical and radiological improvement.
The reported case illustrates an exacerbated inflammatory response observed after Alemtuzumab infusion. The response seen in our patient is consistent with the time-frame in which B-cell repopulation and peripheral expansion occur following alemtuzumab treatment, therefore further cases might be identified. As such, we suggest that apparent relapses after alemtuzumab treatment should be promptly screened by MRI for the presence of therapy-related inflammation.
Disclosure: Nothing to disclose

Abstract: EP1762

Type: ePoster

Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments

Alemtuzumab is a pan-lymphocyte depleting anti-CD52 antibody approved as escalation therapy for patients with multiple sclerosis (MS) with clinically or image defined active disease. It has been shown effective in reducing relapse rate and brain volume loss. However concerns have been raised due to its numerous adverse effects. We report a case of severe nervous system inflammatory response following Alemtuzumab infusion.
On March 2017 a 31-year-old woman was referred to our service due to an acute deterioration of her mental status. She had been diagnosed with multiple sclerosis in 2007 after attacks of dizziness and left hemiparesis with typically disseminated T2 lesions fulfilling diagnostic criteria on magnetic resonance imaging (MRI) and oligoclonal band (OCB) positivity on cerebrospinal fluid analysis. Despite the use of several immunomodulatory therapies - interferon beta-1a, glatiramer acetate, cyclophosphamide and natalizumab- the patient maintained frequent relapses and persistent disease activity on MRI. Alemtuzumab was first infused in January of 2017 and in March 2017 the patient presented with severe trigeminal neuralgia, marked cognitive impairment including apraxia and left-dominant tetraparesis. The MRI showed two new lesions on T1 weighted image with ring contrast enhancement in periventricular white matter, thickening and enhancement of nerve roots in bulbar (V, VII and XI nerves) and cervical segments. Infection was ruled out and the patient received 5000mg of methylprednisolone which led to marked clinical and radiological improvement.
The reported case illustrates an exacerbated inflammatory response observed after Alemtuzumab infusion. The response seen in our patient is consistent with the time-frame in which B-cell repopulation and peripheral expansion occur following alemtuzumab treatment, therefore further cases might be identified. As such, we suggest that apparent relapses after alemtuzumab treatment should be promptly screened by MRI for the presence of therapy-related inflammation.
Disclosure: Nothing to disclose

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