Due to poor response, she was subsequently treated with two cycles of alemtuzumab 12 months apart. She was diagnosed with MS and treated with beta interferon followed by natalizumab. Her past medical history included alopecia totalis, vitiligo, asthma, and psoriasis. These cases highlight that (a) MOGAD can be misdiagnosed as MS and, (b) alemtuzumab may be ineffective in MOGAD.Ī Caucasian woman in her early thirties presented with numbness of left arm and tongue as well as left-sided ptosis followed by another episode of left arm, leg, and trunk numbness, urinary frequency, and vertigo five months later. The diagnosis of MOGAD was finally established with antibody testing by flow cytometry live cell-based assay. We present three cases of anti-MOG encephalomyelitis initially diagnosed as MS and treated with alemtuzumab followed by multiple relapses and worsening disability on alemtuzumab. MOGAD is an autoimmune condition characterised by the synthesis of IgG antibodies against MOG, a glycoprotein found on the outer membrane of the myelin sheath in the central nervous system. While bilateral ON and longitudinally extensive TM are more characteristic presentations in MOGAD, the phenotypes that do overlap with MS include unilateral ON and short TM. Typically, these patients present with optic neuritis (ON) (bilateral ON more frequent than unilateral ON), acute demyelinating encephalomyelitis (ADEM), transverse myelitis (TM), and cortical seizures in the absence of brain lesions consistent with MS. MOG antibody-associated disease (MOGAD) is one of the demyelinating diseases that can be misdiagnosed as MS. Moreover, it has recently been reported that alemtuzumab can also induce diffuse alveolar bleeding. A well-established adverse effect of alemtuzumab therapy is the emergence of secondary autoimmune conditions such as Graves’ disease and immune thrombocytopenia. Similarly confirmed disability worsening (CDW) was reduced by 70% in patients receiving alemtuzumab compared with those in the IFNB-1a group, highlighting the very effective therapeutic potential of alemtuzumab in the treatment of RRMS. At 3 years, the annualised relapse rate was significantly reduced by 70% in patients who received alemtuzumab compared to IFNB-1a. In the CAMMS223 study, patients with relapsing–remitting MS (RRMS) and Expanded Disability Status Scale (EDSS) score of 0–3 were randomized to treatment with alemtuzumab or interferon beta 1a (IFNB-1a). One of the immunomodulatory medications for the treatment of MS is alemtuzumab, a monoclonal antibody that leads to reduced levels of T and B lymphocytes via its targeting of the cell-surface glycoprotein CD52. It can be misdiagnosed with other demyelinating disorders due to overlapping imaging features and clinical presentations, which can vary widely between different patients and within the same patient over time. Multiple sclerosis (MS) is a demyelinating disease of the central nervous system with a characteristic clinical and radiological profile. These cases highlight that if a patient suspected to have MS does not respond to conventional treatments such as alemtuzumab, a search for alternative diagnoses such as MOG antibody disease may be warranted. Subsequently, all three cases were found to have anti-MOG antibody in their serum. Unexpectedly, all three patients did quite poorly on this medication, with a decline in their clinical status with worsening of expanded disability status scale (EDSS) and an increasing lesion load on magnetic resonance imaging of the brain. We present three cases initially diagnosed as MS and then treated with alemtuzumab. Thus, clinically and radiologically, MOGAD can mimic MS and clinical vigilance is required for accurate diagnostic workup. However, the presence of clinical phenotypes including unilateral ON and short TM in some patients with MOGAD may lead to their misdiagnosis as MS. ADEM phenotype is the most common presentation of MOGAD in children. Myelin Oligodendrocyte Glycoprotein antibody-associated disease (MOGAD) is most classically associated in both children and adults with phenotypes including bilateral and recurrent optic neuritis (ON) and transverse myelitis (TM), with the absence of brain lesions characteristic of multiple sclerosis (MS).
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