Hospital Fundación Favaloro

Author Of 1 Presentation

Neuromyelitis Optica and Anti-MOG Disease Poster Presentation

P0682 - Aggressive and fulminant course of Anti-myelin oligodendrocyte glycoprotein antibody associated disease in a solid organ receptor (ID 1514)

Speakers
Presentation Number
P0682
Presentation Topic
Neuromyelitis Optica and Anti-MOG Disease

Abstract

Background

Anti-myelin oligodendrocyte glycoprotein (MOG) antibody (ab)-associated disease or MOG-IgG-associated encephalomyelitis (MOG-EM) was previously considered a benign entity but mounting evidence shows there are patients who experience severe and frequent relapses and ultimately acquire significant neurological disability.

There are some evidence about (MOG-EM) in hematopoietic receptors, with good prognosis, but these information is limited in solid organ receptors.

Objectives

To describe a case of MOG EM with aggressive course treated with steroids, azathioprine and rituximab in a solid organ receptor

Methods

We report a case of MOG EM with aggressive course treated with steroids, azathioprine and rituximab in a kidney organ recipient.

Results

He was diagnosed with a haemolytic uremic syndrome during his childhood, so he progressed to end stage kidney failure. At age of 20 he received a kidney transplant from his mother and a second new transplant at age 29 was indicated due to solid organ rejection. In the following months, a malign mammary nodule appeared so he was under tamoxifen for the next year. At 38 yo, he presented to the emergency department referred a 15-days-history of bilateral optic neuritis(ON) without other focal signs at the neurological exam and under treatment with deltisone, cyclosporine and micofenolate for immunosuppression, enalapril, and lovastatine. Acute renal failure was detected due to kidney confirmed through biopsy. Brain MRI and Lumbar puncture were made, CSF, Anti aqp4 and Anti Mog were unremarkable and treated with methylprednisolone and plasmapheresis. The diagnosis was atypical ON by inmunosupression drugs in the context of decreased glomerular filtrate. His visual acuity improved in the consecutives months. Against he received methylprednisolone and plasmapheresis. Throated out others causes, Azathioprine was started.

A new relapse was presented in few days, showing a long extensive transverse myelitis (LETM) at dorsal levels appeared, without supratentorial lesions; CSF with increased proteins levels, against infectious causes was dismissed, MOG-Ab were positive in CSF and plasma. Steroids, plasmapheresis and rituximab were started. Two months after encephalopathy signs appeared. A new MRI showed acute supratentorial lesion and LETM at cervical levels. A pulmonary sepsis appeared like a complication an instable haemodynamic, so we had a wide range of treatment. The patient died few days after.

Conclusions

MOG EM is a heterogenous sometimes severe disease. We report an aggressive and fulminant form in a previous immunosuppressive patient. We discuss the presence of Anti MOG disease as comorbidity in association to other immunological conditions. The aim of this report is increased the experience in this condition

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