SC08 Does Low Vitamin D3 Confer a Greater Risk For Relapse In ADEM: A Pediatric Case Series

Thursday, May 30, 2013
Allen DeSena, MD, MPH , Neurology & Neurotherapeutics - MS Clinic, UT Southwestern Medical Center, Dallas, TX
Donna C Graves, MD , Neurology & Neurotherapeutics - MS Clinic, UT Southwestern Medical Center, Dallas, TX
Benjamin Greenberg, MD, MHS , Children's Medical Center, Dallas, TX

Background: Vitamin D3, the activated form of which is vitamin 1,25, is becoming an increasingly recognized factor in autoimmune diseases.  In both murine and rat models, it has been demonstrated to have multiple impacts modulating immune system function to suppress acute activity and reduce risk of relapses in experimental allergic encephalomyelitis.  In addition, clinical trials and other observational studies have shown benefit with higher levels of vitamin D3 in reducing risk for relapses in multiple sclerosis, although it has not been extensively studied acutely or subacutely.1-10 Furthermore, there is a paucity of data with respect to vitamin D3 and acute disseminated encephalomyelitis and idiopathic transverse myelitis, both of which are typically monophasic autoimmune inflammatory events.  Because both of these disorders can lead to permanent neurologic disability, potential beneficial acute impact of vitamin D3 would be especially relevant.  

Objectives: To describe contrasting cases of acute disseminated encephalomyelitis with low and normal vitamin D3 with respect to their clinical courses.

Methods: None or not applicable.

Results: We describe 3 cases of acute disseminated encephalomyelitis with relapses within 12 weeks of onset, all of which had low vitamin D3 levels at presentation or briefly following hospitalization that we suspect may be related to risk for relapses in acute disseminated encephalomyelitis.   In all 3 of these cases, the patients had vitamin D3 levels < 20 ng/mL either at presentation or shortly following their hospitalization; all 3 of these patients had radiologic and clinical progression of their disease, 2 of which failed first-line therapies of intravenous methylprednisolone and subsequently required plasma exchange, intravenous immunoglobulin, and intravenous cyclophosphamide.  In this series, we present a detailed timeline of their presenting symptoms and their imaging as they progressed.  We contrast these cases with 2 patients with monophasic acute disseminated encephalomyelitis: one patient with a normal level and another patient with an initial low level that was normal following supplementation.  Both of these patients responded well to high-dose intravenous methylprednisolone and plasma exchange in combination.  

Conclusions: To our knowledge, this is the first report discussing low vitamin D3 levels as a risk factor for recurrence within 12 weeks of acute disseminated encephalomyelitis, and we feel it is something that should be studied in a larger series of patients as acute or subacute supplementation of vitamin D3 would be a potentially easily modifiable risk factor for acute disseminated encephalomyelitis.

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