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The systemic sarcoidosis and multiple sclerosis dilemma: Serum Amyloid A in cerebrospinal fluid as a useful marker to exclude neurosarcoidosis out of the equation
Author(s): ,
M. Reyes-Mantilla
Affiliations:
Neurology-Neuroimmunology, Johns Hopkins University School of Medicine, Baltimore, MD
,
D.J. Kimbrough
Affiliations:
Neurology-Neuroimmunology, Johns Hopkins University School of Medicine, Baltimore, MD; Neurology-Neuroimmunology, Partners Multiple Sclerosis Center, Harvard Medical School, Boston, MA, United States
,
P.A. Calabresi
Affiliations:
Neurology-Neuroimmunology, Johns Hopkins University School of Medicine, Baltimore, MD
C.A. Pardo-Villamizar
Affiliations:
Neurology-Neuroimmunology, Johns Hopkins University School of Medicine, Baltimore, MD
ECTRIMS Online Library. Reyes-Mantilla M. Oct 12, 2018; 228889
Maria Reyes-Mantilla
Maria Reyes-Mantilla
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Abstract: P1048

Type: Poster Sessions

Abstract Category: Clinical aspects of MS - Comorbidity

Background: In patients with systemic sarcoidosis, the attribution of neurological symptoms to other neurological disorders besides neurosarcoidosis (NS) is challenging. Previous work has outlined the potential role of serum amyloid A(SAA), an innate regulator of the granulomatous inflammation, as a more sensitive and specific biomarker of NS.
Goals of the study: To evaluate the coexistence of systemic sarcoidosis in multiple sclerosis (MS/systemic sarcoidosis) patients and to examine the diagnostic value of SAA, a novel biomarker for neurosarcoidosis, in this group of patients.
Methods: Retrospective records review of patients with systemic sarcoidosis and multiple sclerosis (MS) referred to the Johns Hopkins Hospital between 2000 and 2018. SAA levels in cerebrospinal fluid (CSF) were measured by enzyme-linked immunosorbent assay (ELISA).
Results: Thirteen patients were diagnosed with MS and systemic sarcoidosis based on clinical criteria. Three clinical scenarios were identified regarding this diagnostic association: 46% (n=6) first developed MS, 38.4% (n=5) first developed systemic sarcoidosis and the remaining 15.6% (n=2) had a simultaneous diagnosis of both entities. Patients with initial MS, were exposed to glatiramer acetate (n=4), type I interferons (n=4), natalizumab (n=2) and daclizumab (n=2). SAA in CSF was measured in patients with NS (n = 41), MS (n = 20), MS/systemic sarcoidosis (n = 6) and neuromyelitis optica (NMO) (n =15). The median concentrations were 37.2, 2.27, 5.27 and 3.94 ng/ml respectively. SAA in the MS samples was significantly lower compared with NS (p< 0.0001) but not different from MS/systemic sarcoidosis (p=0.57) or NMO (p=0.49).
Conclusions: Systemic sarcoidosis can either follow diagnosis of MS or precede it. CSF SAA measurement may be useful to distinguish neurosarcoidosis from MS in the setting of systemic sarcoidosis.
Disclosure: Maria I Reyes-Mantilla: Nothing to disclose
Carlos Pardo-Villamizar: Nothing to disclose
Peter A. Calabresi has received personal compensation for activities with Abbott and Vertex as a consultant. Dr. Calabresi has received research support from Novartis, MedImmune and Biogen.
Dorlan Kimbrough: Dr. Kimbrough is a previous participant in the National Institutes of Health T32 Training Program at Johns Hopkins University; has received a previous educational grant from Teva; and has received consulting fees from Medical Logix LLC.

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