Contributions
Abstract: EP1559
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Objective: Chi3l1 is a biomarker related to chronic inflammation. It has been described in cancer and chronic inflammation outside the central nervous system (CNS) and it has been shown to be a prognostic biomarker for CIS conversion to CDMS and disease progression. However, scarce information exists regarding its concentration in acute disseminated encephalomyelitis (ADEM).
Aims: Our purpose was to describe Chi3l1 changes in a series of cases of ADEM and compare its concentration with a cross-sectional cohort of Multiple Sclerosis (MS) patients (Valencia cohort).
Methods: Chi3l1 levels were measured in CSF samples in patients with ADEM (n=4) with ELISA assay. CSF samples were obtained within 15 days from disease onset in three patients, and four months after recovery in one. Clinical data were recorded during admision and in the follow up. The obtained concentrations were compared to median values in MS patients (n=156) and historical controls (HC) (n=20) detected with the same methodology. Variability intra-assay CV% was 6,49 and inter-assay 5,18.
Results: Chi3l1 levels were very elevated in the acute episode in the three reported cases (730,00 ng/ml, 1106,00 ng/ml, and 601,90 ng/ml) with a four-fold increase respect to median values in MS patients (134.7 ng/ml, RRMS 115,35, PMS 171,45 ng/ml) including patients with active inflammation (clinical attack or gadolinium-enhancing lesions) in which median values were not significantly elevated (133.15 ng/ml). In the fourth case, after complete clinical recovery, Chi3l1 returned to HC levels. A biopsy performed in one patient in the acute phase showed a dense inflammatory infiltrate composed mainly by TMEM119+/YKL-40+ microglial cells and less prominent CD4+ lymphocytic component.
Conclusion: Our results indicate that acute inflammation occurring in ADEM patients might be related to innate immune response, expressed as Chi3l1 secretion, and that there is a different profile in the inflammation that takes place in clinical attacks in MS, with possible pathogenic implications. Summed to other clinical variables, Chi3l1 levels could be useful for differential diagnosis at first symptoms.
Disclosure: SGP is funded by Health Institute Carlos III Rio Hortega CM12/00014. LCN, JCV, JGM, SC, ME: nothing to disclose. BCE serves on the scientific advisory board for Novartis, Genzyme, TEVA and Merck Pharmaceuticals, and is funded by Health Institute Carlos III, grant number PS13/00663 (BC) and a local grant from Hospital La Fe VlcBiomed (UV/IIS la Fe #33-2015-A). FPM serves on the scientific advisory board for Novartis, Genzyme, TEVA, Almirall, and Roche Pharmaceuticals. CAV serves on the scientific advisory board for Genzyme. FG serves on the scientific advisory board for Genzyme and Roche Pharmaceuticals
Abstract: EP1559
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Objective: Chi3l1 is a biomarker related to chronic inflammation. It has been described in cancer and chronic inflammation outside the central nervous system (CNS) and it has been shown to be a prognostic biomarker for CIS conversion to CDMS and disease progression. However, scarce information exists regarding its concentration in acute disseminated encephalomyelitis (ADEM).
Aims: Our purpose was to describe Chi3l1 changes in a series of cases of ADEM and compare its concentration with a cross-sectional cohort of Multiple Sclerosis (MS) patients (Valencia cohort).
Methods: Chi3l1 levels were measured in CSF samples in patients with ADEM (n=4) with ELISA assay. CSF samples were obtained within 15 days from disease onset in three patients, and four months after recovery in one. Clinical data were recorded during admision and in the follow up. The obtained concentrations were compared to median values in MS patients (n=156) and historical controls (HC) (n=20) detected with the same methodology. Variability intra-assay CV% was 6,49 and inter-assay 5,18.
Results: Chi3l1 levels were very elevated in the acute episode in the three reported cases (730,00 ng/ml, 1106,00 ng/ml, and 601,90 ng/ml) with a four-fold increase respect to median values in MS patients (134.7 ng/ml, RRMS 115,35, PMS 171,45 ng/ml) including patients with active inflammation (clinical attack or gadolinium-enhancing lesions) in which median values were not significantly elevated (133.15 ng/ml). In the fourth case, after complete clinical recovery, Chi3l1 returned to HC levels. A biopsy performed in one patient in the acute phase showed a dense inflammatory infiltrate composed mainly by TMEM119+/YKL-40+ microglial cells and less prominent CD4+ lymphocytic component.
Conclusion: Our results indicate that acute inflammation occurring in ADEM patients might be related to innate immune response, expressed as Chi3l1 secretion, and that there is a different profile in the inflammation that takes place in clinical attacks in MS, with possible pathogenic implications. Summed to other clinical variables, Chi3l1 levels could be useful for differential diagnosis at first symptoms.
Disclosure: SGP is funded by Health Institute Carlos III Rio Hortega CM12/00014. LCN, JCV, JGM, SC, ME: nothing to disclose. BCE serves on the scientific advisory board for Novartis, Genzyme, TEVA and Merck Pharmaceuticals, and is funded by Health Institute Carlos III, grant number PS13/00663 (BC) and a local grant from Hospital La Fe VlcBiomed (UV/IIS la Fe #33-2015-A). FPM serves on the scientific advisory board for Novartis, Genzyme, TEVA, Almirall, and Roche Pharmaceuticals. CAV serves on the scientific advisory board for Genzyme. FG serves on the scientific advisory board for Genzyme and Roche Pharmaceuticals