
Contributions
Abstract: P1792
Type: Poster Sessions
Abstract Category: N/A
Background and goals: The presentation of optic neuritis (ON) can be very heterogeneous in visual acuity, computerized visual field, optical coherence tomography. Response to high dose iv corticosteroid treatment can also vary and in some forms prognosis as to visualrecovery can be poor. In multiple sclerosis (MS) ischemic events have been found to coexist with inflammation and are mediated by endothelin-1 (ET-1), a potent vasoconstrictor. Also, in MS a reduced ocular and extraocular blood flow has been reported in patients with high ET-1 titers, and following administration of an ET-1 antagonist an incremented global cerebral blood flow is described. We aimed to disclose an association between ON clinical and morpho-functional features and the serum and cerebrospinal fluid (CSF) concentrations of endothelin (ET)-1 and interleukin (IL)-6, as potential marker of ischemic damage and inflammation respectively.
Methods: ON was defined as 'aggressive' (A-ON) if at least one of the following criteria was met: central visus < 5/10 or central visus > 5/10 but expressed through the search for residual receptive fields; presence of a paracentral scotoma with a single point < 10 dB or with at least 3 adjacent points below 4 dB; presence of a large and deep papillomacular fascicular defect; presence of contemporary phlogistic-ischemic changes of the post-chiasmatic optical pathways; presence of a defect of oculomotion with onset of visual impairment. In all other cases, ON was 'non aggressive' (NA-ON). ET-1 and IL-6 levels were measured in serum and CSF with commercially available ELISA kits.
Results: We identified 16 A-NO and 6 NA-ON. CSF mean concentrations and the CSF/serum ratio of ET-1 were significantly higher in A-ON than in NA-ON (10.55 pg/ml vs. 4 pg/ml, p = 0.011, and 10.64 pg/ml vs 3.80 pg/ml, p=0.008, respectively). No differences were found between A-ON and NA-ON for serum ET-1 levels (8.29 pg/ml vs. 10.70 pg/ml, p=0.369), as well as for serum and CSF IL-6 concentrations (8.75pg / ml vs. 9.60pg / ml, p = 0.572, and 9.41pg / ml vs 6, 5pg / ml, p = 0.572, respectively).
Conclusions: Increased CSF levels of ET-1 are associated with A-ON suggesting that poorprognosis in visual recovery in A-ON lies in ischemic damage and the potential beneficial role of ET-1 antagonists to prevent irreversible ischemic damage in ON.
Future studies are however needed to investigate on the role of ET-1 in relation to markers of inflammation and corticosteroid treatment in MS.
Disclosure: MC: nothing to disclose. GL: nothing to disclose. MVR: nothing to disclose. EB: TEVA, Merck (travel grants); TEVA, Biogen, Genzyme (teaching grants). MLC: TEVA (travel grants); TEVA, Biogen, Genzyme (teaching grants). PP: nothing to disclose. MP: Bayer Schering, Genzyme, Biogen, Merck Serono (Advisory Board); Almirall, Bayer Schering, Biogen Idec, Genzyme, Merck Serono, Novartis, Sanofi-Aventis and Teva Neurosciences (Travel or Speaker honoraria)
Abstract: P1792
Type: Poster Sessions
Abstract Category: N/A
Background and goals: The presentation of optic neuritis (ON) can be very heterogeneous in visual acuity, computerized visual field, optical coherence tomography. Response to high dose iv corticosteroid treatment can also vary and in some forms prognosis as to visualrecovery can be poor. In multiple sclerosis (MS) ischemic events have been found to coexist with inflammation and are mediated by endothelin-1 (ET-1), a potent vasoconstrictor. Also, in MS a reduced ocular and extraocular blood flow has been reported in patients with high ET-1 titers, and following administration of an ET-1 antagonist an incremented global cerebral blood flow is described. We aimed to disclose an association between ON clinical and morpho-functional features and the serum and cerebrospinal fluid (CSF) concentrations of endothelin (ET)-1 and interleukin (IL)-6, as potential marker of ischemic damage and inflammation respectively.
Methods: ON was defined as 'aggressive' (A-ON) if at least one of the following criteria was met: central visus < 5/10 or central visus > 5/10 but expressed through the search for residual receptive fields; presence of a paracentral scotoma with a single point < 10 dB or with at least 3 adjacent points below 4 dB; presence of a large and deep papillomacular fascicular defect; presence of contemporary phlogistic-ischemic changes of the post-chiasmatic optical pathways; presence of a defect of oculomotion with onset of visual impairment. In all other cases, ON was 'non aggressive' (NA-ON). ET-1 and IL-6 levels were measured in serum and CSF with commercially available ELISA kits.
Results: We identified 16 A-NO and 6 NA-ON. CSF mean concentrations and the CSF/serum ratio of ET-1 were significantly higher in A-ON than in NA-ON (10.55 pg/ml vs. 4 pg/ml, p = 0.011, and 10.64 pg/ml vs 3.80 pg/ml, p=0.008, respectively). No differences were found between A-ON and NA-ON for serum ET-1 levels (8.29 pg/ml vs. 10.70 pg/ml, p=0.369), as well as for serum and CSF IL-6 concentrations (8.75pg / ml vs. 9.60pg / ml, p = 0.572, and 9.41pg / ml vs 6, 5pg / ml, p = 0.572, respectively).
Conclusions: Increased CSF levels of ET-1 are associated with A-ON suggesting that poorprognosis in visual recovery in A-ON lies in ischemic damage and the potential beneficial role of ET-1 antagonists to prevent irreversible ischemic damage in ON.
Future studies are however needed to investigate on the role of ET-1 in relation to markers of inflammation and corticosteroid treatment in MS.
Disclosure: MC: nothing to disclose. GL: nothing to disclose. MVR: nothing to disclose. EB: TEVA, Merck (travel grants); TEVA, Biogen, Genzyme (teaching grants). MLC: TEVA (travel grants); TEVA, Biogen, Genzyme (teaching grants). PP: nothing to disclose. MP: Bayer Schering, Genzyme, Biogen, Merck Serono (Advisory Board); Almirall, Bayer Schering, Biogen Idec, Genzyme, Merck Serono, Novartis, Sanofi-Aventis and Teva Neurosciences (Travel or Speaker honoraria)