Activated microglial cells start producing a number of cytokines such as IL-6, which plays an important role in the development of neuropathic pain [56]. antiCIL-6 therapies in ameliorating neuropathic pain in the clinical setting is controversial; a reduction in pain intensity has been reported with an antiCIL-6 antibody in four studies, namely a case report, a pilot study, a retrospective observational study, and a case series. Pain intensity was evaluated using a numerical rating scale (NRS), with a lower score indicating lesser pain. A reduction in the NRS score was reported in all four studies. However, Butylscopolamine BR (Scopolamine butylbromide) in two randomized controlled trials of another antiCIL-6R antibody, the change in the visual analog scale pain score was not statistically significantly different when compared with placebo. This was attributed to the low mean pain score at baseline in both the trials and the concomitant use of medications for pain in one of the trials, which may have masked the effects of the antiCIL-6R antibody on Butylscopolamine BR (Scopolamine butylbromide) neuropathic pain. Conclusion Thus, antiCIL-6 therapies might have a potential to reduce neuropathic pain, but further investigations are warranted to clarify the Tnf effect of inhibition of IL-6 signaling on neuropathic pain associated with MS and NMOSD. = 2), acute enterocolitis (= 2), acute pyelonephritis (= 1), leukocytopenia, and/or lymphocytopenia (= 3), anemia (= 2), and a slight decline in SBP (= 1)Ringelstein et al., 2015 (ROS) [22] Eight female patients with highly active AQP4-Ab-seropositive NMO (= 6) or NMOSD (= 2)Immunomodulatory or immunosuppressant therapy (e.g., rituximab, interferon beta-1, AZA)6C8 mg/kg at a 4- to 6-week interval followed up to 10C51 monthsNRS, median ((IQR): 6.5 (5.0C7.0)NRS, median (IQR): 2.5 (0.3C4.5) (= 0.02) 7/8 patients had less pain at the last follow-up, with two of them completely pain free Mild post infusion nausea (= 1), transient gastritis (= 1), transient diarrhea (= 1), headache (= 1), fatigue (= 2), recurrent urinary tract infections (= 3), deep venous thrombosis (= 1), transient mild liver enzyme increase (= 3), recurrent CRP elevation (= 1), leukopenia or neutropenia (= 2) and elevation of cholesterol levels (= 6) Araki, 2019 (CS) [23]19 patients with refractory NMOSDCorticosteroids and/or immunosuppressantsDose not specified; monthly infusion up to 6 years and 8 monthsNRS, mean SD: 3.2 2.2NRS at 1 year after treatment: 1.7 2.6 (< 0.001) In one patient with comorbid SLE, severe neuropathic pain disappeared Not reportedYamamura et al., 2019 (CT) [24]83 patients with AQP4-Ab- seropositive or AQP4-Ab- seronegative NMOSD: satralizumab, 41; placebo, 42Oral glucocorticoids, AZA, MMF, AZA + glucocorticoids, and MMF+oral glucocorticoids120 mg s.c. at weeks 0, 2, and 4 and every 4 weeks during the double-blind Butylscopolamine BR (Scopolamine butylbromide) periodaVAS (mean SD Satralizumab group: 27.6 28.2 Placebo group: 34.6 26.1 The between-group difference in the change in the mean VAS pain score was 4.08 (95% CI, ? 8.44 to 16.61, = 0.52)Satralizumab vs placebo (%): Infection (68% vs 62%), IRR Butylscopolamine BR (Scopolamine butylbromide) (12% vs 5%), neoplasmb (7% vs 7%), and serious infection (5% vs 7%)Traboulsee et al, 2020 (CT) [25]95 patients with AQP4-Ab- seropositive or AQP4-Ab-seronegative NMOSD: satralizumab,63; placebo, 32Previous: B-cell depleting therapy and immunosuppressants. Analgesics were permitted during satralizumab therapy120 mg s.c. Butylscopolamine BR (Scopolamine butylbromide) at weeks 0, 2, and 4 and every 4 weeks thereafter in the double-blind period (maximal duration of 1 1.5 years after the random assignment of the last patient enrolled)VAS (mean SD) Satralizumab group: 31.7 28.9 Placebo group: 27.6 30.8 The adjusted mean of the.
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