Infection Risk in Patients on Multiple Sclerosis Therapeutics
详细信息 查看全文
- 作者：Eric M. Williamson (1)
Joseph R. Berger (1)
1. Division of Multiple Sclerosis ; Department of Neurology ; Perelman School of Medicine ; University of Pennsylvania ; 3400 Spruce Street ; 3 Gates Building ; Philadelphia ; PA ; 19104 ; USA - 刊名：CNS Drugs
- 出版年：2015
- 出版时间：March 2015
- 年：2015
- 卷：29
- 期：3
- 页码：229-244
- 全文大小：443 KB
- 参考文献：1. Weinshenker, BG, Bass, B, Rice, GPA (1989) The natural history of multiple sclerosis: a geographically based study. I: clinical course and disability. Brain. 112: pp. 133-146
2. Polman, CH, Reingold, SC, Banwell, B (2011) Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol. 69: pp. 292-302
3. Murta, V, Ferrari, CC (2013) Influence of peripheral inflammation on the progression of multiple sclerosis: evidence from the clinic and experimental animal models. Mol Cell Neurosci. 53: pp. 6-13
4. Stadelmann, C, Wegner, C, Bruck, W (2011) Inflammation, demyelination, and degeneration: recent insights from MS pathology. Biochim Biophys Acta 1812: pp. 275-282
5. Sospedra, M, Martin, R (2005) Immunology of multiple sclerosis. Ann Rev Immunol. 23: pp. 683-747
6. Finsten, B, Owens, T (2011) Innate immune responses in central nervous system inflammation. FEBS Lett. 585: pp. 3806-3812
7. Esiri, MM (1980) Multiple sclerosis: a quantitative and qualitative study of immunoglobulin-containing cells in the central nervous system. Neuropathol Appl Neurobiol. 6: pp. 9-21
8. Wootla, B, Denic, A, Keegan, BM (2011) Evidence for the role of B cells and immunoglobulins in the pathogenesis of multiple sclerosis. Neurol Res Int. 2011: pp. 780712
9. Cotran, R, Kumar, V, Tucker, C (1999) Robbins pathologic basis of disease. WB Saunders, Philadelphia
10. Anthony, DC, Couch, Y, Losey, P, Evans, MC (2012) The systemic response to brain injury and disease. Brain Behav Immun. 26: pp. 534-540
11. Sibley, WA, Bamford, CR, Clark, K (1985) Clinical viral infections and multiple sclerosis. Lancet. 1: pp. 1313-1315
12. Andersen, O, Lygner, PE, Bergstrom, T (1993) Viral infections trigger multiple sclerosis relapses: a prospective seroepidemiological study. J Neurol. 240: pp. 417-422
13. Buljevac, D, Flach, HZ, Hop, WCJ (2002) Prospective study on the relation between infections and multiple sclerosis exacerbations. Brain. 125: pp. 952-960
14. Confavreux, C (2002) Infections and the risk of relapse in multiple sclerosis. Brain. 125: pp. 933-934
15. Coles, AJ, Wing, MG, Molyneux, P (1999) Monoclonal antibody treatment exposes three mechanisms underlying the clinical course of multiple sclerosis. Ann Neurol. 46: pp. 296-304
16. Correale, J, Fiol, M, Gilmore, W (2006) The risk of relapses in multiple sclerosis during systemic infections. Neurology. 67: pp. 652-659
17. Edwards, LJ, Sharrack, B, Ismail, A (2011) Central inflammation versus peripheral regulation in multiple sclerosis. J Neurol. 258: pp. 1518-1527
18. Mikulkova, Z, Praksova, P, Stourac, P (2011) Imbalance in T-cell and cytokine profiles in patients with relapsing-remitting multiple sclerosis. J Neurol Sci. 300: pp. 135-141
19. Trenova, AG, Manova, MG, Kostadinova, II (2011) Clinical and laboratory study of pro-inflammatory and anti-inflammatory cytokines in women with multiple sclerosis. Folia Med (Plovdiv). 53: pp. 29-35
20. Ysrraelit, MC, Gaitan, MI, Lopez, AS, Correale, J (2008) Impaired hypothalamic-pituitary-adrenal axis activity in patients with multiple sclerosis. Neurology. 71: pp. 1948-1954
21. Hauser, SL, Doolittle, TH, Lincoln, R (1990) Cytokine accumulations in CSF of multiple sclerosis patients: frequent detection of interleukin-1 and tumor necrosis factor but not interleukin-6. Neurology. 40: pp. 1735-1739
22. Racke, MK, Lovett-Racke, AE, Karandikar, NJ (2010) The mechanism of action of glatiramer acetate treatment in multiple sclerosis. Neurology 74: pp. S25-30
23. Loma, I, Heyman, R (2011) Multiple sclerosis: pathogenesis and treatment. Curr Neuropharmacol. 9: pp. 409-416
24. Pucci E, Giuliani G, Solari A, et al. Natalizumab for relapsing remitting multiple sclerosis. Cochrane Database Syst Rev. 2011;(10):CD007621.
25. Saidha, S, Eckstein, C, Calabresi, PA (2012) New and emerging disease modifying therapies for multiple sclerosis. Ann N Y Acad Sci. 1247: pp. 117-137
26. Brinkmann, V, Pinschewer, D, Chiba, K, Feng, L (2000) FTY720: a novel transplantation drug that modulates lymphocyte traffic rather than activation. Trends Pharmacol Sci. 21: pp. 49-52
27. Chun, J, Brinkmann, V (2011) A mechanistically novel, first oral therapy for multiple sclerosis: the development of fingolimod (FTY720, Gilenya). Discov Med. 12: pp. 213-228
28. Gasperini, C, Ruggieri, S (2009) New oral drugs for multiple sclerosis. Neurol Sci. 30: pp. S179-S183
29. Gasperini, C, Ruggieri, S (2011) Emerging oral drugs for relapsing-remitting multiple sclerosis. Expert Opin Emerg Drugs. 16: pp. 697-712
30. Gold, R, Kappos, L, Bar-Or, A (2011) Clinical efficacy of BG-12, an oral therapy, in relapsing remitting multiple sclerosis: data from the phase 3 DEFINE trial. Mult Scler J. 17: pp. S34
31. Killestein, J, Rudick, RA, Polman, CH (2011) Oral treatment for multiple sclerosis. Lancet Neurol. 10: pp. 1026-1034
32. Perry, VH, Newman, TA, Cunningham, C (2003) The impact of systemic infection on the progression of neurodegenerative disease. Nat Rev Neurosci. 4: pp. 103-112
33. Ransohoff, R (2005) Natalizumab and PML. Nat Neurosci. 8: pp. 1275
34. Berger, JR (2010) Progressive multifocal leukoencephalopathy and newer biological agents. Drug Saf. 33: pp. 969-983
35. Doerck, S, Gobel, K, Weise, G (2010) Temporal pattern of ICAM-I mediated regulatory T cell recruitment to sites of inflammation in adoptive transfer model of multiple sclerosis. PLoS One. 5: pp. e15478
36. Schweingruber, N, Reichardt, SD, Luhder, F, Reichardt, HM (2007) Mechanisms of glucocorticoid action and selective glucocorticoid receptor agonists. Mol Cell Endocrinol. 24: pp. 174-182
37. Cutolo, MB, Seriolo, C, Pizzorni, ME (2008) Use of glucocorticoids and risk of infections. Autoimmun Rev. 8: pp. 153-155
38. Delden, C (2006) Infectious risks of immunomodulating therapies in rheumatology [in French]. Rev Med Suisse. 2: pp. 738-740
39. Klein, NC, Go, CH, Cunha, BA (2001) Infections associated with steroid use. Infect Dis Clin North Am. 15: pp. 423-432
40. Stahn, C, Lowenberg, M, Homes, DW, Buttgereit, F (2007) Molecular mechanisms of glucocorticoid action and selective glucocorticoid receptor agonists. Mol Cell Endocrinol. 275: pp. 71-78
41. Spies, CM, Biflsma, JW, Burmester, GR, Buttgereit, F (2010) Pharmacology of glucocorticoids in rheumatoid arthritis. Curr Opin Pharmacol. 10: pp. 302-307
42. Wiendl, H, Toyka, KV, Rieckmann, P (2008) Basic and escalating immunomodulatory treatments in multiple sclerosis: current therapeutic recommendations. J Neurol. 255: pp. 1449-1463
43. Johnson, KP (2012) Glatiramer acetate for treatment of relapsing-remitting multiple sclerosis. Expert Rev Neurother. 12: pp. 371-384
44. Karussis, D (2013) Immunotherapy of multiple sclerosis: the state of the art. Bio Drugs. 27: pp. 113-148
45. Winkelman, A, Loebermann, M, Reisinger, EC, Zettl, UK (2014) Multiple sclerosis treatment and infectious issues: update. Clin Exp Immunol. 175: pp. 425-438
46. Fridkis-Hareli, M, Strominger, JL (1998) Promiscuous binding of synthetic copolymer-1 to purified HLA-DR molecules. J Immunol. 160: pp. 4386-4397
47. Ziemsen, T, Kumpfel, T, Klinkert, WE (2002) Glatiramer acetate-specific T-helper 1-and 2-type cell lines produce BDNF: implications for multiple sclerosis therapy. Brain-derived neurotrophic factor. Brain. 125: pp. 2381-2391
48. Hong, J, Li, N, Zhang, X (2005) Induction of CD4+CD25+ regulatory T cells by copolymer-1 through activation of transcription factor Foxp3. Proc Natl Acad Sci. 102: pp. 6449-6454
49. Johnson, KP, Brooks, BR, Cohen, JA (1995) Copolymer 1 reduces relapse rate and improves disability in relapsing-remitting multiple sclerosis results of a phase III multicenter, double-blind placebo-controlled trial. The Copolymer 1 Multiple Sclerosis Study Group. Neurology. 45: pp. 1268-1276
50. Johnson, KP, Brooks, BR, Cohen, JA (1998) Extended use of glatiramer acetate (Copaxone庐) is well tolerated and maintains its clinical effect on multiple sclerosis relapse rate and degree of disability. Copolymer 1 Multiple Sclerosis Study Group. Neurology. 50: pp. 701-708
51. Marriott, JJ, Miyasaki, JM, Gronseth, G, O鈥機onnor, PW (2010) Evidence report: the efficacy and safety of mitoxantrone (Novantrone庐) in the treatment of multiple sclerosis. Neurology. 74: pp. 1463-1470
52. Martinelli, V, Radaelli, M, Straffi, L (2009) Mitoxantrone: benefits and risks in multiple sclerosis patients. Neurol Sci. 30: pp. S167-S170
53. Millefiorini, E, Gasperini, C, Pozzilli, C (1997) Randomized placebo-controlled trial of mitoxantrone in relapsing-remitting multiple sclerosis: 24-month clinical and MRI outcome. J Neurol. 244: pp. 153-159
54. Edan, G, Miller, D, Clanet, M (1997) Therapeutic effect of mitoxantrone combined with methylprednisolone in multiple sclerosis: a randomised multicentre study of active disease using MRI and clinical criteria. J Neurol Neurosurg Psychiatry. 62: pp. 112-118
55. Hartung, H, Gonsette, R, Konig, N (2002) Mitoxantrone in progressive multiple sclerosis: a placebo-controlled, double-blind, randomised, multicentre trial. Lancet. 360: pp. 2018-2025
56. Leger, OJ, Yednock, TA, Tanner, L (1997) Humanization of a mouse antibody against human alpha-4- integrin: a potential therapeutic for the treatment of multiple sclerosis. Hum Antibodies. 8: pp. 3-16
57. Biogen Idec. Tysabri庐 prescribing information and safety update. Available at: https://medinfo.biogenidec.com/. Accessed 2 Mar 2015.
58. Kleinschmidt-DeMasters, BK, Tyler, KL (2005) Progressive multifocal leukoencephalopathy complicating treatment with natalizumab and interferon beta-1a for multiple sclerosis. N Engl J Med. 353: pp. 369-374
59. Langer-Gould, A, Atlas, SW, Green, AJ (2005) Progressive multifocal leukoencephalopathy in a patient treated with natalizumab. N Engl J Med. 353: pp. 375-381
60. Assche, G, Ranst, M, Sciot, R (2005) Progressive multifocal leukoencephalopathy after natalizumab therapy for Crohn鈥檚 disease. N Engl J Med. 353: pp. 362-368
61. Brooks, BR, Walker, DL (1984) Progressive multifocal leukoencephalopathy. Neurol Clin. 2: pp. 299-313
62. Berger, J, Pall, L, Lanska, D, Whiteman, M (1998) Progressive multifocal leukoencephalopathy in patients with HIV infection. J Neurovirol 4: pp. 59-66
63. Astrom, KE, Mancall, EL, Richardson, EP (1958) Progressive multifocal leukoencephalopathy: a hitherto unrecognized complication of chronic lymphatic leukemia and Hodgkin鈥檚 disease. Brain. 81: pp. 93-111
64. Berger, J, Aksamit, MD, Clifford, D (2013) PML diagnostic criteria consensus statement from the AAN Neuroinfectious Disease Section. Neurology. 80: pp. 1430-1438
65. Berger, J, Khalili, K (2011) The pathogenesis of progressive multifocal leukoencephalopathy. Discov Med. 12: pp. 495-503
66. Bechtel, M, Sanders, C, Bechtel, A (2009) Neurological complications of biologic therapy in psoriasis: a review. J Clin Aesthet Dermatol. 2: pp. 27-32
67. Grinyo, J, Charpentier, B, Medina, J (2010) An integrated safety profile analysis of belatacept in kidney transplant recipients. Transplantation. 90: pp. 1521-1527
68. Nived, O, Bengtsson, AA, Jonsen, A, Sturfelt, G (2008) Progressive multifocal leukoencephalopathy: the importance of early diagnosis illustrated in four cases. Lupus. 17: pp. 1036-1041
69. Kothary, N, Diak, I, Brinker, A (2011) Progressive multifocal leukoencephalopathy associated with efalizumab use in psoriasis patients. J Am Acad Dermatol. 65: pp. 546-551
70. Waggoner, J, Martinu, T, Palmer, S (2009) Progressive multifocal leukoencephalopathy following heightened immunosuppression after lung transplant. J Heart Lung Transplant. 28: pp. 395-398
71. Neff, RT, Hurst, FP, Falta, EM (2008) Progressive multifocal leukoencephalopathy and use of mycophenolate mofetil after kidney transplantation. Transplantation. 86: pp. 1474-1478
72. Gonzalez, H, Bolgert, F, Camporo, P, Leblond, V (1999) Progressive multifocal leukoencephalitis (PML) in three patients treated with standard-dose fludarabine (FAMP). Hematol Cell Ther. 41: pp. 183-186
73. Leonard, S, Hulin, C, Anxionnat, R (2002) Multifocal progressive leukoencephalitis in a patient given fludarabine for chronic lymphoid leukemia [in French]. Rev Neurol (Paris). 158: pp. 1121-1123
74. Saumoy, M, Castells, G, Escoda, L (2002) Progressive multifocal leukoencephalopathy in chronic lymphocytic leukemia after treatment with fludarabine. Leuk Lymphoma. 43: pp. 433-436
75. Lejniece, S, Murovska, M, Chapenko, S (2011) Progressive multifocal leukoencephalopathy following fludarabine treatment in a chronic lymphocytic leukemia patient. Exp Oncol. 33: pp. 239-241
76. Warnatz, K, Peter, HH, Schumacher, M (2003) Infectious CNS disease as a differential diagnosis in systemic rheumatic diseases: three case reports and a review of the literature. Ann Rheum Dis. 62: pp. 50-57
77. Rahmlow, M, Shuster, E, Domnik, J (2008) Leflunomide-associated progressive multifocal leukoencephalopathy. Arch Neurol. 65: pp. 1538-1539
78. Ermis U, Wiesmann M, Nolte K, et al. Fumaric acid-associated progressive multifocal leukencephalopathy (PML), treatment and survival in a patient with psoriasis [abstract no. 84]. In: Presented at Kongress der Deutschen Gesellschaft fur Neurologie mit Fortbidlunsakademie. Nurnberg; 2011.
79. Oosten, B, Killestein, J, Barkhof, F (2013) PML in a patient treated with dimethyl fumarate from a compounding pharmacy. N Engl J Med. 368: pp. 17
80. Biogen Idec. Tecfidera庐 package insert. http://www.tecfidera.com/pdfs/full-prescribing-information.pdf. Accessed 25 Jan 2015.
81. Zaheer, F, Berger, J (2012) Treatment-related progressive multifocal leukoencephalopathy: current understanding and future steps. Ther Adv Drug Saf. 3: pp. 227-239
82. Kappos, L, Bates, D, Hartung, H (2007) Natalizumab treatment for multiple sclerosis: recommendations for patient selection and monitoring. Lancet Neurol. 6: pp. 431-441
83. Bloomgren, G, Richman, S, Hotermans, C (2013) Risk of natalizumab-associated progressive multifocal leukoencephalopathy. N Engl J Med. 366: pp. 1870
84. Fine, AJ, Sorbello, A, Kortepeter, C, Scarazzini, L (2013) Central nervous system herpes simplex and varicella zoster virus infections in natalizumab-treated patients. Clin Infect Dis. 57: pp. 849-852
85. Bourdette, D, Gilden, D (2012) Fingolimod and multiple sclerosis: four cautionary tales. Neurology. 79: pp. 1942-1943
86. Yeung, J, Cauquil, C, Saliou, G (2013) Varicella-zoster virus acute myelitis in a patient with MS treated with natalizumab. Neurology. 80: pp. 1812-1813
87. Bourre, B, Lefaucheur, R, Ahtoy, P (2013) Varicella-zoster virus acute myelitis in a patient with MS treated with natalizumab. Neurology. 81: pp. 1966-1967
88. Kwiatkowski, A, Gallois, J, Bilbault, N (2012) Herpes encephalitis during natalizumab treatment in multiple sclerosis. Mult Scler. 18: pp. 909-911
89. Shenoy, ES, Mylonakis, E, Hurtado, RM, Venna, N (2011) Natalizumab and HSV meningitis. J Neurovirol. 17: pp. 288-290
90. Fragoso, YD, Brooks, JB, Gomes, S, Oliveira, FT, Gama, PD (2013) Report of three cases of herpes zoster during treatment with natalizumab. CNS Neurosci Ther. 19: pp. 280-281
91. Hauser, SL, Waubant, E, Arnold, DL (2008) B-cell depletion with rituximab in relapsing-remitting multiple sclerosis. N Engl J Med. 358: pp. 676-678
92. Hawker, K, O鈥機onnor, P, Freedman, MS (2009) Rituximab in patients with primary progressive multiple sclerosis: results of a randomized double-blind placebo-controlled multicenter trial. Ann Neurol. 66: pp. 460-471
93. Lanini, S, Molloy, AC, Fine, PE (2011) Risk of infection in patients with lymphoma receiving rituximab: systematic review and meta-analysis. BMC Med. 9: pp. 36
94. Carbone, J, Pozo, N, Gallego, A, Sarmiento, E (2011) Immunological risk factors for infection after immunosuppressive and biologic therapies. Expert Rev Anti Infect Ther. 9: pp. 405-413
95. Molloy, E, Calabrese, L (2008) Progressive multifocal leukoencephalopathy in patients with rheumatic diseases: are patients with systemic lupus erythematosus at particular risk?. Autoimmun Rev. 8: pp. 144-146
96. Carson, K, Evens, A, Richey, E (2009) Progressive multifocal leukoencephalopathy after rituximab therapy in HIV-negative patients: a report of 57 cases from the Research on Adverse Drug Events and Reports project. Blood. 113: pp. 4834-4840
97. Genentech Personal Communication. San Francisco: July 18, 2014.
98. Fox, EJ (2010) Alemtuzumab in the treatment of relapsing-remitting multiple sclerosis. Expert Rev Neurother. 10: pp. 1789-1797
99. Klotz, L, Meuth, S, Wiendl, H (2012) Immune mechanisms of new therapeutic strategies in multiple sclerosis: a focus on alemtuzumab. Clin Immunol 142: pp. 25-30
100. Cohen, JA, Coles, AJ, Arnold, DL (2012) Alemtuzumab versus interferon beta 1a as first-line treatment for patients with relapsing-remitting multiple sclerosis: a randomized controlled phase 3 trial. Lancet. 380: pp. 1819-1828
101. Coles, AJ, Twyman, CL, Arnold, DL (2012) Alemtuzumab for patients with relapsing multiple sclerosis after disease-modifying therapy: a randomized controlled phase 3 trial. Lancet. 380: pp. 1829-1839
102. Genzyme. Lemtrada庐 package insert. http://www.tecfidera.com/pdfs/full-prescribing-information.pdf. Accessed 6 Feb 2015.
103. Martin, S, Mart, F, Fiumara, K (2006) Infectious complications associated with alemtuzumab use for lymphoproliferative disorders. Clin Infect Dis. 43: pp. 16-24
104. O鈥橲ullivan, C, Dev, KK (2013) The structure and function of the S1P1 receptor. Trends Pharmaco Sci. 34: pp. 401-412
105. Cohen, JA, Chun, J (2011) Mechanisms of fingolimod鈥檚 efficacy and adverse effects in multiple sclerosis. Ann Neurol. 69: pp. 759-777
106. Kappos, L, Radue, EW, O鈥機onnor, P (2010) A placebo-controlled trial of oral fingolimod in relapsing multiple sclerosis. N Engl J Med. 362: pp. 387-401
107. Cohen, JA, Barkhof, F, Comi, G (2010) Oral fingolimod or intramuscular interferon for relapsing multiple sclerosis. N Engl J Med. 362: pp. 402-415
108. Uccelli, A, Ginocchio, F, Mancardi, GL, Bassetti, M (2011) Primary varicella zoster infection associated with fingolimod treatment. Neurology. 76: pp. 1023-1024
109. Kappos, L, Radue, EW, O鈥機onnor, P (2010) A placebo-controlled trial of oral fingolimod in relapsing multiple sclerosis. N Engl J Med. 362: pp. 387-401
110. Kappos, L, Antel, J, Comi, G (2006) Oral fingolimod (FTY720) for relapsing multiple sclerosis. N Engl J Med. 355: pp. 1124-1140
111. Cohen, JA, Barkhof, F, Comi, G (2010) Oral fingolimod or intramuscular interferon for relapsing multiple sclerosis. N Engl J Med. 362: pp. 402-415
112. Francis, G, Kappos, L, O鈥機onnor, P (2014) Temporal profile of lymphocyte counts and relationship with infections with fingolimod therapy. Mult Scler. 20: pp. 471-480
113. Berger, JR (2013) Varicella vaccination after fingolimod: a case report. Mult Scler Related Dis. 2: pp. 391-394
114. Ferraro, D, Biasi, S, Vitetta, F (2014) Recurrent varicella following steroids and fingolimod in a multiple sclerosis patient. J Neuroimmune Pharmacol. 8: pp. 1059-1061
115. Ratchford, JN, Costello, K, Reich, DS, Calabresi, PA (2013) Varicella-zoster virus encephalitis and vasculopathy in a patient treated with fingolimod. Neurology. 81: pp. 306
116. Kern RZ. Dear healthcare Provider. East hanover, NJ: Novartis (E-mail 17 Feb 2015).
117. Fox, RI, Herrmann, ML, Frangou, CG (1999) Mechanism of action for leflunomide in rheumatoid arthritis. Clin Immunol. 93: pp. 198-208
118. O鈥機onnor, P, Wolinsky, JS, Confavreux, C (2011) Randomized trial of oral teriflunomide for relapsing multiple sclerosis. N Engl J Med. 365: pp. 1293-1303
119. Jenks, KA, Stamp, LK, O鈥橠onnell, JL (2007) Leflunomide-associated infections in rheumatoid arthritis. J Rheumatol. 34: pp. 2201-2203
120. O鈥機onnor, PW, Li, D, Freedman, MS (2006) A phase II study of the safety and efficacy of teriflunomide in multiple sclerosis with relapses. Neurology. 66: pp. 894-900
121. Confavreux, C, Li, DK, Freedman, MS (2012) Long-term follow-up of a phase 2 study of oral teriflunomide in relapsing multiple sclerosis: safety and efficacy results up to 8.5聽years. Mult Scler. 18: pp. 1278-1289
122. Treumer, F, Zhu, K, Glaser, R, Mrowietz, U (2003) Dimethylfumarate is a potent inducer of apoptosis in human T cells. J Invest Dermatol. 121: pp. 1383-1388
123. Stoof, T, Flier, J, Sampat, S (2001) The antipsoriatic drug dimethylfumarate strongly suppresses chemokine production in human keratinocytes and peripheral blood mononuclear cells. Br J Dermatol. 144: pp. 1114-1120
124. Gold, R, Linker, RA, Stangel, M (2012) Fumaric acid and its esters: an emerging treatment for multiple sclerosis with antioxidative mechanism of action. Clin Immunol. 142: pp. 44-48
125. Gold, R, Kappos, L, Arnold, DL (2012) Placebo-controlled phase 3 study of oral BG-12 for relapsing multiple sclerosis. N Engl J Med. 367: pp. 1098-1107
126. Fox, RJ, Miller, DH, Phillips, JT (2012) Placebo-controlled phase 3 study of oral BG-12 or glatiramer in multiple sclerosis. N Engl J Med. 367: pp. 1087-1097
127. Ermis, U, Weis, J, Schulz, JB (2013) PML in a patient treated with fumaric acid. N Engl J Med. 368: pp. 1657-1658
128. Sweetser, MT, Dawson, KT, Bozic, C (2013) Manufacturer鈥檚 response to case reports of PML. N Engl J Med. 368: pp. 1659-1661
129. Bundesinstitut Fur Arzneimittel Und Medizinprodukte (BfArM) [Federal Institute for Drugs and Medical Devices]. Adverse events database 2013. http://www.bfarm.de/DE/Pharmakovigilanz/uaw-db-node.html. Accessed 8 Aug 2013.
130. Keating, M, Kantarjian, H, Talpaz, M (1989) Fludarabine: a new agent with major activity against chronic lymphocytic leukemia. Blood. 74: pp. 19-25
131. Sipe, J (2005) Cladribine for multiple sclerosis: review and current status. Expert Rev Neurother. 5: pp. 721-727
132. Sipe, J (2010) Cladribine tablets: a potential new short-course annual treatment for relapsing multiple sclerosis. Expert Rev Neurother. 10: pp. 365-375
133. Giacomini, PS, Bar-Or, A (2012) Laquinimod in multiple sclerosis. Clin Immunol. 142: pp. 38-43
134. Bruck, W, Wegner, C (2011) Insight into the mechanism of laquinimod action. J Neurol Sci. 306: pp. 173-179
135. Brunmark, C, Runstrom, A, Ohlsson, L (2002) The new orally active immunoregulator laquinimod (ABR-215062) effectively inhibits development and relapses of experimental autoimmune encephalomyelitis. J Neuroimmunol. 130: pp. 163-172
136. Gurevich, M, Gritzman, T, Orbach, R (2010) Laquinimod suppress antigen presentation in relapsing- remitting multiple sclerosis: in-vitro high-throughput gene expression study. J Neuroimmunol. 221: pp. 87-94
137. Polman, C, Barkhof, F, Sandberg-Wollheim, M (2005) Laquinimod in relapsing MS. Treatment with laquinimod reduces development of active MRI lesions in relapsing MS. Neurology. 64: pp. 987-991
138. Comi, G, Pulizzi, A, Rovaris, M (2008) Effect of laquinimod on MRI monitored disease activity in patients with relapsing-remitting multiple sclerosis: a multicentre, randomized, double-blind, placebo-controlled phase IIb study. Lancet. 371: pp. 2085-2092
139. Comi, G, Abramsky, O, Arbizu, T (2010) Oral laquinimod in patients with relapsing-remitting multiple sclerosis: 36-week double-blind active extension of the multi-centre, randomized, double-blind, parallel group placebo-controlled study. Mult Scler. 16: pp. 1360-1366
140. Comi, G, Jeffery, D, Kappos, L (2012) Placebo-controlled trial of oral laquinimod for multiple sclerosis. N Engl J Med. 366: pp. 1000-1009
141. Tony, HP, Burmester, G, Schulze-Koops, H (2011) Safety and clinical outcomes of rituximab therapy in patients with different autoimmune diseases: experience from a national registry (GRAID). Arthritis Res Ther. 13: pp. R75
142. Bielekova, B, Howard, T, Packer, AN (2009) Effect of Anti-CD25 Antibody daclizumab in the inhibition of inflammation and stabilization of disease progression in multiple sclerosis. Arch Neurol. 66: pp. 483-489
143. Bielekova, B (2013) Daclizumab therapy for multiple sclerosis. Neurotherapeutics. 10: pp. 55-67
144. Rose, JW, Burns, JB, Bjorklund, J (2007) Daclizumab phase II trial in relapsing and remitting multiple sclerosis. Neurology. 69: pp. 785-789
145. Wynn, D, Kaufman, M, Montalban, X (2010) Daclizumab in active relapsing multiple sclerosis (CHOICE study): a phase 2, randomized double-blind, placebo-controlled, add-on trial with interferon beta. Lancet Neurol. 9: pp. 381-390
146. Liu J, Wang L, Zhan SY, Xia Y. Daclizumab for relapsing remitting multiple sclerosis. Cochrane Database Syst Rev. 2012; (4): CD008127.
147. Gold, R, Giovannoni, G, Selmaj, K (2013) Daclizumab high-yield process in relapsing-remitting multiple sclerosis (SELECT): a randomized, double-blind, placebo-controlled trial. Lancet. 381: pp. 2167-2175
148. Ryschkewitsch, CF, Jensen, PN, Monaco, MC, Major, EO (2010) JC virus persistence following progressive multifocal leukoencephalopathy in multiple sclerosis patients treated with natalizumab. Ann Neurol. 68: pp. 384-391
149. Plavina, T, Subramanyam, M, Bloomgren, G (2014) Anti-JC virus antibody levels in serum or plasma further define risk of natalizumab-associated progressive multifocal leukoencephalopathy. Ann Neurol. 76: pp. 802-812
150. Winkelman, A, Loebermann, M, Reisinger, EC (2011) Fingolimod treatment for multiple sclerosis patients. What do we do with varicella?. Ann Neurol. 70: pp. 673-674 - 刊物主题：Neurology; Psychopharmacology; Pharmacotherapy; Neurosciences; Psychiatry;
- 出版者：Springer International Publishing
- ISSN：1179-1934
文摘
The interface of multiple sclerosis (MS) and infection occurs on several levels. First, infectious disease has been postulated as a potential trigger, if not cause, of MS. Second, exacerbation of MS has been well-documented as a consequence of infection, and, lastly, infectious diseases have been recognized as a complication of the therapies currently employed in the treatment of MS. MS is a disease in which immune dysregulation is a key component. Examination of central nervous system (CNS) tissue of people affected by MS demonstrates immune cell infiltration, activation and inflammation. Therapies that alter the immune response have demonstrated efficacy in reducing relapse rates and evidence of brain inflammation on magnetic resonance imaging (MRI). Despite the altered immune response in MS, there is a lack of evidence that these patients are at increased risk of infectious disease in the absence of treatment or debility. Links between infections and disease-modifying therapies (DMTs) used in MS will be discussed in this review, as well as estimates of occurrence and ways to potentially minimize these risks. We address infection in MS in a comprehensive fashion, including (1) the impact of infections on relapse rates in patients with MS; (2) a review of available infection data from pivotal trials and postmarketing studies for the approved and experimental DMTs, including frequency, types and severity of infections; and (3) relevant risk minimization strategies, particularly as they pertain to progressive multifocal leukoencephalopathy (PML).