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中国经典型多发性硬化患者β干扰素-1b治疗前后血清尿酸水平

徐雁 刘彩燕 张遥 孔令燕 冯逢 金征宇 崔丽英

徐雁, 刘彩燕, 张遥, 孔令燕, 冯逢, 金征宇, 崔丽英. 中国经典型多发性硬化患者β干扰素-1b治疗前后血清尿酸水平[J]. 协和医学杂志, 2012, 3(3): 282-286. doi: 10.3969/j.issn.1674-9081.2012.03.008
引用本文: 徐雁, 刘彩燕, 张遥, 孔令燕, 冯逢, 金征宇, 崔丽英. 中国经典型多发性硬化患者β干扰素-1b治疗前后血清尿酸水平[J]. 协和医学杂志, 2012, 3(3): 282-286. doi: 10.3969/j.issn.1674-9081.2012.03.008
Yan XU, Cai-yan LIU, Yao ZHANG, Ling-yan KONG, Feng FENG, Zheng-yu JIN, Li-ying CUI. Serum Uric Acid Levels in Chinese Patients with Classic Multiple Sclerosis: Before and After Treatment with Interferon-beta 1b[J]. Medical Journal of Peking Union Medical College Hospital, 2012, 3(3): 282-286. doi: 10.3969/j.issn.1674-9081.2012.03.008
Citation: Yan XU, Cai-yan LIU, Yao ZHANG, Ling-yan KONG, Feng FENG, Zheng-yu JIN, Li-ying CUI. Serum Uric Acid Levels in Chinese Patients with Classic Multiple Sclerosis: Before and After Treatment with Interferon-beta 1b[J]. Medical Journal of Peking Union Medical College Hospital, 2012, 3(3): 282-286. doi: 10.3969/j.issn.1674-9081.2012.03.008

中国经典型多发性硬化患者β干扰素-1b治疗前后血清尿酸水平

doi: 10.3969/j.issn.1674-9081.2012.03.008
详细信息
    通讯作者:

    崔丽英 电话:010-69156373, E-mail:pumchcly@yahoo.com.cn

  • 中图分类号: R741

Serum Uric Acid Levels in Chinese Patients with Classic Multiple Sclerosis: Before and After Treatment with Interferon-beta 1b

More Information
  • 摘要:   目的  探讨中国经典型多发性硬化(classical multiple sclerosis, CMS)患者β干扰素-1b治疗前后血清尿酸(uric acid, UA)水平的变化及其与复发率、扩展残疾状态评分(Expanded Disability Status Scale, EDSS)和颅内增强病灶(contrast-enhancing lesions, CELs)数目间的关系。  方法  12例CMS患者(10例女性, 2例男性, 年龄:24~54岁)被纳入至一项为期6个月的疗效观察研究。在疾病缓解期, 给予β干扰素-1b(250 μg, 皮下注射, 隔日1次)治疗。治疗前后评估患者EDSS评分、年复发次数、颅内CELs数目和血清UA水平。  结果  治疗后, 患者年复发次数(0.0比0.9, P=0.011)和颅内CELs数目(0.0比1.5, P=0.007)较治疗前明显减低; EDSS评分有降低趋势(2.0比2.8), 但差异无统计学意义(P=0.064);血清UA水平从222.2 μmol/L升高至234.9 μmol/L, 但差异亦无统计学意义(P=0.213)。进一步研究发现, 血清UA水平升高与颅内CELs数目减低显著相关(r=-0.716, P=0.009)。  结论  血清UA水平有可能成为评估CMS患者对β干扰素-1b治疗反应的一个监测指标。
  • 图  1  血清尿酸水平升高与颅内增强病灶数目减少显著相关(r = -0. 716,P =0. 009)

    表  1  β干扰素-1b对患者EDSS、年复发次数、颅内增强病灶数目及血清尿酸水平的影响

    时间 EDSS (中位数) 年复发次数(中位数) 颅内增强病灶数目(中位数) 尿酸(μmol/L,x ± s)
    治疗前(缓解期) 2.8 0.9 1.5 222. 2 ± 28. 9
    治疗后6个月 2.0 0.0 0.0 239. 4 ± 48. 7
    P 0.064 0.011 0.007 0.213
    EDSS:扩展残疾状态评分
    下载: 导出CSV
  • [1] Liu JS, Zhao ML, Brosnan CF, et al. Expression of inducible nitric oxide synthase and nitrotyrosine in multiple sclerosis lesions[J]. Am J Pathol, 2001, 158:2057-2066. doi:  10.1016/S0002-9440(10)64677-9
    [2] Tran EH, Hardin-Pouzet H, Verge G, et al. Astrocytes and microglia express inducible nitric oxide synthase in mice with experimental allergic encephalomyelitis[J]. J Neuroimmunol, 1997, 74:121-129. doi:  10.1016/S0165-5728(96)00215-9
    [3] Mitrovic B, Ignarro LJ, Montestruques S, et al. Nitric oxide as a potential pathological mechanism in demyelination:its differential effects on primary glial cells in vitro[J]. Neuroscience, 1994, 61:575-585. doi:  10.1016/0306-4522(94)90435-9
    [4] Squadrito GL, Cueto R, Splenser AE, et al. Reaction of uric acid with peroxynitrite and implications for the mechanism of neuroprotection by uric acid[J]. Arch Biochem Biophys, 2000, 376:333-337. doi:  10.1006/abbi.2000.1721
    [5] Scott GS, Spitsin SV, Kean RB, et al. Therapeutic intervention in experimental allergic encephalomyelitis by administration of uric acid precursors[J]. Proc Natl Acad Sci U S A, 2002, 99:16303-16308. doi:  10.1073/pnas.212645999
    [6] Hooper DC, Spitsin K, Kean RB, et al. Uric acid, a natural scavenger of peroxynitrite, in experimental allergic encephalomyelitis and multiple sclerosis[J]. Proc Natl Acad Sci U S A, 1998, 95:675-680. doi:  10.1073/pnas.95.2.675
    [7] Zamani A, Rezaei A, Khaeir F, et al. Serum and cerebrospinal fluid uric acid levels in multiple sclerosis patients[J]. Clin Neurol Neurosurg, 2008, 110:642-643. doi:  10.1016/j.clineuro.2008.03.002
    [8] Sotgiu S, Pugliatti M, Sanna A, et al. Serum uric acid and multiple sclerosis[J]. Neurol Sci, 2002, 23:183-188. doi:  10.1007/s100720200059
    [9] Rentzos M, Nikolaou C, Anagnostouli M, et al. Serum uric acid and multiple sclerosis[J]. Clin Neurol Neurosurg, 2006, 108:527-531. doi:  10.1016/j.clineuro.2005.08.004
    [10] Spitsin S, Hooper DC, Mikheeva T, et al. Uric acid levels in patients with multiple sclerosis:analysis in mono- and dizygotic twins[J]. Mult Scler, 2001, 7:165-166. doi:  10.1177/135245850100700305
    [11] Toncev G, Milicic B, Toncev S, et al. Serum uric acid levels in multiple sclerosis patients correlate with activity of disease and blood-brain barrier dysfunction[J]. Eur J Neurol, 2002, 9:221-226. doi:  10.1046/j.1468-1331.2002.00384.x
    [12] Mostert JP, Ramsaransing SM, Heersema DJ, et al. Serum acid levels and leukocyte nitric oxide production in multiple sclerosis patients outside relapses[J]. J Neurol Sci, 2005, 231:41-44. doi:  10.1016/j.jns.2004.12.008
    [13] Kastenbauer S, Kieseier BC, Becker BF. No evidence of increased oxidative degradation of urate to allantoin in the CSF and serum of patients with multiple sclerosis[J]. J Neurol, 2005, 252:611-612. doi:  10.1007/s00415-005-0697-z
    [14] Ramsaransing GSM, Heersema DJ, De Keyser J. Serum uric acid, dehydroepiandrosterone sulphate, and apolipoprotein E genotype in benign vs. progressive multiple sclerosis[J]. Eur J Neurol, 2005, 12:514-518. doi:  10.1111/j.1468-1331.2005.01009.x
    [15] Drulovic J, Dujmovic I, Stojsavljevic N, et al. Uric acid levels in sera from patients with multiple sclerosis[J]. J Neurol, 2001, 248:121-126. doi:  10.1007/s004150170246
    [16] Karg E, Klivenyi P, Nemeth I, et al. Nonenzymatic antioxidants of blood in multiple sclerosis[J]. J Neurol, 1999, 246:533-539. doi:  10.1007/s004150050399
    [17] Peng F, Zhang B, Zhong X, et al. Serum uric acid levels of patients with multiple sclerosis and other neurological diseases[J]. Mult Scler, 2008, 14:188-196. doi:  10.1177/1352458507082143
    [18] Constantinescu C, Freitag P, Kappos L. Increase in serum levels of uric acid, endogenous antioxidant, under treatment with glatiramer acetate for multiple sclerosis[J]. Mult Scler, 2000, 6:378-381. doi:  10.1177/135245850000600603
    [19] Guerrero AL, Martín-Polo J, Laherrán E, et al. Variation of serum uric acid levels in multiple sclerosis during relapses and immunomodulatory treatment[J]. Eur J Neurol, 2008, 15:394-397. doi:  10.1111/j.1468-1331.2008.02087.x
    [20] Polman CH, Reingold SC, Edan G, et al. Diagnostic criteria for multiple sclerosis:2005 revisions to the "McDonald Criteria"[J]. Ann Neurol, 2005, 58:840-846. doi:  10.1002/ana.20703
    [21] Lövblad KO, Anzalone N, Dörfler A, et al. MR imaging in multiple sclerosis:review and recommendations for current practice[J]. AJNR Am J Neuroradiol, 2010, 31:983-989. doi:  10.3174/ajnr.A1906
    [22] Mowry EM, Beheshtian A, Waubant E, et al. Quality of life in multiple sclerosis is associated with lesion burden and brain volume measures[J]. Neurology, 2009, 72:1760-1785. doi:  10.1212/WNL.0b013e3181a609f8
    [23] Brex PA, Molyneux PD, Smiddy P, et al. The effect of IFN beta-1b on the evolution of enhancing lesions in secondary progressive MS[J]. Neurology, 2001, 57:2185-2190. doi:  10.1212/WNL.57.12.2185
    [24] Milanese C, Mantia LL, Palumbo R, et al. A post-marketing study on interferon-beta 1b and 1a treatment in relapsingremitting multiple sclerosis:different response in drop-outs and treated patients[J]. J Neurol Neurosurg Psychiatry, 2003, 74:1689-1692. doi:  10.1136/jnnp.74.12.1689
    [25] Barkhof F, Polman CH, Radue EW, et al. Magnetic resonance imaging effects of interferon beta-1b in the BENEFIT study:integrated 2-year results[J]. Arch Neurol, 2007, 64:1292-1298. doi:  10.1001/archneur.64.9.1292
    [26] Gaindh D, Jeffries N, Ohayon J, et al. The effect of interferon beta-1b on size of short-lived enhancing lesions in patients with multiple sclerosis[J]. Expert Opin Biol Ther, 2008, 8:1823-1829. doi:  10.1517/14712590802510629
    [27] Khan OA, Tselis AC, Kamholz JA, et al. A prospective, open-label treatment trial to compare the effect of IFNβ-1a (Avonex), IFNβ-1b (Betaseron), and glatiramer acetate (Copaxone) on the relapse rate in relapsing-remitting multiple sclerosis[J]. Eur J Neurol, 2001, 8:141-148. doi:  10.1046/j.1468-1331.2001.00189.x
    [28] Etemadifar M, Janghorbani M, Shaygannejad V. Comparison of Betaferon, Avonex, and Rebif in treatment of relapsing-remitting multiple sclerosis[J]. Acta Neurol Scand, 2006, 113:283-287. http://europepmc.org/abstract/MED/16629762
    [29] Flechter S, Vardi J, Finkelstein Y, et al. Cognitive dysfunction evaluation in multiple sclerosis patients treated with interferon beta-1b:an open-label prospective 1 year study[J]. Isr Med Assoc J, 2007, 9:457-459. http://www.ncbi.nlm.nih.gov/pubmed/17642394
    [30] Lily O, McFadden E, Hensor E, et al. Disease-specific quality of life in multiple sclerosis:the effect of disease modifying treatment[J]. Mult Scler, 2006, 12:808-813. doi:  10.1177/1352458506070946
    [31] Trojano M, Paolicelli D, Zimatore GB, et al. The IFNbeta treatment of multiple sclerosis (MS) in clinical practice:the experience at the MS Center of Bari, Italy[J]. Neurol Sci, 2005, 26:S179-S182. doi:  10.1007/s10072-005-0511-9
    [32] Trojano M, Liguori M, Paolicelli D, et al. Interferon beta in relapsing-remitting multiple sclerosis:an independent postmarketing study in southern Italy[J]. Mult Scler, 2003, 9:451-457. doi:  10.1191/1352458503ms948oa
    [33] Flechter S, Vardi J, Pollak L, et al. Comparison of glatiramer acetate (Copaxone) and interferon beta-1b (Betaferon) in multiple sclerosis patients:an open-label 2-year follow-up[J]. J Neurol Sci, 2002, 197:51-55. doi:  10.1016/S0022-510X(02)00047-3
    [34] Grossman RI, Braffman BH, Brorson JR, et al. Multiple sclerosis:serial study of gadolinium-enhanced MR imaging[J]. Radiology, 1988, 169:117-122. doi:  10.1148/radiology.169.1.3420246
    [35] Jimenez J, Jy W, Mauro LM, et al. Elevated endothelial microparticle-monocyte complexes induced by multiple sclerosis plasma and the inhibitory effects of interferon-beta 1b on release of endothelial microparticles, formation and transendothelial migration of monocyte-endothelial microparticle complexes[J]. Mult Scler, 2005, 11:310-315. doi:  10.1191/1352458505ms1184oa
    [36] Minagar A, Long A, Ma T, et al. Interferon (IFN) -beta 1a and IFN-beta 1b block IFN-gamma-induced disintegration of endothelial junction integrity and barrier[J]. Endothelium, 2003, 10:299-307. doi:  10.1080/10623320390272299
    [37] Trojano M, Defazio G, Avolio C, et al. Effects of rIFN-beta-1b on serum circulating ICAM-1 in relapsing remitting multiple sclerosis and on the membrane-bound ICAM-1 expression on brain microvascular endothelial cells[J]. J Neurovirol, 2000, 6(Suppl 2):S47-S51. http://www.ncbi.nlm.nih.gov/pubmed/10871785
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  • 收稿日期:  2012-05-03
  • 刊出日期:  2012-07-30

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