动态增强MRI定量评价强直性脊柱炎骶髂关节炎症活动度的价值

目的探讨动态增强MRI(DCE-MRI)定量评价强直性脊柱炎(AS)炎症活动度的价值。方法收集我院2016年1月～2018年1月24例AS患者的临床和影像学资料,24例经临床病理确诊的AS患者行双侧骶髂关节DCE-MRI检查,运用动态增强专用血流动力学软件测量双侧骶髂关节滑膜病变区定量参数:容积转移常数(Ktrans),采用t检验比较分析滑膜炎症不同活动度组间Ktrans值的差异。结果 24例AS骶髂关节滑膜病变Ktrans值为(1.32±0.08)mL/min,8例滑膜炎症为重度,16例滑膜炎症为轻度。滑膜炎症重度组Ktrans值明显高于轻度组(t=4.07,P0.01)。结论 DCE-MRI的Ktrans值可用于反映AS患者骶髂关节的炎症活动程度。     

中西医结合治疗强直性脊柱炎

目的:观察英平系列中药为主的中西医结合治疗强直性脊柱炎效果。方法:按中医辨证组合使用中成药,结合血疗、钙疗、免疗等治疗患者105例,疗程1年。结果:显效70例(66.67%),有效25例(23.81%),总有效率达90%。结论:辨证组合使用中成药是本治疗方法的特点,符合中医治疗原则,综合治疗更具优势,临床应用效果良好。     

补肾活血方对强直性脊柱炎患者RANKL/OPG表达的影响

目的:观察补肾活血方对强直性脊柱炎(AS)患者细胞核因子-κB受体活化因子配体(RANKL)、护骨素(OPG)的影响。方法:将65例AS患者随机分为2组:西医组(32例)采用柳氮磺胺吡啶治疗;中西医结合组(33例)采用补肾活血方联合柳氮磺胺吡啶治疗,均治疗3月。运用ELISA法测血清RANKL、OPG、骨钙素(OC)、Ⅰ型胶原C端肽(CTX)的表达水平。结果:2组治疗后血清RANKL含量均较治疗前明显下降(P<0.05,P<0.01),OPG含量均较治疗前明显升高(P<0.05),RANKL/OPG比值显著下降(P<0.05,P<0.01)。治疗后2组RANKL、RANKL/OPG比值比较,差异也有显著性意义(P<0.05)。治疗后2组血清OC水平均较治疗前显著升高(P<0.05,P<0.01),CTX水平均较治疗前显著降低(P<0.05,P<0.01),且中西医结合组OC水平变化更为显著(P<0.05)。结论:补肾活血方影响R ANKL/R ANK/OPG系统可能是其阻止AS骨质破坏的作用机理之一。     

施杞从痹论治强直性脊柱炎经验初探

强直性脊柱炎（ankylosing spondylitis,AS）是一种原因不明、以侵犯中轴关节为主的慢性炎症性自身免疫性疾病,属于血清阴性脊柱关节病的一种,多见于青少年男性,具有种族差异性和家族遗传倾向性;病变主要累及骶髂关节、脊柱,引起其强直和纤维化,并伴有不同程度的眼、肺、心血管、肾等多个器官的病变。     

中西医结合长疗程治疗强直性脊柱炎临床分析

目的探讨在强直性脊柱炎临床治疗中运用中西医结合方法的临床效果。方法选取我院2013—2016年收治的90例强直性脊柱炎患者作为本次研究对象,按照治疗方式不同将所选病例分为采取中西医结合治疗的观察组与单纯运用西医治疗的对照组,比较两组治疗效果。结果观察组本次治疗总有效率明显高于对照组,差异有统计学意义(P0.05);治疗后两组患者ESR、CRP均有不同程度地降低,但观察组上述两项指标降低的程度显著优于对照组,差异有统计学意义(P0.05)。结论在强直性脊柱炎临床治疗中采取中西医结合治疗临床效果显著,明显降低患者ESR、CRP指标,值得临床推广应用。     

Angiotensin-Receptor Blockade Improves Inflammation and Endothelial Dysfunction in Ankylosing Spondylitis: ARB-AS Study

Cardiovascular (CV) disease is the leading cause of premature death in ankylosing spondylitis (AS). Atherosclerosis and AS share similar pathogenic mechanisms. The proven benefits of angiotensin-receptor blockers (ARBs) in atherosclerotic cardiovascular disease and their role in immune mediation provide strong rationale to investigate its impact with olmesartan on inflammation and endothelial dysfunction in AS. To investigate the effect of olmesartan on inflammation and endothelial dysfunction in AS. 40 AS patients were randomized to receive 24 weeks of treatment with olmesartan (10 mg/day, n  = 20) and placebo ( n  = 20) as an adjunct to existing stable antirheumatic drugs. Markers of endothelial function included the following: flow-mediated dilation (FMD) assessed by AngioDefender, endothelial progenitor cells (EPCs) estimated by flow cytometry, nitrite (nitric oxide surrogate), intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and inflammatory measures including Bath ankylosing spondylitis disease activity index (BASDAI), ankylosing spondylitis disease activity score (ASDAS) and bath ankylosing spondylitis functional index (BASFI); erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); proinflammatory cytokines (interleukin-1 [IL-1], IL-6, tumor necrosis factor-α [TNF-α]) and marker of oxidative stress– thiobarbituric acid reactive substances (TBARS) estimated at baseline and after treatment. Health assessment questionnaire disability index (HAQDI), 36-item short form survey (SF-36), and systematic coronary risk evaluation (SCORE) were estimated using standard tools. FMD improved significantly in the olmesartan group (5.83 ± 0.31% to 7.68 ± 0.27%, p  ≤  0.05) as compared with placebo (5.89 ± 0.35% to 6.04 ± 0.32%, p  = 0.33). EPC population, nitrite, VCAM-1, and TBARS levels improved significantly in olmesartan group as compared with placebo ( p ≤ 0.05). Olmesartan significantly decreased ASDAS, BASDAI, BASFI, ESR, CRP, IL-6, TNF-α, and SCORE as compared with placebo. HAQDI and SF-36 (PH) scores improved significantly in olmesartan group as compared with placebo. Olmesartan reduces inflammatory disease activity, improves quality of life (QOL), and decreases CV risk demonstrating the immunomodulatory, vasculoprotective, and cardioprotective potential of this drug in AS.     

Ankylosing spondylitis susceptibility loci defined by genome-search meta-analysis

In genome scans of ankylosing spondylitis (AS), with the exception of the HLA loci, linkage has not been easy to replicate across studies. We applied the genome-search meta-analysis (GSMA) method to genome scans of AS and spondyloarthropathy (SpA) to assess evidence for linkage across studies. Three AS genome scans and one SpA scan including 430 families with 1,048 affected individuals were used. All four original genome scans mainly analyzed Caucasian families. Seven bins had both Psumrnk and Pord<0.05, suggesting these bins most likely contain AS-linked loci; bin 6.2, 6.1, 6.3, 16.3, 19.2, 17.1, and 16.4. The GSMA produced significant genome-wide evidence for linkage on chromosome 6p22.3–6p21.1 (Psumrnk=0.000003), including the HLA locus. In addition to the HLA-B27 locus, strong linkage evidence was found on chromosome 6p25.3–6p22.3 (Psumrnk=0.0013) and 6p21.1–6p15 (Psumrnk=0.043). In the GSMA of four genome scans including one SpA study, the bin 9.4 (9q21.32–9q33.1) was newly found for linkage (Psumrnk=0.043, Pord=0.013). This GSMA added the evidence of the HLA loci as the greatest susceptibility factor to AS and showed evidences of chromosome 6, 16q, 19, 17p, and 9q as non-HLA susceptibility loci.