一期后路病灶清除病椎置钉短节段内固定加椎间或关节突间植骨治疗单间隙腰椎布鲁杆菌病性脊柱炎

目的 评价一期后路病灶清除、病椎置钉短节段内固定加椎间或关节突间植骨治疗单间隙腰椎布鲁杆菌病性脊柱炎(BS)的可行性及疗效。方法 回顾性分析2015年1月—2016年1月河北北方学院附属第一医院收治的 27例BS患者的临床资料,其中男15例、女12例,年龄42～65岁。患者均为单间隙病变,累及两个椎体,其中L_1～2 1例,L_2～3 3例,L_3～4 8例,L_4～5 12 例,L₅～S₁ 3例;患者均合并不同程度神经功能损伤,术前至少经过一个疗程的规范药物治疗。均选用一期后路病灶清除、病椎置钉短节段内固定加椎间或关节突间植骨术治疗。对比手术前后Cobb角、VAS、美国脊髓损伤协会(ASIA )脊髓功能评定、红细胞沉降率(ESR)、C反应蛋白(CRP)、虎红平板凝集试验(RBPT)指标,以及X线片、CT、MRI影像学表现,结合临床预后进行临床疗效评价。结果 术后27例均获随访,随访时间12～25个月,平均18个月,无一例发生窦道形成及复发。侧凸Cobb角术前及术后3、6个月分别为14.89°±1.48°、4.00°±1.44°和4.01°±0.87°,VAS术前及术后3、6、12个月分别为(8.4±1.6)、(3.1±0.3)、(1.1±0.3)及(0.7±0.2)分,术后各时间点均较术前显著改善,差异均有统计学意义(P值均＜0.05);ASIA脊髓功能分级较术前明显好转,差异均有统计学意义(P值均＜0.01);随时间推移,术后ESR、CRP、Cobb角明显减小,术后各时间点与术前比较,差异均有统计学意义(P值均＜0.01)。RBPT术后转阴率(正常率)逐渐增高,术后3个月为48.14%,6个月为100%。临床疗效评价:术后3、6、12个月治愈率分别为59.25%(治愈16例、改善10例、无效1例)、81.48%(治愈22例、改善5例)、96.29%(治愈26例、改善1例),后一个时间点治愈率与前一个时间点比较,差异均有统计学意义(P值均＜0.05)。结论 在应用有效的药物控制前提下,一期后路病灶清除、病椎置钉短节段内固定加椎间或关节突间植骨治疗单间隙BS是可行的,其在解除疼痛、稳定脊柱及恢复神经功能等方面具有较好的临床疗效。     

长节段椎弓根钉系统内固定与个性化截骨方法治疗强直性脊柱炎后凸畸形

背景：生物力学的观点认为：强直性脊柱炎的矫形在后凸的顶点处截骨最佳,但术中脊髓损伤的风险大。 目的：分析联合应用椎板间截骨+椎体截骨+长节段椎弓根钉系统内固定治疗强直性脊柱炎后凸畸形的临床效果。 方法：强直性脊柱炎患者共36例,均采用PSO(Pedicle Subtraction Osteotomy)截骨+SPO(Smith-Peterson Osteotomy)联合截骨治疗。随访时间3个月至2年。 结果与结论：36例患者未发现植入物修复后矢状位失平衡者,矢状位失衡的改善率为64%。患者植入物修复后胸腰椎后凸角的到恢复,改善率为60%;颌眉角的改善率为98%,疼痛症状缓解程度为64%,ODI指数95%;均未发生拔钉、断钉、断棒现象。说明选择性截骨矫形技术+长节段内固定手术能够获得稳定的内固定疗效,防止出现矢状位失平衡,以及强直性脊柱炎因骨质疏松导致的拔钉、断钉、断棒现象的发生。中国组织工程研究杂志出版内容重点：人工关节;骨植入物;脊柱;骨折;内固定;数字化骨科;组织工程全文链接：     

HLA-B27 polymorphism and worldwide susceptibility to ankylosing spondylitis

HLA-B27 is strongly associated to ankylosing spondylitis (AS) and represents a family of eleven B27 alleles (B*2701–11). Our aim was to analyze the distribution of B27 subtypes by PCR/SSOP and genomic sequencing in a large group of populations ( n =17). 711 B27-positive samples from Caucasoid, Asian, African, Amerindian and Polynesian populations were selected to ascertain transracial gene mapping of the B27 subtypes. 476 of these were AS patients, chosen to investigate the contribution of B27 alleles to AS susceptibility. Some significant new findings have arisen from this study: 1) B*2705 was the predominant subtype in circumpolar and subarctic areas. B*2702 was found to be practically restricted to Caucasian populations, showing a higher frequency in Middle-East (Jews) and North Africa (Arabs/Berbers) groups. 2) B*2703 appears associated with AS in Western Africans. This is of remarkable interest since it was suggested that B*2703 would be negatively disease-associated. 3) Although B*2706 appears negatively associated with AS in Thais, we identified two patients from northern China carrying it. This may be a reflection of a disease heterogeneity and could indicate that more than one pathogenic agent can be involved in AS. B*2709 has been recently described as negatively associated with AS in Sardinians. The molecular changes His 114Asp (B*2706) and Asp 116His (B*2709) could modify the genetic susceptibility to AS.     

Lack of carboxyl–terminal tyrosine distinguishes the B2706–bound peptide repertoire from those of B2704 and other HLA–B27 subtypes associated with ankylosing spondylitis

B*2704 and B*2706 are two closely related HLA-B27 subtypes, which differ from the common B*2705 by the Asp>Ser77, Val>Glu152, and Ala>Gly211 amino acid changes. In addition, B*2706 differs from B*2704 by the His>Asp114 and Asp>Tyrl 16 changes. In spite of their similarity B*2704, but not B*2706, was associated to ankylosing spondylitis in a same population. We have carried out pool sequence analyses of the peptides naturally bound to each of these subtypes, and of several individual peptide ligands. B*2704 and B*2706 shared with B*2705, among other features, their selectivity for Arg² and their allowance for some aliphatic and aromatic C-terminal residues in their bound peptides. The main features that distinguished both subtypes from B*2705 were: 1) their failure to present peptides with C-terminal basic residues, and 2) their allowance for both polar and nonpolar residues at peptide position 3. A major difference between B*2704 and B*2706 was that C-terminal Tyr was prominent among the peptides bound to B*2704, but was not detected among those from B*2706. The use of Tyr as a C-terminal anchor motif is the only functional feature shared by the disease-associated B*2705, B*2702, and B*2704 subtypes that is absent in B*2706. This suggests that the ability of HLA-B27 to present peptides with C-terminal Tyr might be critical for its association to spondyloarthropathy,     

HLA-B27 (B*2701) specificity for peptides lacking Arg2 is determined by polymorphism outside the B pocket

B*2701 differs from B*2705 by three amino acid changes: DY74, DN77, LA81, and from B*2702 only by two: DY74 and T180. Tyr74 is located in the C/F cavity of the peptide-binding site, and is unique to B*2701 among HLA-B27 subtypes. Binding of natural B*2705 and B*2702 ligands to B*2701, and to mutants mimicking subtype changes, was analyzed. In addition, sequencing of the peptides bound in vivo by B*2701 and the Y74 mutant was carried out. The main distinctive feature of B*2701 was its presentation of peptides with Gln2. Synthetic analogs bound in vitro similarly as the corresponding ligands with Arg2. Moreover, both Gln2 and Arg2 were dominant upon pool sequencing of B*2701- bound peptides, and 2 of 8 natural ligands contained Gln2. Suitability of Gln2 was largely determined by the Y74 change, as indicated by: 1) binding of Gln2 analogs to this mutant, and 2) detection of Gln2 by pool sequencing of Y74-bound peptides. B*2701 bound peptides with C-terminal aromatic or Leu residues, and interacted with these motifs more strongly than B*2702. The Y74 mutation alone was not responsible for poor binding of peptides with C-terminal basic residues to B*2701, since they bound efficiently and at least one was presented in vivo by this mutant. Most peptides bound to the A81 mutant worse than to B*2705, but frequently better than to B*2701 or B*2702, suggesting that other subtype changes were compensatory. The peptide specificity of B*2701 suggests that this subtype may determine susceptibility to spondyloarthropathy.     

No association of KIR3DL1 or KIR3DS1 or their alleles with ankylosing spondylitis

Abstract
We determined the alleles of KIR3DL1 and KIR3DS1 in a cohort of British Caucasian ankylosing spondylitis (AS) patients and HLA-B27-positive controls. We found no association in frequencies of the alleles of these genes in AS. In addition, no differences were found when the patients and controls were differentiated by gender.     

HLA-B27 polymorphism in patients with juvenile and adult-onset ankylosing spondylitis in Southern China

Abstract
Distribution of B27 subtypes in juvenile and adult-onset ankylosing spondylitis (JAS and AAS) in Southern China was studied. A total of 505 patients belonged to Han population were included (145 JAS and 360 AAS patients), and 1368 healthy individuals were included as controls. Human leukocyte antigen (HLA)-B27 typing was performed by Luminex liquid array combining polymerase chain reaction-sequence specific oligonucleotide probe (PCR-SSOP) and/or serological method. HLA-B27 subtyping was performed by polymerase chain reaction-sequence specific primer (PCR-SSP). The sequence-based typing was performed for the B*2715 samples to verify the PCR-SSP results. HLA-B27 was presented in 453 of 505 patients (89.7%), compared with 74 of 1368 controls (5.41%). B*2704 subtype in AS group was significantly higher than controls and B*2705 subtype significantly lower. B*2715 and B*2702 were found in 1.32% and 0.66% of the B27-positive patients but none in controls, and there was no significant difference between either of them and controls. B27-positive patients were 134 (92.4%) in JAS group and 319 (88.6%) in AAS group. There was no significant difference for B27 subtypes distribution between JAS (B*2704, 05, 15) and AAS (B*2704, 05, 15, 02) groups. The frequency of B*2715 in two groups was 3 (2.24%) and 3 (0.94%), respectively. The onset age of three JAS patients carrying B*2715 was 5, 9 and 13 years old, respectively. Our results suggested that B*2704 was the predominant subtype in AS patients in Southern China. B*2715 was observed in AS group only and slightly more in JAS than in AAS, and the patients carrying this allele tended to have early onset, B*2715 may be disease-association subtype.     

中晚期强直性脊柱炎伴脊柱骨折的损伤机制及影像学特点

目的：探讨强直性脊柱炎(AS)伴发脊柱骨折的损伤机制及影像学特点,减少漏诊、误诊。方法回顾15例 AS伴脊柱骨折患者的影像和临床资料,及37例普通脊柱骨折患者的资料,并对其进行分析。结果在 AS患者中,有明确外伤史的11例,影像学上表现为三柱骨折的9例,可见明确椎管受压或脊髓损伤的7例,骨折经过椎间部位的6例;在普通脊柱骨折患者中,有明确外伤史的36例,影像学上表现为三柱骨折的4例,可见明确椎管受压或脊髓损伤的5例,无骨折经过椎间部位。统计分析发现：AS伴脊柱骨折患者与普通脊柱骨折患者相比,无外伤原因所占比率差异有统计学意义(χ2=4.565,P<0.05),患者发生三柱骨折的比率差异有统计学意义(χ2=11.274,P<0.05),骨折导致椎管受压或脊髓损伤的比率差异有统计学意义(χ2=4.873,P<0.05),骨折经过椎间部位发生的比率差异有统计学意义(χ2=13.041,P<0.05)。结论 AS伴发脊柱骨折与普通脊柱骨折损伤机制有明显的差异,X线、CT和 MRI在显示 AS伴脊柱骨折方面各有优势,有效地运用这些差异以及选用合适的影像检查将有助于减少漏、误诊。     

经椎弓根截骨术治疗强直性脊柱炎继发颈胸段后凸畸形

目的评估后路经椎弓根截骨术(PSO)治疗强直性脊柱炎(AS)继发颈胸段后凸畸形的临床疗效。方法2009年1月—2015年3月,本院采用PSO治疗AS继发颈胸段后凸畸形患者7例。患者翻身至手术床之前,先放置石膏床于患者腹侧,并在患者颈胸段与石膏床的空隙处填充数个长方形棉垫。术中C6~T1后方截骨及经C7椎弓根椎体截骨完成后,由台下助手缓慢逐个抽取垫于患者和石膏床之间的长方形棉垫。待棉垫抽取完毕后,患者颈胸段的曲度在重力的作用下恢复至近似直线。然后采用体内弯棒技术进一步增加颈胸段前凸曲度。记录手术时间及术中出血量,用颈胸段(C_2~T_1)后凸Cobb角、颏眉角(CBVA)、C_2~T_1矢状面偏移距离(SVA)、疼痛视觉模拟量表(VAS)和健康调查量表(SF-36)评估临床疗效。结果 7例患者平均手术时间260 min,术中平均出血量1 571 m L,平均随访24.4个月,术前C_2~T_1 Cobb角平均为26.2°,末次随访时为-5.4°。术前CVBA平均为43.1°,术后改善至-0.9°。术前C_2~T_1 SVA平均为6.7 cm,术后改善至3.0 cm。末次随访时,患者的VAS评分由术前的85.0分改善至17.1分;SF-36躯体机能评分(PCS)由术前的20.7分改善至79.3分;SF-36精神机能评分(MCS)由术前的12.8分改善至81.6分。结论 PSO治疗AS继发颈胸段后凸畸形可以有效地恢复颈胸段的矢状位平衡,较好地改善患者前方视野受限、颏-胸畸形等症状,采用术中体内原位弯棒技术安全可靠。     

强直性脊柱炎骨髓间充质干细胞诱导Th17/Treg失衡

目的观察强直性脊柱炎(AS)患者外周血白介素(IL)-17A、IL-23水平及Th17/Treg比例,探讨骨髓间充质干细胞(BMSCs)与Th17/Treg体外相互作用,为研究AS发生机制提供理论依据。方法研究对象为48例活动期AS患者[实验组,男43例、女5例,年龄(26.2±5.2)岁,均为HLA-B27~+]和49例健康志愿者[对照组,男44例、女5例,年龄(25.9±4.8)岁,HLA-B27~+43例、HLA-B27~-6例]。ELISA检测外周血清中IL-17A及IL-23水平,流式细胞术检测外周血单个核细胞(PBMCs)中的CCR4~+CCR6~+Th细胞(Th17)及Treg细胞数量。分离健康志愿者的PBMCs,将PBMCs分别与AS患者及健康志愿者的BMSCs体外共培养72 h,收集PBMCs行流式细胞术检测,评价BMSCs与Th17/Treg体外的相互作用。结果实验组与对照组血清IL-17A及IL-23的表达水平相近(P0.05);实验组Th17细胞明显高于对照组(P0.05),而Treg细胞明显低于对照组(P0.05)。与健康志愿者BMSCs共培养72 h后的PBMCs中Th17较培养前轻度下降,Treg轻度上升,差异无统计学意义(P0.05);而与AS患者BMSCs共培养72 h的PBMCs中Th17较培养前及对照组均明显上升,Treg均明显下降,差异均有统计学意义(P0.05)。结论 AS患者PBMCs中Th17/Treg细胞亚群失衡。免疫抑制能力明显下降的BMSCs极可能通过诱导Th17/Treg失衡而在AS免疫发生机制中发挥重要作用。