神经阻滞预防带状疱疹后神经痛及其高危因素分析
Prevention of Postherpetic Neuralgia by Nerve Block and Analysis of Risk Factors
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摘要: 目的 探讨神经阻滞对治疗带状疱疹 (HZ) 和预防带状疱疹后神经痛 (PHN) 的效果, 探寻影响PHN发生的因素.方法 2015年1月至2016年9月昆明医科大学第一附属医院疼痛科收治的首次发病且未经任何治疗的急性期HZ患者80例.随机分配到病例组 (神经阻滞+常规内科治疗) 40例, 和对照组 (常规内科治疗) 40例.对比2组带状疱症后神经痛发生率, 分析年龄、性别、疱疹部位、前驱性疼痛、初始疼痛程度、结痂时间、和治疗1周时的疼痛缓解率等, 与PHN发生率的相关关系.结果 病例组有4例 (10.0%) 发生PHN, 较对照组19例 (47.5%) 显著降低 (P<0.001) .病例组住院天数减少 (7.43±1.80) d vs (12.90±2.36) d, P<0.001, 结痂时间缩短 (6.33±0.86) d vs (7.15±0.66) d, P<0.001.高龄 (OR:13.03, 95%CI:2.7362.34) 、发病起始的VAS评分 (OR:8.24, 95%CI:1.6241.96) 和结痂时间延长 (OR:17.99, 95%CI:2.14151.43) , 是PHN的危险因素, 显著增加PHN发生率.治疗1周时的VAS缓解率 (OR<0.000, 95%CI:0.0000.001) , 是PHN的保护因素, 与PHN的发生呈负相关.结论 高龄和发病时疼痛严重的患者, 应注意预防PHN.神经阻滞有助于减少HZ患者住院天数, 缩短结痂时间, 降低PHN发生率.Abstract: Objective To investigate the effect of nerve block on the treatment of herpes zoster (HZ) and prevention of postherpetic neuralgia (PHN) , and to explore the factors that affect the occurrence of PHN.Methods From january 2015 to September 2016 in our hospital 80 acute HZ patients for the first time in the treatment of pain, were randomly assigned to the case group (nerve block + conventional medical treatment) 40 cases, and the control group (conventional medical treatment) 40 cases.The incidence of neuralgia in the two groups was analyzed, and the relationship between the age, sex, herpes, prodromal pain, initial pain, scab time, pain relief rate and PHN.Results PHN occurred in 4 cases (10.0%) in the case group and 19 cases (47.5%) in the control group (P <0.001) . (6.33 ± 0.86 days vs.7.15 ± 0.66 days, P <0.001) .The number of hospital days decreased (7.43 ± 1.80 days vs.12.90 ± 2.36 days, P <0.001) .Ageing (OR: 8.24, 95% CI:1.62-41.96) and prolonged crusting time (OR: 17.99, 95% CI: 2.14-151.43) , are risk factors for PHN, significantly increased the incidence of PHN.The VAS remission rate after 1 week (OR <0.000, 95% CI:0.000-0.001) was a protective factor for PHN and was negatively correlated with PHN.Conclusions Aging and onset of severe pain in patients should pay attention to the prevention of PHN.Nerve block helps to reduce the number of hospital stay in HZ patients, shorten the scab time, and reduce the incidence of PHN.
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Key words:
- Herpes zoster /
- Postherpetic neuralgia /
- High risk factors /
- Nerve block
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随着人们饮食习惯及生活方式的改变,如过度清洁、杀菌剂及抗生素泛用等,人体免疫系统失衡呈现逐年递增趋势。人体免疫系统对外能抵抗病原体的入侵,减少感染性疾病发生;对内有监视作用,能清除发生突变的体细胞遏制肿瘤产生及减少罹患自身免疫性疾病的风险。患儿免疫过强可出现皮疹、出血点、鼻炎、喘息、过敏性休克等症状;免疫功能低下可出现反复感染、严重感染、特殊病原体感染或治疗效果不佳的感染[1],甚至肿瘤发生,严重影响儿童生活质量,甚至危及生命。过敏性紫癜(henoch-schonlein purpura,HSP)是儿童时期较常发生的,以IgA介导的小血管炎,典型症状为非血小板减少性紫癜,伴或不伴腹部、关节、肾脏,甚至其它器官(脑、肺等血管炎)损害。维生素D除调节人体钙磷参与骨代谢外,还具有重要的免疫调控作用[2-3],本研究通过检测HSP患儿及健康儿童维生素D的水平,探讨HSP患儿及健康儿童处于不同免疫状态下维生素D含量的变化,为HSP治疗提供新思路。
1. 资料与方法
1.1 研究对象
将2022年7月至2023年7月在昆明市儿童医院就诊,符合HSP诊断标准[4]的130例患儿纳为观察组,观察组患儿需排外:合并严重感染、其它免疫性疾病、皮肤疾病或其它脏器严重功能障碍、佝偻病、骨质疏松者。HSP患儿年龄3岁5月至11岁4月,平均(6.1±1.5)岁,男72例,女58例。随机选取同时期在昆明市儿童医院儿保科体检的健康儿童100例作为正常对照组,年龄1岁1月~13岁6月,平均(5.6±2.9)岁,男51例,女49例。HSP组与正常对照组儿童年龄、性别构成差异比较,差异无统计学意义(P > 0.05),2组间具有可比性。该研究经医院伦理委员会的批准(2022-03-225-K01),并取得家长知情同意。
1.2 HSP诊断标准
可触性非血小板减少性皮肤紫癜(必要条件)伴以下任1条:(1)腹痛;(2)关节痛或关节炎;(3)肾脏病变(血尿或蛋白尿);(4)任意部位病检示IgA沉积。但临床中部分患儿仅有单纯皮疹而无其它临床症状。2012年在长沙召开的儿童过敏性紫癜诊治会议上,专家提议:对于急性发作典型皮疹的患儿,排除其它相关疾病可行临床诊断,但对于非急性发作或皮疹不典型的患儿,仍需严格按照诊断标准,必要时完善皮肤病检诊断[4]。
1.3 检测
所有研究对象采集早晨空腹血3 mL,注入生化促凝管内,经3000 r/min的速度离心5 min,分离血清后注入EP管,放2~8 ℃冰箱当天送昆明金域医学检验所检测。利用Agilent高效液相色谱串联质谱仪测定血清25(OH)D含量。14岁以内血清25(OH)D正常参考值范围为50~250 nmol/L, < 50 nmol/L为维生素D不足[5]。
1.4 统计学处理
所测数据通过SPSS 21.0统计软件进行统计学分析。正态分布的计量资料以均数 ± 标准差($ \bar x \pm s $)表示,HSP组与正常对照组儿童维生素D含量的比较采用两独立样本t检验,HSP组与正常对照组儿童维生素D不足率为计数资料,以n(%)表示,采用χ2检验,P < 0.05为差异有统计学意义。
2. 结果
2.1 HSP组与正常对照组25(OH)D含量的比较
HSP组患儿血清中25(OH)D含量较正常对照组降低,差异有统计学意义(P < 0.01),见表1。
表 1 HSP组与正常对照组25(OH)D含量的比较[($\bar x \pm s $),nmol/L]Table 1. Comparison of 25(OH) D between HSP and control group [($\bar x \pm s $),nmol/L]组别 25(OH)D HSP组 45.44±16.31 对照组 86.6±28.62 t 18.234 P < 0.001 * *P < 0.05。 2.2 HSP组与正常对照组中25(OH)D不足率的比较
HSP组患儿血清中25(OH)D不足率高于正常对照组,差异有统计学意义(P < 0.01),见表2。
表 2 HSP组与正常对照组25(OH)D不足率的比较Table 2. Comparison of vitamin D deficiency in children with HSP and control group组别 25(OH)D不足例数(n ) 25(OH)D不足比例(%) HSP组 87 66.9 对照组 5 5.0 χ2 90.304 P < 0.001 * *P < 0.05。 3. 讨论
维生素D是一种神经内分泌-免疫调节剂,维生素D可与免疫细胞相互作用。免疫细胞(T淋巴细胞、B淋巴细胞、抗原呈递细胞、巨噬细胞)可表达1-α羟化酶,将维生素D变为有生物活性的1,25-(OH)2D;免疫细胞(T淋巴细胞、B淋巴细胞、树突状细胞、单核/巨噬细胞、中性粒细胞)表达维生素D受体(vitamin D receptor,VDR)[6],维生素D与VDR结合从而发挥调节免疫及参与钙磷代谢等作用。维生素D可增强机体固有免疫反应、抑制适应性免疫反应。维生素D通过促进固有免疫从而增强机体抵抗病原体入侵的能力,降低感染性疾病的发生。维生素D通过阻碍适应性免疫反应诱导免疫耐受,从而减少罹患自身免疫性疾病及缓解炎症后对机体的损伤。维生素D仅少量来源于食物,大多经日光照射合成或来源于维生素D营养补充剂,维生素D在人体肝脏、肾脏中分别经25-羟化酶、1-α羟化酶的2次羟化,变为有生物活性的1,25(OH)2D3[7-8]。因25(OH)D在血液中浓度高、半衰期长、相对稳定,被认为是维生素D营养评价的最好指标[9]。本文通过研究HSP及健康儿童25(OH)D的水平,探讨HSP患儿及健康儿童处于不同免疫状态下维生素D含量的变化,为儿童HSP治疗提供新策略。
本研究显示HSP患儿25(OH)D含量较正常儿童降低,HSP患儿维生素D不足率高于正常儿童,提示HSP发病可能与维生素D不足有关。HSP是儿童时期较常发生的免疫介导性小血管炎。在HSP发病中B淋巴细胞起重要作用,B细胞活性增强时可使浆细胞分泌到血液中的IgA、D、E、M、G增多,进而强化机体内体液免疫应答。其中IgA增多可引起儿童多系统IgA免疫复合物介导的小血管炎从而加重HSP症状。维生素D可通过抑制机体内B细胞的增值和诱导其凋亡,抑制浆细胞产生免疫球蛋白,从而减少HSP发病及缓解HSP症状[10]。HSP发生与免疫、遗传、感染等有关,微生物感染会诱发HSP。维生素D可增强机体固有免疫,减少感染性疾病的发生,维生素D促使单核细胞分化为有吞噬作用的巨噬细胞,并可提高巨噬细胞的吞噬及杀伤功能[11-12];维生素D在促进中性粒细胞杀菌等免疫防御体系中起关键作用,维生素D可提高中性细胞抗菌肽活性,抗菌肽可致微生物膜失稳,影响细胞的通透性,导致病原体裂解[13]。维生素D不足与感染性疾病发生呈正相关,维生素D不足可能增加HSP发病率。综上所述,维生素D作为新型免疫调节剂,在HSP防治中具有积极作用。此外,维生素D亦可通过调节钙磷途径,改善HSP患儿使用激素时的钙缺乏症状,促进HSP患儿病情恢复。故在HSP患儿常规治疗的同时,需要强调维生素D的补充。
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