Risk factors for intussusception in children with Henoch-Schönlein purpura:A case-control study

BACKGROUND The etiology of Henoch-Schönlein purpura(HSP)with intussusception remains undefined.AIM To investigate the risk factors for intussusception in children with HSP and gastrointestinal(GI)involvement.METHODS Sixty children with HSP and concomitant intussusception admitted to the Beijing Children’s Hospital of Capital Medical University between January 2006 and December 2018 were enrolled in this study.One hundred pediatric patients with HSP and GI involvement but without intussusception,admitted to the same hospital during the same period,were randomly selected as a control group.The baseline clinical characteristics of all patients,including sex,age of onset,duration of disease,clinical manifestations,laboratory test results,and treatments provided,were assessed.Univariate and multiple logistic regression analyses were performed to identify possible risk factors.RESULTS The 60 children in the intussusception group comprised 27 girls(45%)and 33 boys(55%)and the 100 children in the non-intussusception group comprised 62 girls(62%)and 38 boys(38%).The median age of all patients were 6 years and 5 mo.Univariate and multiple regression analyses revealed age at onset,not receiving glucocorticoid therapy within 72 h of emergence of GI symptoms,hematochezia,and D-dimer levels as independent risk factors for intussusception in children with HSP(P<0.05).CONCLUSION The four independent risk factors for intussusception in pediatric HSP with GI involvement would be a reference for early prevention and treatment of this potentially fatal disease.

Henoch-Schönlein purpura nephritis in children:incidence,pathogenesis and management

Background:Henoch-Schönlein purpura(HSP)is one of the most common vasculitides in children.It is manifested by skin purpura,arthritis,abdominal pain,renal involvement,etc.Typically,HSP is considered to be self-limiting,although renal involvement(HSP purpura nephritis,HSPN)is the principal cause of morbidity from this disease.For this reason,it is important to clarify the mechanism of onset and clinical manifestations of HSPN and to ascertain the most appropriate treatment for HSPN.In this article,we review the updated pathophysiology and treatment strategies for HSPN.Data sources:We searched databases including PubMed,Elsevier and Wanfang for the folowing key words:Henoch-Schönlein purpura,nephritis,mechanism and treatment,and we selected those publications written in English that we judged to be relevant to the topic of this review.Results:Based on the data present in the literature,we reviewed the following topics:1)the possible pathogenesis of HSPN:several studies suggest that immunoglobulin A immune complexes deposit in the mesangium and induce renal injury;2)multiple-drug treatment for HSPN:although there have been few evidence-based treatment strategies for HSPN,several studies have suggested that immunosuppressive drugs and multiple drug combination therapy were effective in ameliorating proteinuria and histological severity.Conclusions:HSPN is a severe disease of childhood.To better understand this disease,detailed investigations into the pathogenesis of HSPN and prospective randomized controlled treatment studies on children with severe HSPN are needed.

Clinicopathological features and prognosis of membranoproliferative-like Henoch-Schönlein purpura nephritis in children

Background: The aim of this retrospective study was to defi ne the clinical manifestations, pathological features and prognosis of children with membranoproliferative-like Henoch-Schönlein purpura nephritis (HSPN), representing International Study of Kidney Disease in Children (ISKDC) grade VI. Methods: Among 245 patients with HSPN treated in our hospital between 2008 and 2010, nine patients (3.7%) were diagnosed with HSPN of ISKDC grade VI (males=5, females=4, age: 9.5±2.03 years, mean±SD). The clinical features, laboratory and pathologicalfi ndings, treatment and outcome of the 9 patients were retrospectively analyzed. Results: Of the 9 patients, 7 (78%) presented with hematuria and nephrotic syndrome, and were treated with steroids (oral prednisone or intravenous methylprednisolone pulse therapy) and immunosuppressants (oral tripterygium glycosides or intravenous cyclophosphamide pulse therapy). One (11%) patient had hematuria and nephrotic range proteinuria (>50 mg/kg per 24 hours) and was treated with oral prednisone and tripterygium glycosides. Another (11%) patient presented with hematuria and moderate proteinuria (25-50 mg/kg per 24 hours) and was treated with oral tripterygium glycoside only. Histopathological examination showed diffuse glomerular mesangial and endocapillary proliferation, mesangial interposition, double-contour formation, podocyte hypertrophy, shedding, and cytoplasmic absorption droplets. The percentages of glomeruli with small cellular crescents varied from 4%-25% in 6 of 9 patients. Follow-up for 2 to 4 years showed excellent recovery in all patients. Conclusions: The main clinical feature of ISKDC grade VI HSPN in children is a nephrotic syndrome with hematuria. The excellent prognosis of the disease was probably related to early diagnosis and treatment with steroids and/or immunosuppressants, and mild degree of glomerulosclerosis and tubulointerstitial damage.

Effect of intestinal flora from children with Henoch-Sch?nlein purpura on visceral sensitivity, gastrointestinal hormones and cytokines secretion in pseudo-sterile rats

Objective:To investigate the effect of intestinal flora from Henoch-Schönlein purpura(HSP)on visceral sensitivity,gastrointestinal hormones and cytokines in pseudo-sterile rats.Methods:The pseudo-sterile rat model was established.The rats were was given fecal microbiota solutions of children with abdominal HSP and healthy children,respectively.The visceral sensitivity was determined by abdominal withdrawal reflex(AWR)which was induced by rectal balloon distention in all the rats.And serum gastrin(Gas),motilin(MTL),cholecystokinin(CCK),substance P(SP),tumor necrosis factor(TNF)-αand interleukin(IL)-6 levels in rats were measured with ELISA method.Results:The volume of rectum water injection under the score 3 of AWR in the rats administrated with fecal microbiota solution from HSP children(HSP group)was significantly decreased compared with that in the rats administrated with fecal microbiota solution from healthy children(HC group),and there was significant difference between these two groups(P<0.05).The serum Gas,MTL,CCK and SP levels were higher in HSP group than those in HC group.And serum MTL,CCK and SP levels in HSP group were significantly different from those in the HC group.The serum TNF-αandIL-6 levels were higher in HSP group than those in HC group,there was significant difference between these two groups(P<0.05).Conclusion:Intestinal flora from HSP can induce the production of visceral sensitivity,inhibit gastrointestinal hormone secretion and prompt cytokine production.

Effect of Activation of the Ca2+-Permeable Acid-Sensing Ion Channel 1a on Acid-Induced Vascular Endothelial Cell Injury of Henoch-Schönlein Purpura Children

Acidosis in local environment plays a critical role in cell injury. One key mediator of acidosis-induced cell injury is the acid-sensing ion channels (ASICs), particularly ASIC1a. Herein, we investigated the role of ASIC1a in acid-induced vascular endothelial cell injury of Henoch-Schonlein purpura (HSP) children. Acid-induced ASIC1a, Calpain and Calcineurin expression in vascular endothelial cells pretreated with IgA1 isolated from HSP were detected by real time quantitative polymerase chain reaction and western blot methods, respectively. Cell cytotoxicity was measured by interleukin-8 and nitric oxide production with ELISA. The results showed acid-induced ASIC1a, Calpain and Calcineurin expression in cells increased, especially at PH6.5. The cytotoxicity of vascular endothelial cells was increased by extracellular acidosis. Moreover non-specific or specific blockers of ASIC1a, Amiloride and PcTX-1 could remarkably decrease these parameters. These findings show that increased [Ca2+]i, mediated via ASIC1a, might contribute to acid-induced vascular endothelial cell injury of HSP.

Severe Henoch-Schonlein purpura with infliximab forulcerative colitis

Infliximab （IFX） is an anti-tumor necrosis factorchimeric antibody that is effective for treatment ofautoimmune disorders such as Crohn＇s disease andulcerative colitis （UC）. IFX is well tolerated with alow incidence of adverse effects such as infections,skin reactions, autoimmunity, and malignancy.Dermatological manifestations can appear as infusionreaction, vasculitis, cutaneous infections, psoriasis,eczema, and skin cancer. Here, we present anunusual case of extensive and sporadic subcutaneousecchymosis in a 69-year-old woman with severe UC,partial colectomy and cecostomy, following her initialdose of IFX. The reaction occurred during infliximabinfusion, and withdrawal of IFX led to gradual alleviationof her symptoms. We concluded that Henoch-Sch？nleinpurpura, a kind of leukocytoclastic vasculitis, mighthave contributed to the development of the bruising.Although the precise mechanisms of the vasculitis arestill controversial, such a case highlights the importanceof subcutaneous adverse effects in the management ofUC with IFX.

Henoch-Schnlein purpura complicating adalimumab therapy for Crohn's disease

Anti-tumour necrosis factor-α(TNF) therapy has revolutionised the management of chronic inflammatory conditions.With ever increasing numbers of patients being treated with these agents,uncommon adverse reactions will inevitably occur more frequently.Cutaneous manifestations are associated with many of these chronic conditions and can complicate anti-TNF therapy in about 20% of cases.Vasculitic complications are rarely associated with anti-TNF therapy.Henoch-Schnlein purpura(HSP),a small vessel vasculitis,has been described following infliximab and etanercept therapy but never with adalimumab,a fully humanized TNF antibody.The risk of such immune-mediated reactions is theoretically less with adalimumab compared to infliximab but can still occur.Here we report the f irst case in the literature of HSP that can be attributed to the use of adalimumab in a 19-year-old male with recalcitrant Crohn's disease.

一项回顾性研究:261例Henoch-Schnlein性紫癜患儿胃肠道表现

目的:小儿Henoch-Schonlein性紫癜(HSP)为儿童的一种IgA介导的自身免疫性血管炎。其常见症状为:紫癜性皮疹、腹痛、肾脏或关节受累等。HSP患儿以腹痛常见,但常被疑为肠套叠或肠穿孔。本文用粪便隐血试验和影像学方法来鉴别腹痛。方法:回顾性研究1991年12月至2001年12月间261例HSP患儿。对腹痛患儿进行影像学检测,包括:腹部超声、腹部CT。

国医大师丁樱治疗过敏性紫癜用药规律研究

目的挖掘丁樱教授治疗过敏性紫癜的用药规律,探析丁樱教授治疗过敏性紫癜的学术思想与临床经验。方法选取2013年1月-2020年1月河南中医药大学第一附属医院丁樱教授儿科门诊的过敏性紫癜处方,通过名医传承一体化平台,建立药物-药物、药物-症状网络,对其核心药组及关联规律进行深层次分析。结果纳入病案195则,涉及585诊次、处方585首、中药153种,药物总频次为8017。药性以寒、温、平为主,药味以苦为主,归经以肝经、心经为主。药物权重等级分析显示,生地黄、当归、连翘、忍冬藤、牡丹皮、紫草、川芎、地肤子、海风藤、络石藤、徐长卿、雷公藤、薏苡仁、黄芩、水牛角、砂仁、白芍、浮萍、甘草为治疗过敏性紫癜的核心处方。药物-药物共现性分析显示,生地黄-当归、生地黄-牡丹皮、连翘-牡丹皮、地肤子-忍冬藤、川芎-忍冬藤、忍冬藤-当归、地肤子-连翘、牡丹皮-紫草、当归-牡丹皮、生地黄-连翘、连翘-川芎、生地黄-忍冬藤为治疗过敏性紫癜的常用药对;聚类分析显示出10个潜在药物群。结论丁樱教授治疗过敏性紫癜强调病、证、症相结合及对药的应用,临证施治遵循“祛邪安络”思想,善用清热解毒类药、清热祛风类药、清热祛湿类药以“祛邪”,善用活血凉血类药、养血通络类药以“安络”。

祛湿化斑颗粒通过调控IL/STAT信号通路对过敏性紫癜性肾炎大鼠的影响

探讨祛湿化斑颗粒(QSHB Gr)通过调控IL/STAT信号通路对过敏性紫癜性肾炎大鼠的影响及可能机制。将幼龄清洁(SPF)级SD大鼠36只随机分为6组:对照组、模型组、QSHB Gr/0.2剂低剂量组、QSHB Gr/0.4剂中剂量组、QSHB Gr/0.8剂高剂量组及霉酚酸酯(MMF 0.3 g/kg)组。综合模拟IgA肾病与血热证动物模型,复合成为过敏性紫癜肾炎大鼠(HSPN)模型;病理学检测肾脏损伤;测定血清肾脏生化指标总蛋白(TP)、白蛋白(ALB)的质量浓度以及肌酐(Cre)和血尿素氮(BUN)的浓度;收集24 h尿观察尿量并检测尿蛋白排泄情况;免疫组织化检测肾脏免疫复合物IgA、IgG沉积;Elisa法检测IL-17、IL-6、IL-2及TGF-β1的含量;Western blot检测STAT3、STAT5、RORγt、FoxP3蛋白表达。结果显示:与HSPN大鼠相比,QSHB Gr治疗可以通过减轻肾脏组织病理损伤、升高血清TP、ALB浓度,降低Cre、BUN浓度及24 h尿蛋白水平(P<0.01)显著改善HSPN大鼠肾脏损伤,且各个指标随QSHB Gr剂量增加变化越明显。QSHB Gr治疗可以显著抑制肾脏免疫复合物IgA、IgG沉积;显著降低IL-17、IL-6及TGF-β1的含量(P<0.05或P<0.01),升高IL-2含量(P<0.01);显著升高STAT5与FoxP3的表达水平(P<0.05或P<0.01),降低STAT3与RORγt的表达水平(P<0.01),各个指标随QSHB Gr剂量增加而变化越明显。以祛湿化斑颗粒(QSHB Gr)治疗可以改善过敏性紫癜性肾炎,可能是HSPN临床治疗的潜在候选药物。其机制可能与抑制IgA和IgG沉积及IL-6/STAT3与IL-2/STAT5信号通路调控密切相关。

过敏性紫癜患儿预后影响因素及其预测价值研究

目的:探讨过敏性紫癜(HSP)患儿预后的影响因素及其预测价值。方法:选取HSP患儿150例为研究对象。根据患儿治疗后有无复发分为预后不良组(47例)和预后良好组(103例)。比较两组患儿一般资料及生化指标(白细胞计数、血小板计数、血清总蛋白、乳酸脱氢酶、碱性磷酸酶、C-反应蛋白、免疫球蛋白A)。分析HSP患儿预后的影响因素及其对患儿预后不良的预测价值。结果:预后不良组皮疹反复发作、初次发病伴肾损害和呼吸道感染比例高于预后良好组(均P<0.05)。预后不良组血小板计数、C-反应蛋白及免疫球蛋白A水平高于预后良好组(均P<0.05)。皮疹反复发作、初次发病伴肾损害、呼吸道感染、血小板计数、C-反应蛋白及免疫球蛋白A为HSP患儿预后的独立影响因素(均P<0.05)。皮疹反复发作、呼吸道感染、血小板计数、C-反应蛋白及免疫球蛋白A对HSP患儿预后不良具有预测价值(均P<0.05)。结论:皮疹反复发作、初次发病伴肾损害、呼吸道感染、血小板计数、C-反应蛋白及免疫球蛋白A为HSP患儿预后的独立影响因素。除初次发病伴肾损害指标外,其余指标对HSP患儿预后不良具有一定预测价值。

儿童IgA血管炎临床研究进展

IgA血管炎(IgAV)是一种由IgA沉积在小血管引起的自身免疫性疾病,除了非血小板减少性紫癜表现,还有胃肠道、关节及肾脏受累。该病具有自限性,少数累及肾脏者,可在晚年发展为终末期肾脏疾病。文章对儿童IgAV临床特征及累及肾脏的相关机制进行综述,并探讨该病的治疗及预后。

儿童过敏性紫癜的营养状况和25-羟基维生素D_(3)水平的临床研究

目的探讨不同营养状况及血清25-羟基维生素D_(3)[25-(OH)D_(3)]水平与儿童过敏性紫癜(HSP)的相关性。方法选取2019年9月至2020年2月于首都医科大学附属北京儿童医院确诊的HSP患儿共119例作为观察组,根据营养状况进一步分为营养正常组(67例)与营养不良组(52例),同时选取同时期于首都医科大学附属北京儿童医院门诊进行健康体检的儿童90例作为对照组。比较分析观察组和对照组、营养正常组和营养不良组儿童的25-(OH)D_(3)水平。结果对照组儿童的25-(OH)D_(3)水平显著高于观察组患儿,差异有统计学意义(P<0.05);营养不良组患儿的25-(OH)D_(3)水平低于营养正常组,差异有统计学意义(P<0.05)。结论HSP患儿25-(OH)D_(3)水平与健康儿童相比明显降低,HSP合并营养不良患儿的25-(OH)D_(3)水平与营养状态正常的HSP患儿相比明显降低。

过敏性紫癜合并器官功能损害的研究现状

过敏性紫癜是临床中最常见的系统性血管炎类疾病,典型临床表现为双下肢的非血小板减少性紫癜,关节、胃肠道及肾损害。随着对此病不断地深入认识,累及其他少见器官的临床表现及诊断值得临床医师关注。该文就近年来国内外过敏性紫癜伴有各个系统损害的临床表现、诊断、危险因素和治疗做一简要综述。

基于文献挖掘的过敏性紫癜动物模型应用特点分析及建模思考

目的研究过敏性紫癜动物模型的造模特点,为其动物模型的规范化提供计量参考。方法在中国知网、万方、维普、中国生物医学文献数据库、PubMed及Web of Science数据库检索过敏性紫癜动物模型相关文献,归纳实验动物品系、年龄、性别、造模方法、成模周期、阳性对照药、检测指标等,构建数据库并进行规范整理、分析。结果共纳入符合标准的46篇文献,包含动物模型实验研究52例。实验动物多选择6周龄、3~4周龄的SD大鼠或3~4周龄、8周龄的KM小鼠,性别多选择雄性或雌雄各半。模型以病证结合复合模型和模拟IgA肾病模型多见;常用造模方法为尾静脉注射印度墨水+灌胃和尾静脉注射麦胶蛋白溶液、灌胃/口服干姜、胡椒、荜茇+腹腔注射卵白蛋白和弗氏完全佐剂混合液+尾静脉/耳缘静脉和皮内注射卵白蛋白0.9%氯化钠溶液;造模周期以14、6、12周多见。阳性对照药应用最多的是西咪替丁、双嘧达莫、雷公藤多苷片。高频检测指标依次为血清相关生化指标、肾组织病理、24 h尿蛋白、肾组织免疫组化、表观指标、尿常规、皮肤组织病理等。结论目前过敏性紫癜动物模型制备方法多样,病证结合复合模型与中西医临床特点吻合度较高,但缺少统一的造模方法及中医证候评价标准等,还需探索其他相关证型的病证模型,并进一步重复验证、完善。

基于数据挖掘的紫癜性肾炎动物模型分析

目的 基于文献挖掘探讨紫癜性肾炎动物模型的造模特点,为制备规范化的紫癜性肾炎动物模型提供参考。方法 通过计算机检索中国知网、万方、维普、中国生物医学文献数据库、PubMed中英文数据库中相关研究文献,获取近20年紫癜性肾炎动物实验文献,将实验动物种类、造模方法、给药剂量、给药周期、成模标准及检测指标进行人工筛选,应用Microsoft Excel 2021软件建立数据库并进行统计分析,运用SPSS Modeler 18.0对高频指标进行关联规则分析并运用Cytoscape 3.6.1软件对关联网络图进行可视化升级。结果 归纳总结符合纳入标准的106篇文献,建立紫癜性肾炎动物模型多选用SD大鼠和KM小鼠,造模方式多选用药源性诱导,造模药物以牛血清白蛋白(bovine serum albumin, BSA)+脂多糖(lipopolysaccharide, LPS)+四氯化碳(carbon tetrachloride, CCl_4)+蓖麻油、卵白蛋白(ovalbumin, OVA)+弗氏完全佐剂、麦胶蛋白+印度墨水、牛血清白蛋白+葡萄糖菌肠毒素B(staphylococcus enterotoxin B,SEB)复刻紫癜性肾炎吻合度较高的动物模型,周期一般在5~14周,成模标准多选用皮肤紫癜,尿红细胞数增多,尿蛋白阳性,肾组织可见肾小球系膜增生及以免疫球蛋白A(immunoglobulin A,IgA)为主的免疫复合物沉积于小血管表示造模成功。检测指标共涉及36个医学指标,其中肾及尿液相关的检测指标23个,血液相关检测指标9个,其中使用频率≥10%的有24 h尿蛋白定量、白细胞介素、肾病理、尿红细胞计数、IgA及循环免疫复合物(circulation immune complex, CIC)、肌酐(creatinine, Cr)等10个指标,对高频指标进行聚类分析,结果表明多采用24 h尿蛋白定量-白细胞介素-肾病理-尿红细胞数-IgA综合评价模型。结论 现有的紫癜性肾炎动物实验多选用SD雄性大鼠和KM雌性小鼠,造模方式多采用药源性诱导,其中瘀热证复合IgA肾病法(病证结合法)具有重复性强、成模率高的优点,可为HSPN动物实验模型选择提供参考。

血液净化治疗儿童过敏性紫癜的研究进展

过敏性紫癜是儿童时期最常见的系统性血管炎,临床主要表现为皮肤瘀点瘀斑、腹痛、关节肿痛及血尿等。因本病的发病率逐渐上升,且重症病例增多,故探寻迅速、有效缓解过敏性紫癜临床症状的方法成为研究重点。本文就血液净化技术在儿童过敏性紫癜中的治疗作一综述。

粪钙卫蛋白在腹型过敏性紫癜中的相关研究进展

腹型过敏性紫癜(abdominal type of Henoch-Sch nlein purpura,AHSP)是一种由IgA介导的全身性血管炎,常发于儿童。AHSP由于症状非典型,故早期筛查诊断难度较大,常规通过胃肠镜检查确诊。钙卫蛋白由S100A8和S100A9蛋白亚体组成,一般来源于中性粒细胞,具有多种生物学作用。粪钙卫蛋白浓度与肠道炎症相关,用于评估胃肠道炎症。鉴于AHSP常伴胃肠道疾病,粪钙卫蛋白具备作为AHSP早期诊断指标的潜力。本研究综述了粪钙卫蛋白在AHSP早期诊断中的应用价值,旨在为将其作为AHSP的临床诊断指标增加理论依据。

儿童血管内压力增高性紫癜误诊为过敏性紫癜临床分析

目的探讨儿童血管内压力增高性紫癜误诊为过敏性紫癜的原因、鉴别要点及防范措施。方法回顾性分析2023年3月至2024年3月收治的误诊为过敏性紫癜的血管内压力增高性紫癜患儿38例的临床资料。结果38例患儿初诊时出现不同程度的双侧下肢或双足、踝部针尖大小皮疹,散在或密集分布,不高出皮肤,压之不褪色。8例患儿皮疹亦可见于头面部、双侧上肢及躯干部。既往诊断为过敏性紫癜,予相应治疗未见明显缓解,详细询问患儿病史,观察皮疹形态及分布特点,完善实验室检查排除其他血液系统及免疫系统疾病后诊断为血管内压力增高性紫癜,予停药观察,随访24周。38例患儿中27例皮疹复发,未予药物干预自行消退。误诊时间为2~28周。全部病例均未出现肾脏损害。结论血管内压力增高性紫癜临床表现不典型,无特异性检查指标,易被误诊。临床需加强病史询问、皮疹形态的鉴别诊断,及时完善相关检查,减少误诊。

血清IgE、IgA及MMP-13水平在复发性过敏性紫癜患儿中的表达及临床意义

目的探讨复发性过敏性紫癜(HSP)患儿血清中免疫球蛋白E(IgE)、免疫球蛋白A(IgA)以及基质金属蛋白酶-13(MMP-13)的表达水平及其临床意义,以此为临床治疗提供参考。方法选取2020年3月—2023年1月空军军医大学第二附属医院收治的HSP患儿161例为观察组,另选取同期于本院进行体检且各项正常儿童143例为对照组。观察组患儿于入院后次日清晨、对照组研究对象于体检当日早晨空腹状态下抽取静脉血5 mL。对比不同人群血清IgE、IgA、MMP-13水平,分析随访过程中观察组患儿复发情况;分析影响HSP患儿复发的单因素,采用多元logistic回归分析影响HSP复发的多因素。结果观察组患儿IgE、IgA、MMP-13水平均高于对照组,差异具有统计学意义(P<0.05)。经12个月的随访可知,161例HSP患儿中复发了36例(22.36%),其中再次出现关节疼痛15例,再次出现腹痛者10例,再次出现关节积液者7例,再次出现其他临床症状者4例,均归为复发组;随访期间,HSP患儿未出现临床症状的有125例(77.64%),归为未复发组。复发组患儿中饮食控制占比、血小板计数水平均低于未复发组,且乳酸脱氢酶、IgE、IgA、MMP-13水平均高于未复发组,差异均具有统计学意义(P<0.05)。多因素logistic回归分析结果显示:无饮食控制、血小板计数降低、乳酸脱氢酶水平升高、IgE水平升高、IgA水平升高、MMP-13水平升高为影响HSP复发的危险因素(P<0.05)。结论在复发性HSP患儿中,血清IgE、IgA及MMP-13水平均呈现上升趋势,并且三者同饮食不控制、血小板计数降低以及乳酸脱氢酶水平升高,均被视为影响HSP复发的危险因素。