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.

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.

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.

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。

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。

Heat shock protein 70-2 and tumor necrosis factor-α gene polymorphisms in Chinese children with Henoch- Schönlein purpura

Background:Henoch-Schönlein purpura(HSP)or IgAassociated vasculitis is related to immune disturbances.Polymorphisms of the heat shock protein 70-2 gene(HSP70-2)and the tumor necrosis factor-αgene(TNF-α)are known to be associated with immune diseases.The purpose of this study was to investigate the likely association of HSP70-2(+1267A/G)and TNF-α(+308A/G)gene polymorphisms with HSP in children.Methods:The polymerase chain reaction restriction fragment length polymorphism method was used to detect the HSP70-2 and TNF-αpolymorphisms in 205 cases of children with HSP and 53 controls;and the association of these polymorphisms with HSP and HSP nephritis(HSPN)was analyzed.Results:The G/G genotypic frequencies at the+1267A/G position of HSP70-2 in the HSP group(22.9%)were signifi cantly higher than those in the healthy control group(9.4%)(χ^(2)=4.764,P<0.05).The frequencies of the A/A,A/G and G/G genotypes of HSP70-2 in patients in the nephritis-free group and the HSPN group showed no statistically significant difference.The A/A genotype frequency at the+308G/A position of TNF-αin the HSP group was 8.3%,which was higher than that in the control group(χ^(2)=6.447,P<0.05).The A allele frequency of TNF-αin the HSP group was higher than that in the control group,with a statistically significant difference(χ^(2)=7.241,P<0.05).Conclusions:The HSP70-2(+1267A/G)and TNF-α(+308G/A)gene polymorphisms were associated with HSP in children.The G/G homozygosity of HSP70-2 and the A/A homozygosity of TNF-αmay be genetic predisposing factors for HSP.

吗替麦考酚酯治疗以蛋白尿为主的儿童紫癜性肾炎疗效观察

目的评价吗替麦考酚酯(MMF)分散片联合小剂量激素治疗以蛋白尿为主的儿童难治性紫癜性肾炎的临床疗效及安全性。方法选取19例以蛋白尿为主的难治性紫癜性肾炎儿童作为研究对象,其中5例在MMF治疗之前接受肾活检(轻度系膜增殖性肾炎2例,中度系膜增殖性肾炎伴新月体形成1例,重度系膜增殖性肾炎1例,局灶节段性肾小球硬化1例)。泼尼松0.5～1.0 mg/(kg.d),平均0.74 mg/(kg.d),尿蛋白转阴2周后逐渐减量,半月减5～10 mg至5～10 mg/d维持;MMF分散片20～25 mg/(kg.d),2次/d。随访1～1.7年。治疗期间定期复查血常规、尿常规、肾功能、肝功能以及24 h尿蛋白定量等,治疗3个月后进行疗效及安全性评价。结果 MMF分散片联合小剂量激素治疗前、后24 h尿蛋白定量和血清白蛋白差异有统计学意义(P<0.01)。治疗3个月后19例中完全有效17例,部分有效2例。1例应用MMF后2个月合并水痘,1例出现了胃肠道症状,2例一过性白细胞减少。结论吗替麦考酚酯分散片联合小剂量泼尼松能有效缓解以蛋白尿为主的儿童紫癜性肾炎尿蛋白,改善病情,且近期不良反应少,安全性高,依从性好。

初发过敏性紫癜患儿肾脏受累危险因素分析

目的对初发过敏性紫癜(HSP)患儿进行随访,探讨HSP患儿肾脏受累的危险因素。方法前瞻性纳入2009年12月至2010年11月在南京医科大学附属南京儿童医院肾脏科住院的初发HSP患儿,随访6个月,根据肾脏受累定义,将HSP患儿分为肾脏受累组和无肾脏受累组。复习文献提取与肾脏受累可能相关的3项人口学特征、8项临床症状和17项辅助检查指标进行分析,先行单因素分析,对有统计学意义的变量行Logistic回归分析。结果研究期间共纳入初发HSP患儿283例,平均发病年龄为(7.2±2.6)岁(8月龄至16岁)。239/283例(84.5%)完成随访。283例初发HSP患儿均有紫癜样皮疹表现,分别有194/283例(68.6%)和224/283例(79.2%)患儿有消化道和关节症状。80/239例(33.5%)患儿在随访过程中出现肾脏受累,以孤立性蛋白尿为主(44/80例,55.0%)。发病1个月内出现肾脏受累者占50.0%(40/80例),3个月内出现肾脏受累者占88.8%(71/80例)。单因素分析提示年龄≥8岁、皮疹反复、皮疹持续≥2周、无菌性白细胞尿、血清白蛋白、血小板平均容积(MPV)≥10fL、胱抑素C(CysC)≥0.8mg·L-1和血清C3≤0.88g.L-1在肾脏受累组和无肾脏受累组间差异有统计学意义(均P<0.05)。多因素Logistic回归分析结果显示,无菌性白细胞尿:OR=4.178,95%CI:2.061～8.468,皮疹持续≥2周:OR=2.474,95%CI:1.367～4.478,MPV≥10fL:OR=2.948,95%CI:1.533～5.667,CysC≥0.8mg·L-1:OR=2.101,95%CI:1.067～4.134。结论无菌性白细胞尿、皮疹持续≥2周、MPV≥10fL和CysC≥0.8mg·L-1为初发HSP患儿肾脏受累的独立危险因素。

过敏性紫癜患儿血清Tim-1水平及临床意义

目的检测过敏性紫癜(HSP)患儿不同临床类型、不同临床疾病期血清中Tim-1水平,探讨Tim-1与HSP发生的关系。方法不同临床类型HSP患儿共35例,分别在急性期和恢复期空腹采静脉血2 ml,ELISA法测定其血清中Tim-1水平;20例无过敏性疾病史的健康体检儿童作为对照。结果 HSP患儿急性期血清中Tim-1含量较正常对照组显著增高(P<0.001),HSP腹型和肾型急性期血清中Tim-1水平显著高于HSP单纯型(P<0.01),而HSP腹型和肾型急性期血清中Tim-1水平差异无统计学意义。结论 Tim-1与HSP发生及临床类型有关,检测HSP患儿血清中Tim-1水平有助于判断HSP患儿的严重程度及复发可能。

儿童腹型过敏性紫癜的超声表现

目的探讨腹型过敏性紫癜(HSP)的超声表现及诊断价值。方法选择2009年6月至2009年12月83例腹型HSP患儿,其中男性49例,女性34例;年龄2～16岁,平均年龄7.72岁。回顾性分析临床诊断腹型HSP患儿的超声表现。结果病变肠管以小肠为主,肠壁肿胀,内部可分层,血流信号增多,呈乏蠕动状态。可出现盆腔积液或淋巴结增大,肠系膜回声改变等伴发表现。结论儿童腹型HSP的超声表现有一定特异性,可对受累肠管进行细致观察及时随诊,有助于早期提示该病,并可以用于观察其并发症及临床疗效。超声检查可作为儿童腹型HSP的常规首选检查。

十二指肠降部黏膜免疫荧光试验辅助诊断过敏性紫癜的价值及临床局限性

目的探讨十二指肠降部免疫荧光试验与黏膜病变程度在过敏性紫癜(HSP)辅助诊断中的价值和临床局限性。方法收集2014年4月至2015年12月复旦大学附属儿科医院消化科以腹痛为主要症状初诊的HSP或怀疑HSP,且辅助诊断至少有胃镜检查并行十二指肠降部黏膜免疫荧光试验的患儿,从病史中查阅紫癜的记录情况,采集HSP患儿行胃镜检查时十二指肠黏膜病变程度及其组织荧光试验结果;本文以胃镜直视下充血、水肿为轻度病变,糜烂和溃疡为中重度病变;本文以典型皮肤紫癜出现在胃镜检查前为早出紫癜,之后为晚出紫癜;根据免疫荧光试验结果分为阴性和阳性。结果符合本文纳入和排除标准的54例HSP患儿进入本文分析,男31例,女23例;平均(8.1±2.7)岁;门诊病例14例,住院病例40例;早出紫癜36例(76.7%),晚出紫癜18例。十二指肠降部黏膜均受累,免疫荧光阳性31例(57.4%),阴性23例(其中弱阳性6例)。十二指肠降部黏膜轻度病变14例(25.3%),重度病变40例(其中糜烂19例,溃疡21例)。免疫荧光阴性的HSP患儿中黏膜中重度病变的比例明显多于阳性,差异有统计学意义[91.3%(21/23)vs61.3%(19/31),P=0.013];早出紫癜的HSP患儿黏膜轻度病变免疫荧光阳性比例(10/31,32.2%)多于阴性(2/23,8.7%),差异有统计学意义(P=0.039);不论免疫荧光结果阳性与否:早或晚出紫癜HSP患儿黏膜病变轻度与中重度比例差异均无统计学意义、晚出紫癜的HSP患儿黏膜轻度病变的比例差异无统计学意义、早出或晚出紫癜的HSP患儿黏膜中重病变的比例差异亦均无统计学意义。结论十二指肠降部黏膜较皮肤组织免疫荧光试验阳性率低,可能与取活检处黏膜的病变严重程度有关,不排除与取活检的部位、数量、深度及器械等多种因素有关。

儿童紫癜性肾炎的诊断、治疗与预后

紫癜性肾炎是儿童较常见的继发性肾脏疾病,部分患者随着病情进展,肾功能逐渐减退,最终需长期肾脏替代治疗,预后欠佳。其治疗方案受到国内外广泛关注但尚未有统一确定的结论,血管紧张素受体拮抗剂、糖皮质激素、细胞毒药物、免疫抑制剂等治疗方法在文中进行介绍。国内外学者报道紫癜性肾炎远期预后终末期肾损害发生率高低不等,与其预后密切相关的因素尚需更多高质量的循证医学方面的证据以进一步明确。

紫癜性肾炎患儿肾组织podocalyxin的表达及其与尿足细胞数的相关分析(英文)

目的：分析肾脏足细胞特异蛋白podocalyxin（PCX）的表达和尿足细胞数在紫癜性肾炎（Henoch-Schnlein purpura nephritis,HSPN）病理进展过程中的变化。方法：56例HSPN患儿为病例组,根据肾脏病理改变分为4组：HSPN Ⅱ（Ⅱa＋Ⅱb）级组（n=10）,Ⅲ（Ⅲa＋Ⅲb）级组（n=21）,Ⅳ级组（n=16）和Ⅴ级组（n=9）;另取非肾脏疾病死亡病例尸检切取的肾脏标本4例作为正常肾组织对照组;同时收集8例健康儿童的晨尿作正常尿液对照组。应用免疫荧光方法检测PCX在4例正常肾组织及56例HSPN肾组织中的表达,并对其结果进行定量分析;同时检测8例健康儿童及56例HSPN患儿尿足细胞阳性的发生率和尿足细胞数。结果：在正常对照组和HSPN Ⅱ（Ⅱa＋Ⅱb）级组的肾组织中,PCX表达完整,2组之间肾组织PCX阳性面积占肾小球面积的百分比差异无统计学意义（P〉0.05）;在HSPN Ⅲ（Ⅲa＋Ⅲb）级﹑Ⅳ级和Ⅴ级组的肾组织中,PCX表达均有不同程度缺失,从Ⅲ（Ⅲa＋Ⅲb）~Ⅴ级其表达依次下降,各组间比较差异有统计学意义（P〈0.01）;病理分级在Ⅲ（Ⅲa＋Ⅲb）级以上的HSPN,尿中有PCX的阳性表达,提示尿中有足细胞存在;肾组织PCX荧光阳性面积占肾小球的百分比与尿中足细胞数呈负相关（r=-0.637,P〈0.01）。结论：足细胞损伤在儿童HSPN病理进展中发挥一定作用;可以在一定程度上反映HSPN的病理损伤程度。

彩色多普勒检测过敏性紫癜患儿肾血流变化的价值

目的:探讨彩色多普勒检测过敏性紫癜(HSP)患儿肾血流变化的临床意义。方法:用彩色多普勒超声仪检测35例HSP患儿肾血流动力学变化,以30例健康儿童作为对照组,同时检测HSP患儿尿常规、尿微量白蛋白。结果:HSP患儿肾血流频谱为高速高阻型,肾主动脉、叶间动脉、弓状动脉的收缩期最大峰值流和阻力指数均高于正常对照组。35例HSP患儿中彩超肾血流异常31例(88.6%),尿常规异常8例(22.9%),尿微量白蛋白异常25例(71.4%)。检测的敏感性由高到低依次为彩超肾血流、尿微量白蛋白、尿常规。结论:多普勒肾血流检测是早期发现过敏性紫癜患儿肾损害的敏感指标。

抗核抗体在儿童过敏性紫癜发病中的作用

目的:研究抗核抗体在儿童过敏性紫癜(Henoch-Sch9nlein purpura,HSP)发病中的作用。方法:回顾性分析临床HSP患儿病史,并分成紫癜型、关节型、腹型和肾炎型HSP;同时收集健康体检儿童血样。分析抗核抗体滴度及抗核抗体谱在HSP以及不同临床亚型中的检出率,抗核抗体阳性对体液免疫(C3、C4、Ig A、Ig G、Ig M)及细胞免疫(CD3^+、CD3^+CD4^+、CD3^+CD8^+、CD3-CD19^+、CD19^+CD23^+、CD3-CD16^+CD56^+细胞)的影响,体液免疫、细胞免疫对抗核抗体阳性的影响。结果:共收集同龄健康体检儿童82例,HSP患儿436例。HSP患儿抗核抗体阳性66例(15.14%),其中关节型HSP 17例,紫癜型HSP 25例,腹型HSP 13例,肾炎型HSP 11例;抗核抗体滴度介于1∶100~1∶320,抗核抗体谱阳性介于弱阳性及阳性之间。抗核抗体在HSP不同临床亚型之间的检出率差异无统计学意义(P=0.213)。抗核抗体阳性HSP患儿的Ig A、Ig G、Ig M水平较健康对照明显升高(P均<0.01),补体C3、C4差异无统计学意义(P>0.05);细胞免疫中HSP患儿CD3^+、CD3^+CD4^+和CD3-CD16^+CD56^+细胞比例显著下降(P分别为<0.01、<0.01、0.009),而CD3^+CD8^+、CD3-CD19^+和CD19^+CD23^+细胞显著升高(P分别为0.011、<0.01、<0.01)。将各HSP临床亚型患儿根据抗核抗体结果分为自身抗体阳性和阴性两组,结果显示两组体液和细胞免疫各指标的差异均无统计学意义(P均>0.05)。Logistic回归分析显示,体液免疫及细胞免疫指标均不是影响抗核抗体阳性的主要因素。结论:抗核抗体阳性不是影响HSP患儿体液免疫及细胞免疫的主要因素,HSP患儿免疫功能的变化也不是影响抗核抗体阳性的主要因素;HSP患儿中低滴度或非强阳性抗核抗体可能是自身免疫机制中产生的非特异性抗体。

紫癜性肾炎伴高血压患儿临床病理特征及预后分析

目的分析过敏性紫癜性肾炎(henoch-Schonlein purpura nephritis,HSPN)伴高血压患儿临床和病理特征及预后特点。方法对2015年1月至2019年12月贵阳市妇幼保健院住院诊断为HSPN的148例患儿的临床及病理资料进行回顾性分析,根据患儿是否合并高血压分为HSPN血压正常组和HSPN伴高血压组,分析比较两组患儿临床病理特征及预后的差异。结果(1)148例HSPN患儿中血压正常105例(70.9%),伴高血压43例(29.1%),两组患儿在性别、年龄、起病时间上差异无统计学意义。(2)高血压组患儿夜间高血压发生率明显大于日间高血压发生率(χ^(2)=9.446,P<0.05)。两组患儿异常血压类型(非杓型及反杓型血压)发生率分别为79.1%、77.1%,差异无统计学意义。(3)高血压组24 h尿蛋白定量、尿微量白蛋白、血肌酐、血总胆固醇程度较血压正常组严重,差异有统计学意义(P<0.05),而血补体C3、血白蛋白、血小板计数差异无统计学意义。(4)高血压组临床分型以肾病综合征型为主,较血压正常组重,差异有统计学意义(χ^(2)=35.470,P<0.01)。高血压组病理分型均为Ⅲ型及Ⅲ型以上,较血压正常组重,差异有统计学意义(χ^(2)=25.642,P<0.01)。(5)与血压正常组比较,高血压组预后较差,差异有统计学意义(χ^(2)=6.663,P<0.05)。结论HSPN伴高血压患儿以夜间血压升高为主,其临床分型和病理分型较HSPN血压正常患儿严重,肾脏预后较差,应重视HSPN伴高血压患儿血压管理,改善患儿预后。