人血丙种球蛋白和阿司匹林治疗对川崎病患儿循环内皮祖细胞功能的影响

目的：研究人血丙种球蛋白(IVIG)和阿司匹林(ASP)治疗对川崎病患儿循环内皮祖细胞功能的影响及其可能的机制。方法：抽取10例川崎病患儿IVIG和ASP治疗前及治疗7 d后的外周血,将单个核细胞诱导培养内皮祖细胞。利用MTT法、改良Boyden小室法、细胞培养板贴壁法测定内皮祖细胞的增殖、迁移和贴壁功能。同时测定血浆中肿瘤坏死因子-α（TNF-α）和超敏C反应蛋白（hs-CRP）的浓度。结果：IVIG和ASP治疗7 d后循环内皮祖细胞的功能较治疗前显著提高。IVIG和ASP治疗7 d后血浆中TNF-α和hs-CRP 的浓度显著降低。治疗后TNF-α和hs-CRP 浓度的降低与内皮祖细胞功能的提高呈显著正相关关系。结论：IVIG和ASP治疗可显著改善川崎病患儿循环内皮祖细胞的功能,其机制可能与TNF-α和hs-CRP的浓度降低有关。     

血浆内皮微粒水平变化与川崎病冠状动脉损伤关系的研究

目的 通过观察川崎病患儿血浆内皮微粒(endothelial microparticle,EMP)水平的变化,确定EMP水平变化与川崎病冠状动脉损伤的关系,探讨EMP测定在早期诊断冠状动脉损伤中的价值.方法 30例川崎病患儿均符合日本川崎病研究委员会第4次修订的诊断标准,其中24例为完全型川崎病,6例为不完全型川崎病,并按病程分为急性期、亚急性期、恢复期.根据超声心动图将川崎病组又分为冠状动脉损伤组(6例)和冠状动脉无损伤组(24例).以10例发热伴有皮疹的患儿及10例健康儿童为发热对照组和正常对照组.采用流式细胞术检测血浆中CD31+/CD42b- EMP水平.结果 川崎病患儿急性期血浆EMP水平[(8.18±2.29)％]明显高于恢复期[(2.77±0.85)％]和正常对照组[(1.34±0.38)％](P＜0.01);亚急性期血浆EMP水平[(5.93±1.05)％]明显高于恢复期和正常对照组(P＜0.01);发热对照组血浆EMP水平[(3.66±1.16)％]高于正常对照组(P＜0.05);急性期川崎病患儿中冠状动脉损伤组血浆EMP水平高于冠状动脉无损伤组,差异有统计学意义(P＜0.01).结论 血浆EMP的检测分析有助于川崎病的早期诊断及冠状动脉损伤的早期发现.     

川崎病冠状动脉损伤与纤维蛋白原Bβ-148C/T基因多态性的关系

目的：探讨纤维蛋白原Bβ-148C/T基因多态性与川崎病冠状动脉损伤的关系。方法：收集36例川崎病患儿与49例健康对照儿童的空腹静脉血,用辅助血浆纤维蛋白原活性测定系统测定纤维蛋白原水平和纤维蛋白原的分子功能;采用多聚酶链反应,限制性酶切方法对纤维蛋白原Bβ-148C/T位点的基因型进行测定。结果：川崎病儿童冠状动脉扩张组血浆纤维蛋白原水平明显高于非扩张组及健康对照组(P<0.01); 川崎病儿童冠状动脉扩张组T等位基因频率明显高于健康对照组及非扩张组 (P<0.01)。结论：纤维蛋白原β-148基因多态性及血浆纤维蛋白原水平与川崎病患儿冠状动脉扩张有相关性。［中国当代儿科杂志,2010,12（7）：518-520］     

川崎病患儿血浆脑利钠肽水平改变及其与心功能的关系

目的：探讨脑利钠肽(BNP) 在川崎病(KD)患儿血浆中的变化及其与心功能的关系。方法：选择KD患儿43例作为观察组（KD组）,30例健康儿童作为对照组。对KD急性期、恢复期患儿及对照组儿童采用酶联免疫吸附法测定血浆BNP浓度,KD组常规超声心动图检测左室射血分数(LVEF)、左室短轴缩短率（LVSF）、心脏指数（CI）及舒张期二尖瓣血流频谱速度（E/A）。结果：KD患儿急性期血浆BNP水平明显高于恢复期及对照组,差异有统计学意义(P<0.01)。急性期LVEF、LVSF、CI较恢复期降低,差异有统计学意义（P<0.05）。直线相关分析显示,KD患儿急性期血浆BNP水平与LVEF、LVSF、CI均呈负相关（r=-0.63,-0.52,-0.53,P<0.05）。结论：血浆BNP浓度在KD急性期异常升高,与左室收缩功能呈负相关。血浆BNP水平检测对KD的早期诊断具有重要意义。［中国当代儿科杂志,2010,12（3）：169-171］     

紫绀型先天性心脏病患儿血清VEGF和SDF-1水平与循环EPCs的相关性研究

目的：探讨紫绀型先天性心脏病患儿血清血管内皮生长因子（VEGF）和基质细胞衍生因子（SDF-1）的水平与循环内皮祖细胞（EPCs）数量及功能变化的关系。方法：采用ELISA法检测15例法洛四联症患儿（紫绀组）外周血清SDF-1和VEGF的水平;采用密度梯度离心法分离EPCs体外扩增培养;做免疫荧光鉴定及细胞计数。采用MTT比色法、改良的Boyden小室和黏附能力测定实验,观察EPCs的增殖能力、迁移能力及黏附能力。用回归分析法分析VEGF和SDF-1水平与EPCs数量及功能的相关性。单纯室间隔缺损患儿15例为对照组。结果：紫绀组与对照组相比, VEGF水平增高（201.42±44.74 ng/L vs 113.56±35.62 ng/L）;SDF-1水平增高（3.45±1.07 ng/L vs 1.05±0.99 ng/L,P<0.05）。血清VEGF与SDF-1水平呈正相关（r=0.675,P<0.01）。与对照组相比,紫绀组PEPCs数目明显增多（72.2±9.73）/200倍视野vs （51.2±3.83）/200倍视野,P<0.01; EPCs功能明显增强,其增殖能力、迁移能力及黏附能力明显强于对照组。VEGF,SDF-1的血清水平与EPCs数量及功能变化表现出明显的一致性,相关系数分别为0.8395,0.5491,0.6376和0.7392。结论：紫绀型先天性心脏病外周血EPCs数量及功能较非紫绀组明显增加,同时VEGF和SDF-1血清水平也明显增加,上述变化存在相关性,可能共同影响着患者的一些病理、生理变化。［中国当代儿科杂志,2009,11（4）：267-272］     

心型脂肪酸结合蛋白在川崎病患儿中的变化及其临床意义

目的：通过测定川崎病（KD）患儿血清心型脂肪酸结合蛋白(h-FABP)水平变化,以探讨h-FABP在反映KD患儿心肌损害中的临床价值。方法：选择40例KD患儿为研究对象,以30例正常儿童为对照组。对KD组及对照组采用酶联免疫吸附法检测血清h-FABP、肌钙蛋白I（cTnI）,同时利用杜邦全自动生化分析仪检测肌酸磷酸激酶同功酶（CK-MB）。并行心脏彩色多普勒(UCG)检测冠状动脉内径,将KD组分为冠状动脉病变（CAL）组和非冠状动脉病变（NCAL）组。结果：KD组血清h-FABP浓度、阳性率与对照组比较差异有显著性（P<0.01）,cTnI浓度及阳性率明显高于对照组(P<0.05),而CK-MB浓度和阳性率与对照组比较差异无显著性（P>0.05）;h-FABP与cTnI阳性率比较差异有显著性（P<0.01）;CAL组和NCAL组血清h FABP浓度对比差异有显著性（P<0.01）。结论：血浆h-FABP、cTnI浓度可作为KD患儿早期心肌损害的生化标志物,而h-FABP具有更高的灵敏度和特异性;血浆h-FABP浓度对川崎病以及川崎病合并冠状动脉病变的早期诊断、指导治疗具有重要的临床意义。     

内源性血管弹性蛋白酶在川崎病冠状动脉重构中的作用研究

目的 探讨内源性血管弹性蛋白酶（EVE）对川崎病患儿冠状动脉重构的影响。方法 2012年1月至2013年4月诊断为川崎病的60例患儿作为病例组,分别于发病0~11 d（病理Ⅰ期）、发病12~25 d（病理Ⅱ期）抽取外周静脉血3 mL;60例同期因发热就诊的非川崎病患儿作为对照组,均于发热急性期空腹抽取外周静脉血3 mL。应用酶联免疫法（ELISA）检测各组血清中EVE、IL-6及血浆中血管内皮生长因子（VEGF）水平;病例组分别于发病的第一周末、第二周末和第四周末以超声心动图检查冠状动脉受损情况;Pearson相关分析评价EVE与IL-6和VEGF的相关性。结果 病例组Ⅰ期和Ⅱ期血清EVE和IL-6水平均明显高于对照组,而血浆VEGF水平均低于对照组（均PPPPr=0.915、-0.769,均P结论 EVE可能参与川崎病患儿冠状动脉重构,干预其活性可能缓解和阻止冠状动脉损害。     

川崎病冠脉瘤患儿远期血管内皮功能的研究

目的：评估川崎病（KD）冠脉瘤患儿远期血管内皮功能。方法：选择病程大于1年的合并中型以上冠脉瘤的川崎病患儿31例为研究对象,采用高分辨率超声仪进行肱动脉内皮依赖性和非依赖性舒张功能（FMD）、颈动脉僵硬度指数（SI）和颈动脉内中膜厚度（IMT）的检测。选择年龄相近的正常儿童21例作为对照。结果：31例KD冠脉瘤患儿中,中型冠脉瘤9例,冠脉巨大瘤22例,其中12例有心肌缺血。与对照组比较,KD冠脉瘤组患儿肱动脉血管内皮依赖性FMD减低（P＜0.05）,颈动脉SI增加（P＜0.05）,颈动脉IMT增厚（P＜0.05）。与无心肌缺血患儿相比,有心肌缺血患儿血管内皮依赖性FMD显著降低（P＜0.05）。结论：KD冠脉瘤患儿远期存在血管内皮功能障碍,且合并心肌缺血患儿的血管内皮功能障碍尤为显著。     

一氧化氮和内皮型一氧化氮合成酶与血管迷走性晕厥发病的关系

目的：探讨一氧化氮和内皮型一氧化氮合成酶与儿童血管迷走性晕厥发病的关系。方法：血管迷走性晕厥患儿14例（A组）,其他原因引起晕厥患儿10例（B组）,健康志愿者20例（C组）。于倾斜试验（HUT）前和倾斜不同时间测定A组与B组患儿的血浆一氧化氮（NO）水平,同时对3组儿童进行内皮型一氧化氮合成酶（eNOS）基因G894T多态性检测。结果：①A组患儿出现阳性反应时血浆NO水平较平卧时显著升高（76.7±9.6 vs 90.0±11.4 μmol/L, P<0.05）;②A组患儿在症状好转后血浆NO水平较试验前显著降低（82.7±9.2 vs 61.5±6.9 μmol/L,P<0.01）;③B组患儿倾斜时血浆NO水平较平卧时差异无显著性;④A,B两组患儿的血压、心率变化与NO水平无显著相关性;⑤A组患儿eNOS基因G894T突变型基因频率显著高于B组与C组(42.9% vs 10%, P<0.05)。结论： 倾斜体位时血浆NO水平异常升高可能参与了血浆血管迷走性晕厥的发病机制,而其升高水平可能与eNOS基因G894T多态性表达有关。     

川崎病患儿血浆可溶性血栓调节蛋白的检测及其意义

目的探讨川崎病(KD)患儿治疗前后血浆可溶性血栓调节蛋白(sTM)含量变化及其临床意义。方法2004-07—2006-07入住南京医科大学附属南京儿童医院的KD患儿67例,将患儿分为无冠状动脉损伤组(39例)和冠状动脉损伤组(28例),按病程分为急性期、亚急性期和恢复期;另以28例健康儿童作为正常对照组。应用酶联免疫吸附法检测血浆sTM水平。结果急性期有、无冠状动脉损伤组血浆sTM质量浓度均明显高于正常对照组(均P<0.01),且冠状动脉损伤组血浆sTM蛋白水平亦显著高于无冠状动脉损伤组(P<0.01);治疗后sTM水平降低,冠状动脉损伤组KD患儿的血浆sTM水平急性期[(74.04±16.68)ng/mL]、亚急性期[(46.48±14.12)ng/mL]和恢复期[(38.94±12.93)ng/mL]均高于健康对照组[(14.00±5.58)ng/mL],差异有显著性(P<0.01);无冠状动脉损伤组KD患儿急性期[(37.06±14.55)ng/mL]、亚急性期[(34.04±12.47)ng/mL]sTM水平亦显著升高,与健康对照组相比差异有显著性(P<0.01),恢复期[(16.42±9.16)ng/mL]与正常组差异无显著性(P>0.05)。结论sTM可能参与了KD冠状动脉损伤的病理过程,检测sTM的水平对评估KD冠状动脉病变具有重要意义。     

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目的探讨川崎病(KD)冠脉瘤远期血管改变及其与冠脉粥样硬化的关系。方法选择首都医科大学附属北京儿童医院2008年6月至2009年6月病程大于1年且合并中型以上冠脉瘤的KD患儿31例为研究对象(KD冠脉瘤组),以CD34/CD133/KDR+为血管内皮祖细胞(EPC)表面分子标记,用流式细胞仪测定血周血EPC数量;采用酶联免疫法测定血清超敏C反应蛋白(hs-CRP);全自动生化分析仪测定血脂及载脂蛋白。选取年龄、性别匹配的21名健康体检儿童作对照(对照组)。结果 KD冠脉瘤组患儿病程1.0～12.5年,中位病程2.5年;中型冠脉瘤9例,巨大瘤22例,12例存在心肌缺血证据。KD冠脉瘤组血清hs-CRP为(2.77±1.06)mg/L,对照组为(1.60±1.53)mg/L,KD冠脉瘤组显著升高(P<0.01)。外周血EPC及血脂两组比较差异无统计学意义(P>0.05)。结论 KD冠脉瘤组恢复期血清hs-CRP显著升高,提示仍有慢性炎症反应,可能与KD成年后早发动脉粥样硬化有关。     

Effect of pravastatin on endothelial dysfunction in children with medium to giant coronary aneurysms due to Kawasaki disease

Background

Ongoing low-grade inflammation and endothelial dysfunction persist in children with coronary lesions diagnosed with Kawasaki disease (KD). Statins, frequently used in the management of high cholesterol, have also shown to improve surrogate markers of inflammation and endothelial dysfunction. This study was undertaken to investigate the efficacy and safety of pravastatin in children with coronary artery aneurysms due to KD.

Methods

The study enrolled 14 healthy children and 13 male children, aged 2–10 years, with medium-to-giant coronary aneurysms for at least 12 months after the onset of KD. Pravastatin was given orally to the KD group at a dose of 5 mg/day for children under 5 and 10 mg/day for children older than 5 years. To determine the effects of pravastatin on endothelial function, high-frequency ultrasound was performed before the start of the study and 6 months after pravastatin therapy. The parameters measured were brachial artery flow-mediated dilation (FMD), non-flow mediated dilation (NMD), and carotid artery stiffness index (SI). High sensitive C-reactive protein (hs-CRP) levels, the circulating endothelial progenitor cells (EPCs) number, and serum lipid profiles were also determined at baseline and after 6 months of pravastatin treatment.

Results

Before treatment, the KD group had significantly decreased FMD (P<0.05) and increased SI and hs-CRP levels (P<0.05) compared with controls. After 6 months of pravastatin therapy, FMD improved significantly compared to the baseline KD group (3.16±6.49 to 10.05±7.74, P<0.05), but remained significantly less than that in the control group with no significant changes in NMD and SI. There were significant decreases in markers of inflammation after treatment. The hs-CRP levels decreased significantly from 2.93±0.81 mmol/L to 2.14±0.82 mmol/L (P<0.05) and the serum apo-B and apo-B/apo-A1 ratio were also reduced (P<0.05) in the KD group. However, the circulating EPC number was not significantly different between baseline and that following pravastatin treatment in the KD group and the control group (P>0.05). No significant complications were noted with paravastatin therapy.

Conclusions

Pravastatin improves endothelial function and reduces low-grade chronic inflammation in patients with coronary aneurysms due to KD. Children with coronary aneurysms due to KD may benefit from statin therapy.     

髓系相关蛋白8和14在川崎病患儿中的表达及其与循环内皮细胞的关系

目的 研究髓系相关蛋白8、14（MRP-8、-14）在川崎病（KD）患儿中的表达及其与循环内皮细胞数（CECs）的关系。方法 选取41 例KD患儿为研究对象,根据有无冠状动脉扩张分为冠状动脉无扩张KD组和冠状动脉扩张KD组,同时选取年龄和性别与KD患儿相匹配的因急性上呼吸道感染发热的40例患儿为对照组。分别通过ELISA、RT-PCR和流式细胞术检测各组患儿外周血MRP-8/MRP-14二聚体含量、单个核细胞MRP-8和MRP-14 mRNA表达水平及CECs。Pearson积差相关分析法分析MRP-8/MRP-14二聚体含量与CECs的相关性。结果 冠状动脉扩张KD组患儿MRP-8/MRP-14二聚体含量、单个核细胞MRP-8和MRP-14 mRNA表达水平及CECs均高于冠状动脉无扩张KD组（均P<0.05）,且两组上述指标均高于对照组（均P<0.05）;MRP-8/MRP-14二聚体含量与CECs呈正相关（r=0.69,P<0.05）。结论 MRP-8、MRP-14表达增高在KD的发病中起重要作用,且与CECs增高显著相关,是引起KD患儿血管损伤、冠状动脉扩张的重要因素。     

Endothelial Function Evaluated by Flow-Mediated Dilatation in Pediatric Vascular Disease

The endothelial function of children with and without vascular disease, consisting of 41 controls, 24 with Kawasaki disease (KD), and 46 with diabetes mellitus (DM), was examined. Age at examination ranged from 3 to 23 years (mean, 12.0 ± 4.7). The flow-mediated dilatation (FMD) and intima-media complex in the common carotid artery were measured. In controls age at examination was not associated with FMD or intima-media complex. FMD significantly decreased in children with KD and DM compared with the control group (control vs KD or DM: 11.7 ± 14.7 vs 3.0 ± 11.0 or 6.4 ± 8.5%, respectively; p < 0.05). However, there was no significant difference for intima-media complex among the groups. Furthermore, FMD in KD patients with coronary arterial aneurysm was lower than that in KD patients without aneurysm (-0.5 ± 9.2 vs 8.3 ± 9.1%, p < 0.05). In DM patients, FMD in the high HbA1c group (HbA1c = 7%) was lower than that in the normal HbA1c group (HbA1c < 7%) (4.8 ± 8.1 vs 11.4 ± 7.8%, p < 0.05). In conclusion, FMD detected endothelial impairment in children with KD or type 1 DM regardless of overt vascular complications, and FMD impairment occurs prior to intima-media complex thickening. By measuring both FMD and intima-media complex, useful information for predicting vascular complications may be obtained.     

Endothelial dysfunction in adult patients with a history of Kawasaki disease

To assess the existence of endothelial dysfunction and the possibility of the early onset of atherosclerosis in the chronic stage of Kawasaki disease (KD), we examined endothelial function in adult patients late after the onset of KD. We evaluated two age-matched groups: 35 adult KD patients (KD group) (mean age, 27.0 years; mean interval time, 24.1 years), and 36 healthy adults (control group). To assess vascular endothelial function, flow-mediated dilatation (%FMD) of the brachial artery and urinary nitrites and nitrates (NOx) were examined. We also measured adhesion molecules and several coagulation-fibrinolysis markers. In addition, we measured high-sensitive C-reactive protein (hs-CRP) as a chronic inflammatory marker, and brachial-ankle pulse wave velocity (baPWV) as a marker for arterial stiffness. %FMD was significantly reduced in the KD group when compared with that of the control group (KD group, 10.4 ± 2.6%; control group, 14.4 ± 3.2%, p<0.05), particularly in patients with coronary artery lesions. Thrombin-antithrombin III complex values were higher in the KD group, although no significant differences were observed in the other markers for endothelial function. Hs-CRP was significantly elevated only in the patients with coronary aneurysms. Furthermore, in the male KD patients, the baPWV values were significantly higher than those in the control subjects. This study revealed that the adult patients with a history of KD had systemic vascular endothelial dysfunction, and also suggested that a history of KD was possibly one of the risk factors for early onset of atherosclerosis.     

Evaluation of Preclinical Atherosclerosis by Flow-Mediated Dilatation of the Brachial Artery and Carotid Artery Analysis in Patients with a History of Kawasaki Disease

Cardiac sequelae of Kawasaki disease are an important cause of ischemic heart disease in young adults. The possibility of early progression of atherosclerosis following Kawasaki disease is therefore of great concern. We examined whether preclinical atherosclerotic changes are seen in patients with a history of Kawasaki disease, and whether these changes appear in all or in only a proportion of patients. Sixty-five patients with a history of Kawasaki disease, aged 13.1 ± 2.1 years, and 20 aged-matched controls participated in the study. All subjects underwent flow-mediated dilatation (FMD) of the brachial artery and analysis of carotid artery size and pulse-wave transmission. Patients were classified into four groups depending on the severity of the maximum coronary artery lesion: group 0 (normal), group 1 (mild), group 2 (moderate), and group 3 (severe). There was no statistical difference in the carotid artery analyses between the four groups. FMD (mean ± SD) was significantly lower in groups 2 and 3 than in groups 0 and 1 and the control group (group 0, 19.4 ± 3.9%; group 1, 19.5 ±4.1%; group 2, 8.9 ± 2.8%; group 3, 4.2 ± 1.5%; control group, 18.8 ± 2.8%; p < 0.0001). There was a significantly negative correlation between the severity of the coronary artery lesion and FMD (p < 0.0001 for both). Endothelial dysfunction was revealed by FMD in patients with persistent coronary artery lesions subsequent to Kawasaki disease. Preclinical atherosclerosis may be present only in patients with coronary aneurysms.     

The number and function of circulating endothelial progenitor cells in patients with Kawasaki disease

Kawasaki disease (KD) is associated with coronary artery injury. Studies have shown that the endothelial progenitor cell (EPC) participates in the process of arterial repair. Data have been reported that the number of EPC increased significantly in the subacute phase of KD. However, until now, there are no data about the functions of EPC in KD patients. The present study was designed to further investigate the number and functions of EPC in KD. Ten KD patients in the acute phase and ten healthy volunteers were recruited and attributed to the KD group and control group, respectively. The circulating CD34/kinase insert domain-containing receptor double positive cells were evaluated in the two groups using flow cytometry. In vitro assays were used to measure the functions of EPC, including proliferation, adhesion, and migration activities. The plasma levels of nitric oxide (NO), tumor necrosis factor-α (TNF-α), and high sensitivity C-reactive protein (hs-CRP) were also assessed in both groups. The number of EPC in the KD group was significantly higher than that of the control group (0.021 ± 0.007% vs. 0.014 ± 0.003%, P < 0.05). The migratory response of EPC was significantly decreased in the KD group, compared with that of the control group (5.50 ± 1.78 vs. 3.40 ± 1.35 cells/high power field, P < 0.01). Similarly, the proliferative and adhesive activities of EPC in the KD group were also decreased (0.47 ± 0.08 vs. 0.66 ± 0.07, P < 0.01; 6.5 ± 2.12 vs. 11.2 ± 2.04 cells/high power field, P < 0.01). The plasma NO, TNF-α, and hs-CRP levels in the KD group were higher than those of the control group (54.10 ± 11.78 vs. 38.80 ± 11.10 μmol/l, P < 0.01; 48.20 ± 7.42 vs. 37.00 ± 11.12 pg/ml, P < 0.05; 87.10 ± 30.18 vs. 5.30 ± 3.37 mg/l, P < 0.01). The number of circulating EPC positively correlated with the level of NO (r = 0.92, P < 0.001), and the functions of EPC negatively correlated with the levels of TNF-α and hs-CRP, respectively. In Kawasaki disease, the number of EPC was enhanced and the functions of EPC were attenuated. The two-way regulation of circulating EPC in KD patients may be associated with the disorders of cytokines or messengers in KD patients.     

小儿急性细菌性痢疾血循环内皮细胞的变化和意义

目的：观察小儿急性细菌性痢疾时血循环内皮细胞(CEC)的变化和意义。方法：将患儿分为观察组(急性细菌性痢疾患儿30例)及对照组(病毒性肠炎30例),其中观察组又分为观察组Ⅰ(中毒型8例)和观察组Ⅱ(普通型22例)。采用流式细胞仪检测患儿在发病第1天及第5天时的血循环内皮细胞(CEC)数。结果：观察组患儿第1天CEC水平(4.57±0.69)个/mm3高于该组第5天(1.06±0.15)个/mm3及对照组第1天(1.22±0.23)个/mm3、第5天(1.18±0.20)个/mm3 CEC水平,差异有显著性(P<0.01)。观察组Ⅰ第1天CEC水平(5.43±0.50)个/mm3,明显高于观察组Ⅱ第1天的CEC水平(4.25±0.44),P<0.01;而二者第5天CEC水平(0.98±0.12 vs 1.10±1.15)差异无显著性(P>0.05)。结论：CEC可能对鉴别急性细菌性痢疾具有重要意义,并可能成为此类疾病早期诊断,选择积极治疗的重要指标。