Genetic studies of human apolipoproteins. VII. Population distribution of polymorphisms of apolipoproteins A-I, A-II, A-IV, C-II, E, and H in Nigeria.

Familial porphyria cutanea tarda (PCT) results from a generalized deficiency of uroporphyrinogen decarboxylase (URO-D) activity. The molecular defect responsible for this disorder has not been characterized. To determine whether decreased levels of URO-D mRNA are responsible for subnormal URO-D activity, steady-state levels of URO-D mRNA in lymphoblastoid cells were determined. Northern blots were hybridized with a URO-D cDNA probe and quantified by densitometry. No difference in the levels of URO-D mRNA was detected between affected individuals and their normal relatives. Thus, the deficiency of URO-D activity in two familial PCT pedigrees characterized here does not arise from a deficiency of URO-D mRNA.     

Familial porphyria cutanea tarda: hybridization analysis of the uroporphyrinogen decarboxylase locus

Familial porphyria cutanea tarda (PCT) results from a deficiency of uroporphyrinogen decarboxylase (URO-D) activity. Hybridization analysis of genomic DNA from unrelated normal individuals and PCT pedigree members failed to detect any major deletions, rearrangements or restriction fragment length polymorphisms at the URO-D locus.     

Serum Procalcitonin Levels are Associated with Clinical Outcome in Intracerebral Hemorrhage

Procalcitonin (PCT) has emerged as a new prognostic inflammatory marker in a variety of diseases. This study aimed to evaluate whether PCT is associated with increased risk of unfavorable outcome in intracerebral hemorrhage (ICH) patients. During January 2015–December 2016, we conducted a prospective cohort investigation involved 251 primary ICH patients who were admitted within 24 h after the onset of symptoms. We assessed serum PCT levels for all patients at admission. The functional outcome after 3 months was evaluated by modified Rankin Scale (mRS) and dichotomized as favorable (mRS 0–2) and unfavorable (mRS 3–6). The independent risk factors for unfavorable outcome and mortality after 3 months were examined by binary logistic regression. Of 251 ICH patients, the median PCT concentration was 0.053 µg/L (interquartile range 0.035–0.078 µg/L). Unfavorable outcome and mortality at 3 months were observed in 161 (64.1%) and 51 (20.3%) patients, respectively. After adjusting for potential confounders, patients with PCT levels in the top quartile (>0.078 ug/L), compared with the lowest quartile (<0.035 μg/L) were more likely to have a higher risk of poor functional outcome [odds ratio (OR) 7.341; 95% confidence interval (CI) 2.770–21.114; P = 0.001] and mortality (OR 7.483; 95% CI 1.871–24.458, P = 0.006). Furthermore, the area under the receiver operating characteristic curve of PCT showed 0.701 (95% CI 0.635–0.767) for worse functional prognosis, and 0.652 (95% CI 0.569–0.735) for mortality. This study demonstrated that elevated PCT levels at admission were independently associated with unfavorable clinical outcome in ICH patients.     

Crystal structure of human uroporphyrinogen decarboxylase.

Uroporphyrinogen decarboxylase (URO-D) catalyzes the fifth step in the heme biosynthetic pathway, converting uroporphyrinogen to coproporphyrinogen by decarboxylating the four acetate side chains of the substrate. This activity is essential in all organisms, and subnormal activity of URO-D leads to the most common form of porphyria in humans, porphyria cutanea tarda (PCT). We have determined the crystal structure of recombinant human URO-D at 1.60 A resolution. The 40.8 kDa protein is comprised of a single domain containing a (beta/alpha)8-barrel with a deep active site cleft formed by loops at the C-terminal ends of the barrel strands. Many conserved residues cluster at this cleft, including the invariant side chains of Arg37, Arg41 and His339, which probably function in substrate binding, and Asp86, Tyr164 and Ser219, which may function in either binding or catalysis. URO-D is a dimer in solution (Kd = 0.1 microM), and this dimer also appears to be formed in the crystal. Assembly of the dimer juxtaposes the active site clefts of the monomers, suggesting a functionally important interaction between the catalytic centers.     

Substrate Shuttling between Active Sites of Uroporphyrinogen Decarboxylase Is Not Required to Generate Coproporphyrinogen

Uroporphyrinogen decarboxylase (URO-D; EC 4.1.1.37), the fifth enzyme of the heme biosynthetic pathway, is required for the production of heme, vitamin B12, siroheme, and chlorophyll precursors. URO-D catalyzes the sequential decarboxylation of four acetate side chains in the pyrrole groups of uroporphyrinogen to produce coproporphyrinogen. URO-D is a stable homodimer, with the active-site clefts of the two subunits adjacent to each other. It has been hypothesized that the two catalytic centers interact functionally, perhaps by shuttling of reaction intermediates between subunits. We tested this hypothesis by construction of a single-chain protein (single-chain URO-D) in which the two subunits were connected by a flexible linker. The crystal structure of this protein was shown to be superimposable with wild-type activity and to have comparable catalytic activity. Mutations that impaired one or the other of the two active sites of single-chain URO-D resulted in approximately half of wild-type activity. The distributions of reaction intermediates were the same for mutant and wild-type sequences and were unaltered in a competition experiment using I and III isomer substrates. These observations indicate that communication between active sites is not required for enzyme function and suggest that the dimeric structure of URO-D is required to achieve conformational stability and to create a large active-site cleft.     

Accelerated development of uroporphyria in mice heterozygous for a deletion at the uroporphyrinogen decarboxylase locus

Three weeks after a single dose of iron-dextran and Aroclor 1254, mice maintained continuously on delta-aminolevulinic acid supplemented drinking water showed significantly elevated levels of hepatic uroporphyrin and depressed (25% of normal) uroporphyrinogen decarboxylase (URO-D) activity. Depressed URO-D activity was paralleled by the ability of heat denatured cytosol to inhibit rhURO-D activity. Mice heterozygous for a targeted disruption at the URO-D locus (URO-D+/-) exhibited half the URO-D activity of homozygous controls prior to treatment. After treatment, these animals showed URO-D activity and rhURO-D inhibitory activity comparable to similarly treated wild type (URO-D +/+) mice but with significantly greater uroporphyrin accumulation. With only 10 days of treatment, URO-D +/- but not URO-D +/+ mice showed changes similar in magnitude to those seen after 21 days. Prior to treatment, URO-D genotype did not influence overall hepatic P450 concentration in either sex and there was no significant difference between sexes. The treatment regimen significantly elevated P450 in animals of either URO-D genotype and in both sexes, although the induction response at the 10-day point was attenuated in URO-D +/- mice. From differences in the CO absorbance maximum, and by P450 activity analysis, this attenuated induction response resulted from an attenuation of the CYP2B not the CYP1A induction.     

内毒素、PCT联合NLR对经皮肾镜碎石术后患者尿源性脓毒血症的预测价值

摘要 目的：探讨内毒素、降钙素原（PCT）联合中性粒细胞与淋巴细胞比值（NLR）对经皮肾镜碎石术（PCNL）术后患者发生尿源性脓毒血症的预测价值。方法：选取2020年5月-2023年5月于西安医学院第二附属医院和空军军医大学第一附属医院泌尿外科行PCNL的患者750例作为研究对象。根据尿源性脓毒症发生情况分为尿源性脓毒血症组（n=45）和非脓毒血症组（n=705）。检测PCNL术前血清内毒素、PCT、中性粒细胞与淋巴细胞水平，并计算NLR。对比两组血清内毒素、PCT水平及NLR。采用多因素Logistic回归模型分析PCNL术后患者发生尿源性脓毒血症的影响因素。绘制受试者工作特征（ROC）曲线分析血清内毒素、PCT联合NLR预测PCNL术后患者发生尿源性脓毒血症的临床效能。结果：与非脓毒血症组相比，尿源性脓毒血症组血清内毒素、PCT及NLR更高（P<0.05）。多因素Logistic回归模型分析结果显示，血清内毒素升高、PCT升高、NLR升高、尿白细胞阳性、术前发热及鹿角型结石是PCNL术后患者发生尿源性脓毒血症的独立危险因素（P<0.05）；ROC曲线分析结果显示，血清内毒素、PCT联合NLR检测预测PCNL术后患者发生尿源性脓毒血症的曲线下面积（AUC）为0.913，高于上述各指标单独检测。结论：PCNL术前血清内毒素、PCT和NLR升高可能与术后患者发生尿源性脓毒血症有关。血清内毒素、PCT水平升高、NLR升高、术前发热、尿白细胞阳性、鹿角型结石是PCNL术后患者发生尿源性脓毒血症的危险因素。血清内毒素、PCT联合NLR检测对PCNL术后患者发生尿源性脓毒血症具有较高预测价值。     

Uroporphyrinogen decarboxylase from mouse mammary carcinoma and liver of normal and tumor-bearing mouse.

1. URO-D was investigated in crude extracts from mouse mammary carcinoma, normal mouse (NM) liver and tumor-bearing mouse (TBM) liver. 2. URO-D from TBM liver and tumor appears to be more sensitive to increasing concentrations of UROgen than the NM liver enzyme. 3. In tumor the rate-limiting step seems to be the decarboxylation of the first carboxyl group, but this was not so clear for the NM and the TBM liver URO-D. 4. URO-D activity was enhanced when incubated at higher temperatures in the presence of its substrate, suggesting that UROgen might afford some protection of the enzyme against heat inactivation. 5. The optimum pH for all three sources is around 7.0.     

Enzymatic and immunological studies of uroporphyrinogen decarboxylase in familial porphyria cutanea tarda and hepatoerythropoietic porphyria

Uroporphyrinogen decarboxylase activity was measured in hemoglobin-free lysates from two patients with hepatoerythropoietic porphyria (HEP) and from 12 unrelated patients with familial porphyria cutanea tarda (PCT). In HEP patients, enzyme activities were 5% of normal, and familial studies clearly confirmed that patients with HEP are cases of homozygous PCT. Immunoreactive uroporphyrinogen decarboxylase was measured by developing a direct and noncompetitive enzyme immunoassay (EIA). For the 12 familial PCT patients, we found an immunoreactive protein decreased (51%) to the same extent as the catalytic activity (48%) [cross-reactive immunological material ( CRIM ) negative]. The children from the HEP family were also CRIM negative, contrasting with another HEP family previously described as CRIM positive; our data support the hypothesis of a heterogeneity in familial uroporphyrinogen decarboxylase deficiency.     

血清降钙素原检测对早期诊断肝衰竭合并感染的临床意义

目的:探讨血清降钙素原(PCT)检测在肝衰竭合并感染早期诊断中的临床意义。方法:选择2014年3月至2017年3月我院收治的由病毒性肝炎导致的肝衰竭患者102例为研究对象,根据有无感染分为感染组(75例)和非感染组(27例),采用干式免疫荧光法检测其血清PCT水平,并检测两组患者白细胞(WBC)水平、C反应蛋白(CRP)水平、中性粒细胞百分比(N%),进行全身炎症反应综合征(SIRS)评分,采用多因素Logistic回归模型分析PCT、WBC、CRP、N%水平和SIRS评分对肝衰竭合并感染的预测价值大小,绘制受试者工作特征曲线(ROC曲线)评价PCT、WBC、CRP、N%水平和SIRS评分对肝衰竭合并感染的诊断价值。结果:感染组PCT、WBC、N%、CRP水平和SIRS评分均高于非感染组(P0.05);不同感染部位患者WBC、N%、CRP水平和SIRS评分比较差异不明显(P0.05);多部位感染患者血清PCT水平均高于其他单部位感染患者(P0.05);多因素Logistic回归分析显示,PCT和N%水平是肝衰竭合并感染的独立危险因素(P0.05);PCT、N%、CRP、WBC水平和SIRS评分诊断肝衰竭合并感染的ROC曲线下面积(AUC)值依次为0.916、0.763、0.752、0.746、0.682,PCT诊断肝衰竭合并感染的AUC值分别与N%、CRP、WBC和SIRS评分比较差异均有统计学意义(Z=3.518、3.672、4.103、5.106,P0.05)。结论:肝衰竭合并感染患者血清PCT水平明显升高,PCT对肝衰竭合并感染的诊断价值优于WBC、CRP、N%和SIRS评分等传统实验室指标。     

Precipitating/aggravating factors of porphyria cutanea tarda in Spanish patients.

Erythrocyte uroporphyrinogen decarboxylase (UROD) activity was measured to classify 118 Spanish patients with porphyria cutanea tarda (PCT) into three subtypes: sporadic-, familial- and type III-PCT. Seventy-four patients (63%) had eythrocyte UROD activity within the normal range (74% to 126% of the mean activity of 43 healthy controls) and were classified as sporadic-PCT (47%) or as type III-PCT (16%) whenever a family history of PCT was documented. Forty-four patients (37%) had decreased UROD activity and were classified as familial-PCT. The frequency of both familial-PCT and type III-PCT was higher than reported in other countries. The clinical expression of PCT was associated with the coexistence of two or more risk factors in 80% of the sporadic-PCT patients and in 89% of the familial-PCT patients. Hepatitis C virus and alcohol abuse were risk factors frequently found in these patients, being unrelated to age of onset of skin lesions. A heavy alcohol intake was the main risk factor for type III-PCT. Estrogens appeared as a precipitating factor for women with familial-PCT. The H63D mutation in the hemochromatosis type 1 gene was more frequently found than the C282Y mutation. Both mutations appeared to play a role as precipitating factors in sporadic-PCT when associated with hepatitis C virus infection and alcohol abuse.     

脓毒症患者血清氧化应激因子、炎症因子水平与APACHEⅡ评分及预后的关系研究

目的:探讨脓毒症患者血清氧化应激因子、炎症因子水平与急性生理学与慢性健康状况II(APACHEⅡ)评分及预后的关系。方法:选择2016年1月-2019年10月我院收治的脓毒症患者76例作为研究组,同期收治的相同基础疾病非脓毒症患者60例作为对照组,比较两组血清氧化应激因子[丙二醛(MDA)、超氧化物歧化酶(SOD)、一氧化氮(NO)]、炎症因子[降钙素原(PCT)、C反应蛋白(CRP)、白细胞介素27(IL-27)]水平及APACHEⅡ评分,根据脓毒症患者预后将其分为死亡组25例、存活组51例,比较两组上述指标,并分析脓毒症患者预后的影响因素及血清氧化应激因子、炎症因子水平与APACHEⅡ评分的相关性。结果:研究组血清MDA、PCT、CRP、IL-27及APACHEⅡ评分显著高于对照组,血清SOD、NO显著低于对照组(P<0.05)。死亡组血清MDA、PCT、CRP、IL-27及APACHEⅡ评分显著高于存活组,血清SOD、NO显著低于存活组(P<0.05)。多因素logistic回归分析显示MDA升高、SOD降低、NO降低、PCT升高、CRP升高、APACHEⅡ评分升高均是脓毒症患者死亡的危险因素(OR=2.293、1.872、1.527、2.472、1.667、1.926,P<0.05)。Pearson相关性分析显示,脓毒症患者血清MDA、PCT、CRP、IL-27水平与APACHEⅡ评分呈正相关(r=0.563、0.582、0.441、0.302,P<0.05),血清NO、SOD水平与APACHEⅡ评分呈负相关(r=-301、-0.386,P<0.05)。结论:脓毒症患者血清MDA、PCT、CRP、IL-27与APACHEⅡ评分异常升高,血清NO、SOD异常降低,可能通过对上述指标进行检测从而判断患者病情及评估其预后。     

降钙素原与APACHEⅡ评分对急性胰腺炎病情严重程度及预后的评估价值

目的:探讨血清降钙素原(PCT)与急性生理学与慢性健康状况评分(APACHE Ⅱ)对急性胰腺炎(AP)患者病情严重程度及预后的评估价值。方法:选取本院2012年5月-2015年5月收治的急性胰腺炎患者280例为研究对象。根据急性胰腺炎患者病情严重程度将其分为低危组(83例)、中危组(102例)和高危组(95例);按患者临床结局将其分为存活组(248例)及死亡组(32例),采用酶联免疫吸附法(ELISA)检测各组血清PCT水平同时记录APACHE Ⅱ评分情况,分别比较PCT水平的差异以及与APACHE Ⅱ评分的相关性,评价血清PCT及APACHEⅡ评分对急性胰腺炎患者病情严重程度及预后的评估价值。结果:低危组、中危组及高危组间血清PCT水平和APACHE Ⅱ评分的差异具有统计学意义(P0.05)。其中,高危组血清PCT水平和APACHE Ⅱ评分最高,中危组次之,低危组最低(P0.05);死亡组PCT水平及APACHE Ⅱ评分显著高于存活组(P0.05)。相关性分析显示血清PCT水平与APACHE Ⅱ评分呈正相关(r=0.64,P0.01)。以PCT2.13 ng/m L为评估急性胰腺炎患者预后不佳界限时,其敏感性和特异性分别79.2%和91.3%;以APACHE Ⅱ评分18.1分为评估急性胰腺炎患者预后不佳界限时,其敏感性和特异性分别为82.7%和90.1%;两者指标串联评估敏感性及特异性分别为86.1%和92.9%,ROC曲线下面积为0.921(95%CI 0.824~0.938)。结论:急性胰腺炎患者血清PCT水平和APACHE Ⅱ评分具有较好的相关性,血清PCT水平越高,APACHEⅡ评分越高,患者病情越严重及预后也越差,二者联合可作为预测急性胰腺炎患者病情严重程度及预后的敏感指标,具有较好的临床应用价值。     

Oxidative state of glutathione in red blood cells and plasma of diabetic patients: in vivo and in vitro study

The oxidative state of glutathione in red blood cells (RBC) and plasma of diabetic patients and of age-matched volunteers has been studied. Oxidized glutathione (GSSG) levels in plasma from diabetic subjects were higher than those from controls (17.2 +/- 2.5 and 3.3 +/- 0.4 micrograms/ml, respectively). This phenomenon was evident also in in vitro experiments: incubated RBC from diabetic patients released very high amounts of GSSG in medium. Thus, erythrocytes are responsible for the enhanced amounts of GSSG found in plasma from diabetic patients. The fall in the conversion of GSSG to reduced glutathione in RBC could be due to a reduced activity of the glucose-6-phosphate dehydrogenase (G6PDH) enzyme which has been observed in diabetic patients. In this way, G6PDH supplies reduced amounts of NADPH to the glutathione reductase enzyme affecting the integrity of the glutathione system; on the other hand, the activation by glucose of the polyol pathway also reduces the levels of NADPH for the glutathione reductase enzyme.     

Major and trace elements in whole blood of phlebotomized patients with porphyria cutanea tarda

Porphyria cutanea tarda (PCT) is a disorder of hem biosynthesis resulting from a decreased activity of the uroporphyrinogen decarboxylase enzyme. Hem precursors are accumulated in the blood, liver and skin. Inherited and acquired factors also contribute to the pathogenesis of PCT. Hem precursors and porphyrins are excreted with urine and faeces. Whole blood of 8 PCT patients and 6 volunteers of Caucasian origin were analysed. In addition to routine laboratory measurements, 19 elements (Al, B, Ba, Ca, Cd, Co, Cu, Fe, K, Li, Mg, Mn, Mo, Na, Ni, P, S, V, Zn) were determined by means of inductively coupled plasma optical emission spectrometry (ICP-OES). Mg, P and S concentrations in whole blood were decreased significantly (p<0.05), whereas Ba was increased in PCT patients compared to controls. Metabolic alterations are reflected in the correlation of parameters. Positive correlations were found between the element pairs of Zn-Al, Zn-Mg, Zn-Mn, B-S, Fe-Mg, K-P, Mg-Mn for PCT patients, whereas in the control group Al-Mn, Ca-Cu, Ca-Na, Cu-Mg, Fe-K, Mg-Na, Zn-P showed positive correlations.     

PCT、IL-6及CRP对新生儿宫内细菌感染的诊断价值

目的:探讨新生儿宫内细菌感染采用降钙素原(PCT)、白细胞介素-6(IL-6)、及C反应蛋白(CRP)诊断的临床价值。方法:根据感染结局将2013年3月~2014年9月在我院分娩且有宫内感染高危因素的179例新生儿分为感染组(34例)和无感染组(145例),检测两组的PCT、IL-6及CRP水平,并比较各项指标对宫内细菌感染的诊断价值。结果:感染组脐带血PCT、IL-6、CRP水平均高于无感染组,差异有统计学意义(P0.05)。感染组各单个指标阳性率、两指标联合的阳性率高于无感染组,差异均有统计学意义(P0.05),感染组中PCT、IL-6阳性率高于CRP,PCT+IL-6的阳性率高于PCT+CRP、IL-6+CRP,差异均有统计学意义(P0.05)。PCT+IL-6的灵敏度、准确率高于单个指标及其他两个指标联合检测的结果,差异有统计学意义(P0.05),各项指标检测的特异性比较,差异无统计学意义(P0.05)。结论:新生儿宫内感染采用脐带血PCT检测具有灵敏度高,特异性好的特点,联合IL-6检测是临床诊断新生儿宫内感染的最有效的方式。     

PCT, IL-6及CRP 对新生儿宫内细菌感染的诊断价值

目的:探讨降钙素原(PCT)、白细胞介素-6(IL-6)及C反应蛋白(CRP)对新生儿宫内细菌感染的诊断价值。方法:根据感染结局将2013年3月-2014年9月在我院分娩且有宫内感染高危因素的179例新生儿分为感染组(34例)和无感染组(145例),检测两组新生儿的PCT、IL-6及CRP水平,并比较其对宫内细菌感染的诊断价值。结果:感染组新生儿脐带血PCT、IL-6、CRP水平均高于无感染组,差异有统计学意义(P0.05)。感染组新生儿各单个指标阳性率、两指标联合检测阳性率高于无感染组,差异均有统计学意义(P0.05),感染组新生儿PCT、IL-6阳性率高于CRP,PCT+IL-6的阳性率高于PCT+CRP、IL-6+CRP,差异均有统计学意义(P0.05)。PCT+IL-6的灵敏度、准确率高于单个指标及其他两个指标联合检测,差异均有统计学意义(P0.05),各项指标检测的特异性比较,差异无统计学意义(P0.05)。结论:新生儿宫内感染采用脐带血PCT检测具有灵敏度高、特异性好的特点,联合IL-6检测是临床诊断新生儿宫内感染的有效方式。     

血培养阳性报警时间联合降钙素原、中性粒细胞/淋巴细胞比值对大肠埃希菌血流感染患者死亡风险的预测价值

摘要 目的：探讨血培养阳性报警时间（TTP）联合降钙素原（PCT）、中性粒细胞/淋巴细胞比值（NLR）对大肠埃希菌血流感染（BSI）患者死亡风险的预测价值。方法：选取2020年1月～2022年6月我院收治的223例大肠埃希菌BSI患者,根据入院后28 d内是否死亡分为死亡组和存活组。收集患者临床资料和血培养TTP,检测PCT、NLR。采用多因素Logistic回归分析大肠埃希菌BSI患者死亡的影响因素。采用受试者工作特征（ROC）曲线分析TTP、PCT、NLR对大肠埃希菌BSI患者死亡风险的预测价值。结果：223例大肠埃希菌BSI患者入院后28 d内死亡率为30.04％（67/223）。死亡组TTP短于存活组,PCT、NLR高于存活组（P均＜0.001）。多因素Logistic回归分析显示,年龄增加、入住重症监护病房（ICU）、气管插管/切开、PCT升高、NLR升高为大肠埃希菌BSI患者死亡的独立危险因素,TTP延长为独立保护因素（P＜0.05）。ROC曲线分析显示,TTP、PCT、NLR联合预测大肠埃希菌BSI患者死亡的曲线下面积大于各指标单独预测。结论：TTP缩短和PCT、NLR升高与大肠埃希菌BSI患者死亡风险增加相关,TTP、PCT、NLR联合预测大肠埃希菌BSI患者死亡风险的价值较高。     

脓毒症患儿血清SAA、PCT、CRP水平与预后的关系及其诊断价值分析

摘要 目的：探讨脓毒症患儿血清淀粉样蛋白A（SAA）、降钙素原（PCT）、C反应蛋白（CRP）与预后的关系,并分析三者对脓毒症的诊断价值。方法：纳入我院于2016年8月～2020年6月期间收治的脓毒症患儿60例开展回顾性研究,作为脓毒症组,选取同期于我院进行体检的健康儿童40例作为对照组,比较两组血清SAA、PCT、CRP水平。根据脓毒症患儿1个月内的生存、死亡情况,分成生存组（n=42）、死亡组（n=18）,比较两组临床资料及血清SAA、PCT、CRP水平,经COX回归模型分析脓毒症患儿死亡的危险因素。绘制受试者工作特征（ROC）曲线分析血清SAA、PCT、CRP对脓毒症的诊断价值。结果：脓毒症组血清SAA、PCT、CRP水平显著高于对照组（P＜0.05）。死亡组器官障碍数量＞2个、脓毒性休克患儿占比分别为55.56%、44.44%,显著高于生存组的19.05%、9.52%（P＜0.05）;死亡组入院后1 h内使用抗菌治疗患儿占比为38.89%,显著低于生存组的69.05%（P＜0.05）;死亡组血清SAA、PCT、CRP水平高于生存组（P＜0.05）。COX多因素分析结果显示,器官障碍数量＞2、脓毒性休克及血清SAA、PCT、CRP水平升高是脓毒症患儿死亡的危险因素（P＜0.05）,而入院后1 h内使用抗菌治疗是脓毒症患儿死亡风险的保护性因素（P＜0.05）。血清SAA、PCT、CRP单独及三者联合诊断脓毒症的曲线下面积（AUC）分别为0.808、0.780、0.761、0.912。结论：脓毒症患儿血清SAA、PCT、CRP明显升高,三者升高均为脓毒症患儿死亡的危险因素,且对脓毒症具有一定诊断价值。