原发性肾小球肾炎患者Th1/Th2细胞因子失平衡状况的研究

目的：探讨原发性肾小球肾炎（PGN）Th1／Th2细胞因子失衡情况，以及不同病理类型、不同病程对Th1／Th2失平衡的影响。方法：采用酶联免疫吸附（ELISA）法测定16例正常人及38例PGN患者血浆IL-18及IL-13水平，同时应用免疫组织化学检测6例正常肾组织和38例PGN患者肾组织IL-18及IL-13的表达量。结果：无论在肾组织抑或外周血，PGN患者IL-18水平及IL-13水平均较正常对照组显著上升（P均〈0．001），但肾组织抑或外周血IL-18／IL-13比率与正常对照组比较无统计学差异（P〉0．05）；在肾组织局部，除膜增生性肾小球肾炎（MPGN）患者IL一18／IL-13显著高于正常对照组（P均〈0．001）外，其他病理类型PGN患者IL-18／IL-13比率与正常人比较无统计学差异（P〉0．05），各病理类型PGN患者血浆IL-18／IL-13比率与正常对照组比较也无统计学差异；虽然外周血及肾组织IL-18及IL-13水平与血清肌酐（Ser）水平具有密切正相关关系，但IL-18／IL-13比率与Ser水平无相关关系（P〉0．05）。结论：除极个别病理类型外，PGN患者免疫紊乱状态似乎不能简单的按Th1优势／Th2优势进行二分法分类，其免疫紊乱状态远较此复杂，试图通过简单的调节Th1／Th2平衡来治疗PGN似乎仍缺乏坚实的理论及实验基础。     

急性肾损伤患者尿液IL-18、NGAL的变化

目的:探讨急性肾损伤(AKI)患者尿液中白细胞介素-18(IL-18)、中性粒细胞明胶酶相关脂蛋白(NGAL)的改变及临床意义。方法:AKI患者30例,原发性慢性肾脏病(CKD)患者30例,健康对照者30例,应用酶联免疫吸附检测法(ELISA)测定三组患者尿液IL-18、NGAL水平的变化;测定三组血清肌酐值。结果:血清肌酐AKI组较CKD组及健康对照组增高(P<0.001),而CKD组与健康对照组比较差异无统计学意义(P>0.05)。AKI组尿IL-18水平高于CKD组(P<0.05),显著高于健康对照组(P<0.001)。CKD组尿IL-18水平高于健康对照组,但差异无统计学意义(P>0.05)。AKI组尿NGAL水平高于CKD组(P<0.05),显著高于健康对照组(P<0.001);CKD组尿NGAL水平高于健康对照组,但差异无统计学意义(P>0.05)。尿IL-18与尿NGAL之间存在正相关关系(r=0.994)。结论:尿IL-18、NGAL在急性肾损伤患者中均增高,是反映AKI较敏感的生物学标志物。     

狼疮肾炎小鼠白细胞介素18的血浆水平及其在肾组织中的表达

目的:探讨白细胞介素18(IL-18)在狼疮性肾炎(LN)发生发展中的作用.方法:应用ELISA和免疫组化方法分别检测雄性BXSB小鼠血浆IL-18水平和肾组织IL-18的表达,并测定血清抗-dsDNA抗体水平和尿蛋白含量,评估肾脏免疫病理和组织病理变化.结果:LN组较对照组小鼠血浆IL-18水平明显升高[(547.7±41.9)pg/ml比(178.8±40.1)pg/ml];肾组织IL-18蛋白表达明显增加[Ng:(0.26±0.05)比(0.10±0.04);Nt:(17.09±1.76)比(10.98±2.84)],LN鼠血浆IL-18水平和肾组织IL-18的表达量与尿蛋白、肾组织病理改变、IgG类免疫复合物的沉积呈正相关.结论:IL-18在LN鼠外周循环和肾组织表达明显增加,可能在LN发病中起重要作用.     

白介素18基因多态性和中国人群原发性肾小球肾炎易感的相关性研究

研究提示，原发性肾小球肾炎（PGN）肾组织IL-18与肾组织损伤程度呈正相关。我们尚未检查索到有关IL-18基因多态性与PGN易感相关性的报道。     

原发性肾小球肾炎患者肾组织白介素18的表达

白细胞介素18(IL-18)是一新发现的主要由单核-巨噬样细胞分泌的单核因子,有多效的免疫调节功能[1]。原发性肾小球肾炎(PGN)肾组织IL-18表达情况如何尚未检索到有关报道。     

狼疮性肾炎患者血浆可溶性内皮细胞蛋白C受体及血栓调节蛋白水平变化及临床意义

目的:比较系统性红斑狼疮与狼疮性肾炎患者与正常对照组血浆可溶性内皮细胞蛋白C受体(sEPCR)及血栓调节蛋白(sTM)水平变化,初步探讨其在系统性红斑狼疮及狼疮性肾炎中的临床意义。方法:收集单纯性系统性红斑狼疮患者32例,狼疮性肾炎患者38例,狼疮性肾炎患者根据肾活检结果病理分型Ⅱ型9例,Ⅲ型6例,Ⅳ型20例,Ⅴ型3例。系统性红斑狼疮病人共70例根据SLEDAI评分分组,SLEDAI≥9分37例,SLEDAI<9分33例。正常对照组20例。采用酶联免疫双抗夹心法(ELISA)检测血浆sEPCR及sTM含量。同时常规检测血凝常规及D-二聚体,并收集所有病例的临床资料及实验室数据。结果:(1)与正常对照组比较,单纯SLE组及LN组sEPCR水平均显著增高(P<0.05,P<0.01),单纯SLE组及LN组sTM水平均显著增高(P<0.01);与单纯SLE组比较,LN组sEPCR水平显著增高(P<0.05),sTM水平显著增高(P<0.01)。(2)与SLEDAI<9分比较,SLEDAI≥9分sEPCR及sTM水平显著增高(P<0.01)。(3)与LNⅣ型比较,Ⅲ型的sTM水平显著降低(P<0.05),Ⅲ型的sEPCR及Ⅱ型的sEPCR及sTM水平显著降低(P<0.01);与Ⅱ型比较,Ⅲ型的sTM水平显著增高(P<0.05)。(4)血浆sEPCR与sTM呈正相关性(r=0.419,P<0.05)。结论:(1)血浆sEPCR与sTM呈正相关,sEPCR可作为反映内皮功能损伤的新指标。(2)单纯性系统性红斑狼疮患者和狼疮性肾炎患者血浆sEPCR和sTM水平明显高于正常对照组,与D-二聚体、ESR、SLEDAI呈正相关,提示sEPCR可能参与了系统性红斑狼疮及狼疮性肾炎的病理生理过程,可能能作为狼疮活动的预测指标。(3)Ⅳ型狼疮患者的sEPCR和sTM水平明显高于其他病理类型,sEPCR和sTM可能能作为狼疮性肾炎病情严重程度的预测指标。     

狼疮肾炎患者血清和尿白细胞介素-18水平检测及其临床意义

目的：检测狼疮肾炎(LN)患外周血清和尿液白细胞介素—18(IL—18)水平并探讨其临尿意义。方法：血清和尿液IL-18含量采用酶联免疫吸附方法(ELISA)。结果：LN组血清IL—18水平显高于正常对照组(P＜0、01)，活动期LN血清IL—18水平显高于缓解期患(P＜0．01)3LN组尿IL—18水平显高于正常对照组(P＜0．05)，活动期LN患尿IL—18水平显高于缓解期患(P＜0．05)。LN患血清IL—18水平与SLEDAI、抗dsDNA抗体成正相关关系，与补体C3呈负相关关系，而与血白蛋白、血肌酐无相关关系；活动期LN患尿IL—18水平与狼疮肾组织活动性指数(AI)、24h尿蛋白排泄量均呈正相关关系。结论：LN血清和尿IL—18水平显增高，IL—18可能在LN的病理生理过程中起重要作用。LN血清和尿IL—18水平均与狼疮病情活动密切相关，可作为判断狼疮疾病活动性的候选参考指标。     

白细胞介素6在狼疮性肾炎患者小管间质的表达及其意义

探讨白细胞介素6(IL-6)在狼疮性小管间质病变中的作用。方法 采用ELISA方法与原位分子杂交技术(后者结合IBAS计算机图像分析系统),分别检测42例活动期狼疮性肾炎(LN)患者尿IL-6浓度与其中的15例肾小管间质IL-6mRNA水平。结果 42例活动期LN患者有36例尿IL-6>5pg/mg·cr,其增高程度与尿β_2-m及NAG活性水平呈显著正相关;其中15例肾组织切片中,肾小管间质均有IL-6mRNA表达,并且小管间质病变愈严重,其表达量愈高,而健康肾组织小管间质几无IL-6mRNA表达。结论 LN患者活动期尿IL-6浓度异常增高与肾小管间质IL-6mRNA异常表达有关,提示IL-6在狼疮性小管间质损害过程中可能具有重要作用。     

肾小球肾炎足细胞脱落与肾组织钠氢交换调节因子2表达的研究

目的探讨肾小球足细胞脱落情况及其与病理改变的关系;探讨6类肾炎中肾组织钠氢交换调节因子2（NHERF2）基因表达量的变化及其与足细胞损伤的关系。方法将患者分为肾炎组（原发性肾炎和狼疮性肾炎）、非肾炎组、健康对照组;用间接免疫荧光法检测尿足细胞数量,用荧光定量PCR检测肾组织NHERF2蛋白,比较不同类型肾炎足细胞脱落情况及NHERF2基因表达量。结果原发性肾炎和狼疮性肾炎（LN）组患者尿足细胞脱落较健康对照组显著增多（P〈0．05）;活动期LN患者尿足细胞脱落较缓解期LN显著增多（P〈0．05）;原发性肾炎组中局灶节段硬化性肾小球肾炎（FSGS）患者尿足细胞脱落最多,其次为膜性肾病（MS）患者,二者与健康对照组相比,差异均有统计学意义（P〈0．05）。MS患者尿足细胞脱落比微小病变性肾病（MCD）患者显著增多（P〈0．05）。原发性肾炎组和LN组患者肾组织NHERF2基因表达量均较非肾炎组显著降低（P〈0．05）。肾炎患者尿足细胞脱落数量和肾组织NHERF2基因表达之间具有相关性（r=0．318,P〈0．05）。结论根据尿足细胞脱落数量可初步推断FSGS和LN的病理改变类型、预测LN的疾病进展和预后,可能为临床MS与MCD的鉴别提供依据;证明肾小球足细胞脱落可能与肾组织NHERF2基因表达减低有关,提示足细胞NHERF2基因表达缺陷可能参与足细胞损伤脱落的机制。     

狼疮肾炎患者白细胞介素13的血浆水平和基因表达

目的探讨狼疮肾炎(LN)患者外周血单个核细胞(PBMC)中白细胞介素13(IL-13)mRNA表达及IL-13血浆水平变化及其意义.方法选择10名正常对照者和16名LN患者.采用逆转录多聚酶链反应(RT-PCR)技术,对LN患者PBMCIL-13mRNA表达量进行分析.同时应用IL-13特异的酶联免疫吸附法(ELISA)测定IL-13血浆水平.结果LN患者PBMC中IL-13mRNA表达量及IL-13血浆水平均较正常对照组增高(IL-13mRNA表达量为1.99±0.29比0.68±0.15,P＜0.001IL-13血浆水平为68.8±14.65比25.92±7.60,P＜0.001).IL-13血浆水平与抗-dsDNA抗体滴度、血清C3浓度、血浆γ球蛋白水平、肾小球活动性指数(GAI)及肾小管间质活动性指数(IAI)均呈一定的等级相关关系(rs分别为0.757、-0.809、0.652、0.854和0.846,P均＜0.01).结论IL-13可能参与LN发病机制.IL-13基因表达及蛋白质分泌水平增高在LN活动性病变中起一定的作用.     

原发性肾病综合征患者IL-18的血浆水平及其在肾组织的表达

目的：初步探讨白细胞介素18(IL—18)在原发性肾病综合征(PNS)发生发展中的作用。方法：采用酶联免疫吸附(ELISA)法测定11例正常人及24例PNS患者血浆IL—18水平，同时用免疫组织化学方法检测6例正常肾组织和上述24例PNS患者肾组织IL—18的表达量。结果：PNS患者血浆IL—18水平与正常对照组IL较无统计学意义；而且各种病理类型间的差异也没有统计学意义(P均＞0．05)；而肾小球及肾小管—间质IL—18表达量却均显著高于正常对照组(P均＜0．01)。不同病理类型PNS肾小球区IL—18表达量存在差异，以膜增生性肾小球肾炎(MPGN)表达量为最高，其次为系膜增生性肾小球肾炎(MesPGN)，而膜性肾病(MD)、局灶节段性肾小球硬化(FSGS)和轻微病变(MCD)的表达量则相对较低，并且肾小球区IL—18表达量与24h尿蛋白排泄量(24h　UPQ)至正相关，与血浆白蛋白浓度(Alb)至负相关(r分别为0．669和－0．727，P均＜0．01)；肾小管—间质区IL—18表达量与小管—间质损害程度至正相关(r＝0．484，P＜0．05)。结论：肾组织IL—18高表达可能参与PNS的发病过程，而又可能以自分泌或/和旁分泌方式起作用。     

Role of the kidney in plasma cytokine removal in sepsis syndrome: a pilot study

BACKGROUND: At the onset of sepsis, endotoxins or other components of the gram-negative capsular wall stimulate the synthesis of pro-inflammatory cytokines by activating the monocyte-macrophage system. In this context, interleukin-1 beta (IL-1), tumor necrosis factor-alpha (TNF) and IL-6 are considered co-responsible for the clinical picture of sepsis syndrome. Many organs can be involved, and kidney dysfunction occurs early with a picture of non-oliguric acute renal failure (NOARF) or oliguric acute renal failure (OARF). This study aimed to investigate the role of the kidney in plasma removal of some pro-inflammatory cytokines in the first 24 hr after the diagnosis of sepsis syndrome, when, according to the peak concentration hypothesis, their plasma concentration is maximal. 18 septic patients, six patients with normal renal function (NRF), six with NOARF and six with OARF were selected for the study. We measured the plasma levels and urinary excretion of IL-1, TNF and IL-6 at the moment of sepsis diagnosis (base-line) and 24 hr later. Moreover, urinary excretion of IL-1 and IL-6 was done in the same interval by measuring the percentage of fractional excretion (FE%) of these cytokines. RESULTS: Multivariate analysis (ANOVA) showed no significant difference in plasma IL-1 levels at baseline in the NRF, NOARF and OARF patients (p=0.11), whereas a significant increase was found in OARF patients at 24 hr, p<0.023. OARF patients presented significantly higher IL-6 plasma levels compared with the other two groups, both at baseline (p<0.0002) and at 24 hr (p<0.0001). Plasma TNF levels were not significantly different at baseline (p=0.184), whereas the OARF group showed a significant increase at 24 hr, (p<0.05). The urinary FE of IL-1 was 1.2 +/- 0.6% in NRF, and 1.0 +/- 0.4% in NOARF (ns), the FE of IL-6 was 1.4 +/- 0.8% in NRF and 1.3 +/- 0.3% in NOARF (ns). A negative in-significant correlation was found between the plasma concentration and FE of IL-1 beta (r=-0.33, p<0.07). Urinary excretion of IL-6 was significantly related with urinary IL-1 beta, both expressed as pg/ml/mg of urinary creatinine (r=0.85, p<0.0001). No significant relation was found between IL-1 and IL-6 plasma concentrations or between plasma concentration and FE of IL-6. CONCLUSION: These results suggest that at disease onset, the kidney removes some pro-inflammatory cytokines from the plasma of septic patients until diuresis is preserved. As it has been demonstrated that NOARF patients have a better prognosis than OARF patients and their survival in sepsis syndrome seems to be inversely related to the plasma pro-inflammatory cytokine levels, diuresis maintenance by diuretic infusion can be important to improve patient prognosis.     

Increased excretions of beta2-microglobulin, IL-6, and IL-8 and decreased excretion of Tamm-Horsfall glycoprotein in urine of patients with active lupus nephritis

Tubulointerstitial nephritis is a less frequently recognized but important complication of systemic lupus erythematosus. We have investigated the cytokine beta2-microglobulin (beta2M) and Tamm-Horsfall glycoprotein (THG) excretions in the urine of systemic lupus erythematosus patients to identify indices for evaluation of tubulointerstitial inflammation in lupus nephritis (LN). Daily urine was collected from 15 patients with active LN, from 12 patients with inactive LN, and from 17 normal subjects. The amounts of soluble interleukin (IL) 2 receptor, IL-6, IL-8, beta2M, and THG in urine were measured. Beta2M and THG were regarded as indicators of proximal and distal renal tubule function, respectively. The urinary excretions of IL-6 and IL-8 were significantly higher in patients with active LN than in those with inactive LN and in normal individuals. The excretion of soluble IL-2 receptor in all three groups of subjects was not significantly different. On the other hand, the excretion of beta2M in patients with LN was significantly higher than that in normal individuals. The excretion of beta2M in patients with active or inactive LN was not significantly different. The THG excretion was lower in patients with active LN and tubulointerstitial inflammation as compared with patients with inactive LN or normal individuals. Six patients underwent pulse cyclophosphamide therapy during the course of experiments. Five of them showed a decrease in IL-8 and IL-6 excretions in urine after the treatment. The excretions of beta2M and THG in urine, in addition to IL-6 and IL-8, can reflect the renal inflammatory activity in patients with lupus tubulointerstitial nephritis as well as in those having lupus glomerulonephritis.     

Daily urinary interleukin-11 excretion correlated with proteinuria in IgA nephropathy and lupus nephritis

Interleukin-11 (IL-11) is a multifunctional cytokine with both thrombopoietic and anti-inflammatory effects. In an animal study IL-11 was shown to reduce proteinuria in mice with necrotizing glomerulonephritis. The purpose of this current study is to explore the role of IL-11 in human glomerulonephritis. Subjects of this study were patients with proteinuria (daily urine protein excretion >40 mg/m² per hour) and underlying pathology of IgA nephropathy (IgAN) (n=20), lupus nephritis (LN) (n=40), and idiopathic nephrotic syndrome (INS) (n=68). Daily urinary IL-11 level was measured by enzyme-linked immunosorbent assay (ELISA). Correlation between urinary IL-11 and urinary protein was determined by Pearson’s correlation coefficient. Another five patients with serial data of urinary protein, IL-11 and IL-11 messenger RNA (mRNA) expression in urine sediment are presented. The correlation between urinary IL-11 and daily urinary protein was significant for patients with IgAN (r=0.596, P=0.006) and LN (r=0.630, P<0.001), but not for patients with INS (r=0.030, P=0.812). Serial data revealed the same correlation. Furthermore, the peak of urinary IL-11 mRNA preceded that of urinary IL-11. We conclude that daily urinary IL-11 excretion is correlated with urinary protein loss in nephritis having local T helper (Th)1 predominant immune response, such as IgAN and LN. Local IL-11 production may serve as a counter cytokine against Th1-mediated inflammation.     

Plasma and urinary adrenomedullin levels in children with renal parenchymal scar and vesicoureteral reflux

Adrenomedullin (AM) is a strong vasodilator peptide with proven antimitogenic and antiproliferative effects in renal mesangial cells, as well as diuretic and natriuretic actions. Its gene expression is stimulated by endotoxins (lipopolysacharides) and cytokines. Consequently, its plasma and urinary levels are known to deviate from normal levels in many renal diseases. The purpose of this study is to determine plasma and urinary AM levels in children with renal parenchymal scar (RPS) and vesicoureteral reflux (VUR). The study was carried out on 74 children with recurrent urinary tract infections, arranged in groups: 25 patients with RPS with VUR (group I), 16 patients with RPS without VUR (group II), 12 patients with VUR without RPS (group III) and 21 healthy children as the control group. Plasma and urinary AM concentrations were both determined by high performance liquid chromotography (HPLC). Plasma AM was measured as picomoles per milliliter (pM/ml) and urinary AM as pM/mg urinary creatinine. In addition, serum creatinine, creatinine clearance and fractional sodium excretion (FE_Na) were measured. All cases with RPS and VUR had normal blood pressure levels. The plasma AM levels were higher, although not significantly, in the control group (56.2±14.0 pM/ml) than in group I (50.6±4.2 pM/ml), group II (49.6±3.7 pM/ml) and group III (50.6±3.6 pM/ml) ( P =0.162). The urinary AM levels were higher in the control group (80.1±33.9 pM/mg) than in the three study groups (52±7.6 pM/mg, 58.6±7.5 pM/mg and 44.2±6.4 pM/mg; P =0.003, P =0.002 and P =0.002, respectively). There were no differences among the 4 groups (group I, group II, group III and the control group) in terms of FE_Na and creatinine clearance ( P >0.05 and P >0.05, respectively). The finding that diminished urinary AM levels in patients with RPS and VUR implies that AM can be a prognostic factor in the long-term follow-up of cases with these diseases.     

Cytokines and adhesion molecules in renal vasculitis and lupus nephritis

Background: Plasma levels of some pro-inflammatory cytokines and soluble adhesion molecules have been suggested to be useful parameters to assess the activity of antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis and lupus nephritis. We hypothesized that the renal activity of these diseases is better reflected by the urinary excretion and fractional excretion of these molecules. Methods: Plasma levels and urinary excretion of tumour necrosis factor-&agr; (TNF-&agr;), interleukin (IL)-6, IL-8, and the soluble cell adhesion molecules sICAM-1 and sVCAM-1 were measured by enzyme-linked immunosorbent assay (ELISA) in 15 patients with ANCA-positive renal vasculitis (eight active, ANCA-A; six in remission, ANCA-R), six patients with active lupus nephritis (LN), 15 patients with IgA nephropathy (IgAN) and nine healthy subjects. Fractional excretion of selected cytokines and adhesion molecules was also calculated. Results: Patients with ANCA-A had increased urinary excretion and fractional excretion of TNF-&agr; (9.27±3.19% vs 0.58±0.02%, P<0.01), IL-6 (120.79±65.83% vs 1.89±0.34%, P<0.01) and increased fractional excretion of IL-8 (23.34±6.38% vs 2.56±1.07%, P<0.01) and sVCAM-1 (0.81±0.33% vs 0.03±0.02%, P<0.01) compared with controls. Urinary excretion of TNF-&agr; and IL-6 and fractional excretion of TNF-&agr;, IL-6 and IL-8 were higher in ANCA-A than in ANCA-R. Patients with LN had increased plasma TNF-&agr; (20.52±2.01 pg/ml vs 12.33±0.23 pg/ml, P<0.05) and sVCAM-1 (1537.88±276.36 ng/ml vs 692.26±44.42 ng/ml, P<0.05) and increased urinary excretion of TNF-&agr; (2.81±0.51 &mgr;g/mol creat vs 0.98±0.05 &mgr;g/mol creat, P<0.01), IL-8 (35.78±14.03 &mgr;g/mol creat vs 12.46±5.19 &mgr;g/mol creat, P<0.05) and sVCAM-1 (48.98±20.20 &mgr;g/mol creat vs 2.92±1.35 &mgr;g/mol creat, P<0.01) compared with controls. Patients with IgAN had, in comparison with controls only increased plasma TNF-&agr; (18.10±0.57 pg/ml vs 12.33±0.23 pg/ml, P<0.05). Conclusions: Urinary excretion and fractional excretion, but not plasma levels of selected proinflammatory cytokines (TNF-&agr;, IL-6 and IL-8) were increased in patients with active ANCA-positive renal vasculitis, but not in ANCA positive vasculitis in remission. These parameters may be useful to monitor the activity of this disease.     

Systemic immunologic and inflammatory response after laparoscopic versus open nephrectomy: a prospective cohort trial

Abstract Purpose: To compare the dynamics of systemic inflammatory indices during laparoscopic nephrectomy (LN) and standard open donor nephrectomy. Patients and Methods: Participants in this cohort study were 54 adults without a history of renal surgery and no evidence of urinary tract infection who underwent transperitoneal LN (n=29) and open donor nephrectomy (n=25, control group). We recorded demographic characteristics, intraoperative parameters, and changes 24 hours postoperatively in systemic inflammatory and immunologic values (body temperature, concentrations of white blood cell count [WBC], C-reactive protein [CRP], interleukin [IL]-6, and tumor necrosis factor [TNF]-α), and compared the mean changes between groups. Results: Mean age was older in the LN group (45.6 vs 30.9 years; P<0.0001), and mean operative time was significantly shorter (83.1?min vs 101.6?min; P=0.004). Mean postoperative increase in IL-6 and body temperature in LN was significantly less than in control: For IL-6, 15.87 vs 29.09?pg/mL, P=0.03; for body temperature, +0.22°C vs +0.71°C, P=0.001). Mean postoperative increases in levels of other inflammatory markers (CRP, TNF-α, WBC) did not differ significantly. No statistical correlation was found between operative time and changes in IL-6, CRP, TNF-α, WBC, or body temperature. Conclusion: Based on the smaller increase in serum IL-6 as the most important indicator of surgical stress, the surgical trauma-induced immune dysfunction may be less intense after LN than open surgery. This may explain the smooth convalescence after LN.     

Plasma leptin levels in patients with burn injury: a preliminary report

The purpose of this study was to investigate the relationship between the plasma leptin level and clinical parameters in patients with burn injury. Six patients with burn injury were admitted to the Emergency and Critical Care Medicine Center of St. Marianna University Hospital within 1h after injury. Plasma levels were monitored for leptin, proinflammatory cytokines (interleukin (IL)-1 beta, IL-6, tumor necrosis factor alpha (TNF alpha)), stress-related parameters (adrenocorticotropic hormone (ACTH), cortisol, and C-reactive protein (CRP)). The change in individual plasma leptin levels did not show similar pattern in all these patients. However, leptin levels remained within the normal range, except in a patient (Case 1) complicated with severe hypovolemic shock. Plasma ACTH and cortisol levels were also elevated in most of the patients. Examination of relationships among plasma leptin, proinflammatory cytokines, and stress-related parameters revealed a significant positive correlation between the plasma leptin level and IL-1 beta or IL-6. These results suggest that the plasma leptin level may have some relations to plasma proinflammatory cytokines in pathophysiologic responses to critical conditions of burn injury.