糖尿病肾病患者血清晚期蛋白氧化产物水平及其临床意义的研究

目的通过检测不同时期糖尿病肾病（DN）患者血清晚期蛋白氧化产物（AoPP）水平,分析其与超氧化物歧化酶（SOD）及单核细胞趋化蛋白-1（MCP-1）的相关性,研究蛋白氧化与DN的关系及临床意义。方法66例2型糖尿病（T2DM）患者根据尿白蛋白排泄率（UAER）将患者分为以下3组：正常白蛋白尿（N-UAlb）组20例（UAER〈30mg／24h）、微量白蛋白尿（M-UAlb）组24例（UAER30-300mg／24h）和大量白蛋白尿（L-UAlb）组22例（UAER〉300mg／24h）,并与20名正常对照（NC）组比较。用Wikto-sarsat介绍的方法改进后测定各组的血清AOPP水平,黄嘌呤氧化酶法测定SOD水平,ELISA法测定血清MCP-1水平。结果随着UAER的增加,血清中AOPP水平逐渐增高,各组间比较均有统计学意义（P〈0．05）;血清中SOD水平逐渐降低,除N—UAlb组与NC组间相比外,其余各组间比较均有统计学意义（P〈0．05）;血清MCP-1水平逐渐增加,除L-UAlb组与M-UAIb组间相比外,其余各组间比较均有统计学意义（P〈0．05）。相关分析表明血清AOPP与SOD呈显著负相关,与BUN、Cr、TG、UAER呈显著正相关,与MCP-1、HDL-C、LDL-C、TC、HbA1c、BMI无相关性。血清SOD与BUN、Cr、UAER、MCP-1呈显著负相关,与TG、TC、LDL-C、HDL-C、HbA1c、BMI无相关性。多重线性回归分析结果显示Cr、1℃、UAER对AOPP有显著影响;Cr、UAER、MCP-1对SOD有显著影响。结论增加的蛋白氧化损伤及氧化应激状态可能在DN的发生发展中起重要作用,增加的蛋白氧化应激可能与DN的氧化应激状态和慢性炎症相关。     

晚期氧化蛋白产物在肝脏疾病中的作用机制

晚期氧化蛋白产物（AOPP）是一类与炎症、氧化应激密切相关的氧化修饰蛋白。围绕AOPP在肝脏疾病中的研究进展情况进行综述,讨论了AOPP的来源及生化特征、生物学作用、与肝脏疾病的相关性研究,旨在为肝脏疾病的发病机制、治疗及预测不良预后寻求新的突破。     

晚期氧化蛋白产物与胃肠道癌的相关性研究进展

晚期氧化蛋白产物(AOPP)是氧化应激下中性粒细胞髓过氧化物酶来源的氯氧化剂次氯酸作用于蛋白质而形成的蛋白质氧化交联产物。本文围绕AOPP与胃肠道癌的相关性研究进展作一综述,旨在为胃肠道癌的发病机制、治疗及预测预后寻求新的突破。     

急性胰腺炎患者血清C反应蛋白改变的临床意义

目的 评估Ｃ反应蛋白（ＣＲＰ）预测重症急性胰腺炎（ＡＰ）的作用。方法 测定４９例起病时间〈４８小时入院的急性胰腺炎患者入院次晨血清ＣＲＰ浓度。结果 重症组ＣＲＰ浓度（１７８．１±６３．５ｍｇ／Ｌ）明显高于轻症组（５０．２±２８．７ｍｇ／Ｌ）,以ＣＲＰ≥１２０ｍｇ／Ｌ为预测重症胰腺炎的指标,其特异性９７％,敏感性７１％,阳性预测值９１％,阴性预值９０％。结论 ＣＲＰ可作为早期预测重症胰炎的可靠指标     

慢性肾脏病患者晚期氧化蛋白产物血症及其与动脉粥样硬化的关系

目的　观察慢性肾脏病(CKD)患者循环中晚期氧化蛋白产物(AOPP)水平,并探讨其与动脉粥样硬化的关系。方法　断面队列研究。选109例CKD患者和71例健康对照者,用高分辨B超测颈动脉内膜中层厚度(IMT)、切面内膜中层面积及粥样斑块。测血清AOPP、丙二醛、谷胱苷肽过氧化物酶活性(GSHPx)和C 反应蛋白水平。结果　CKD患者血清AOPP水平明显高于健康对照者(P<0 01), 62例透析者血清AOPP水平明显高于47例未透析者(P<0 01);未透析者血清AOPP水平与内生肌酐清除率呈负相关(r=-0 292, P<0 05)。38例有颈动脉粥样斑块者血清AOPP水平明显高于71例无颈动脉粥样斑块者(P<0 01)。单因素相关分析和多因素逐步回归分析均显示,血清AOPP水平与颈动脉IMT、切面内膜中层面积呈正相关(r=0 332,r=0 288,P值均小于0 05;β=0 313,P<0 001;β=0 301,P<0 01)。CKD患者血清AOPP水平与丙二醛、C 反应蛋白呈正相关(r=0 300,P=0 01;r=0 255,P<0 05 ),与血清GSHPx呈负相关(r=-0 647,P<0 01 )。结论CKD患者普遍存在高AOPP血症,血清AOPP水平随肾功能减退而增高,并与CKD患者动脉粥样硬化密切相关。     

血清晚期氧化蛋白产物与2型糖尿病患者动脉粥样硬化的关系

目的 探讨血清晚期氧化蛋白产物与2型糖尿病患者动脉粥样硬化性大血管并发症的关系.方法选择90例2型糖尿病患者和60例健康对照者,用酶联免疫吸附法及分光光度法分别检测血清基质细胞衍生因子1α生及晚期氧化蛋白产物水平,采用高分辨超声测定大动脉内膜中膜厚度.结果 2型糖尿病患者血清晚期氧化蛋白产物和基质细胞衍生因子1α水平明显高于健康对照者(P<0.05或P<0.01),2型糖尿病患者高晚期氧化蛋白产物组基质细胞衍生因子1α、空腹血糖、糖化血红蛋白及血清甘油三酯水平和体质指数与正常晚期氧化蛋白产物组比较显著升高(P<0.05),2型糖尿病患者中动脉粥样硬化组晚期氧化蛋白产物及基质细胞衍生因子1α水平明显高于非动脉粥样硬化组(P<0.01或P<0.05).单因素相关分析显示,血清晚期氧化蛋白产物水平与基质细胞衍生因子1α呈正相关(r=0.295,P=0.03),与空腹血糖、糖化血红蛋白、甘油三酯及体质指数呈正相关(r=0.286,P=0.03;r=0.310,P=0.01;r=0.461,P=0.001;r=0.257,P=0.04).结论 2型糖尿病患者蛋白氧化损伤增强,血清晚期氧化蛋白产物增加促进血管内皮细胞基质细胞衍生因子1α表达,晚期氧化蛋白产物增加可能与2型糖尿病动脉粥样硬化相关.     

阻塞性睡眠呼吸暂停综合征患者晚期氧化蛋白产物水平及检测意义

研究显示阻塞性睡眠呼吸暂停综合征(OSAS)患者体内氧化应激水平增强,Carpagnano等〔1〕试验结果显示OSAS患者晨起呼出气冷凝液(EBC)和血浆8-iso-PGF2α水平均高于正常对照者,并且OSAS患者晨起水平均高于其睡前水平,表明OSAS     

妊娠合并阻塞性睡眠呼吸暂停低通气综合征患者血清晚期氧化蛋白产物水平检测的临床价值

目的探讨妊娠合并阻塞性睡眠呼吸暂停低通气综合征（OSAHS）与血清晚期氧化蛋白产物（AOPP）的相关性以及其可能的发病机制。方法选择妊娠合并OSAHS患者56例和正常妊娠组24例行标准多导睡眠呼吸监测系统监测记录呼吸暂停低通气指数（AHI）;采用分光光度法检测血清AOPP水平,同时测定平均动脉压（MAP）和24h尿蛋白。结果正常妊娠组与妊娠合并OSAHS组AOPP、AHI、MAP和24h尿蛋白比较有统计学差异（P均〈0.01）;其中,反映OSAHS病情的指标AHI值与MAP、24h尿蛋白、AOPP呈正相关（r分别为：0.745、0.765、0.798,P均〈0.01）;反映氧化应激指标的AOPP值与MAP、24h尿蛋白呈正相关（r分别为：0.626、0.619,P均〈0.01）。结论妊娠合并OSAHS患者病情与AOPP水平密切相关;妊娠合并OSAHS部分参与了妊娠期高血压疾病（HDCP）的病理过程,并有可能是HDCP中的一个重要的致病因素。     

急性胰腺炎患者检测血清PCT和CRP的临床意义

[目的]探讨急性胰腺炎患者检测血清降钙素原（PCT）和C-反应蛋白（CRP）水平的临床意义.[方法]选择86例急性胰腺炎患者,其中轻症急性胰腺炎（MAP）47例,重症急性胰腺炎（SAP） 39例,另选择35例健康体检者作为对照组.分别对急性胰腺炎患者及对照组进行血清PCT和CRP水平测定.[结果]MAP组和SAP组患者血清PCT及CRP水平均高于对照组（均P＜0.05）,SAP组患者同期PCT及CRP水平均高于MAP组（均P＜0.05）.[结论]监测血清PCT和CRP水平对急性胰腺炎患者病情严重程度和预后的评估具有重要的临床意义.     

晚期氧化蛋白产物与慢性肾脏疾病的关系研究进展

慢性肾脏疾病（ CKD ）是由各种原因引起的慢性肾脏结构和功能的障碍,肾损伤的进展总体上是渐进且不可逆的。目前, CKD已成为世界范围内继心脑血管疾病、肿瘤和糖尿病后严重威胁人类健康的一大公害,在我国患病率达10．8％,患者过早死亡的风险是非慢性肾脏病的100倍。国内外学者在对CKD发病机制的不断探索中已证明,氧化应激、炎症反应都参与了肾小球和肾小管间质的损伤过程,导致肾衰竭的慢性发展,最终至肾衰竭终末期。参与两种反应的化学介质种类繁多,机制复杂,除了既往熟知的超氧阴离子（ O2－）、白介素类、转化生长因子等以外,参与肾脏损伤的新介质不断被发现与证实。晚期氧化蛋白产物（ AOPP）是近年来被认识的一种参与肾脏损伤的新介质。 AOPP潴留所致肾损伤的机制既包括诱导肾脏固有细胞的氧化应激反应,也可诱导炎症因子的产生,另外其对肾脏肾素血管紧张素系统（ RAS ）也有一定的作用。现将AOPP与CKD的关系研究进展综述如下。     

急性胰腺炎合并急性肺损伤与血清中IL-6变化的关联性研究

目的：探讨白细胞介素－6（IL－6）在急性胰腺炎合并急性肺损伤发生发展中的临床意义。方法入选患者96例,分为急性胰腺炎组62例及急性胰腺炎合并急性肺损伤组34例,以健康成人30名为对照组。采用放射免疫法测定血清中IL－6含量变化,进行统计学分析。结果急性胰腺炎组和急性胰腺炎合并急性肺损伤组IL－6值均高于对照组,急性胰腺炎合并急性肺损伤组高于急性胰腺炎组,差异均有统计学意义（ P＜0．05）。结论 IL－6作为炎症启动因子,参与急性胰腺炎合并肺损伤的病理生理过程。     

Peritoneal lavage with aprotinin in patients with severe acute pancreatitis

Summary Conclusion Although high-dose aprotinin given intraperitoneally to patients with severe acute pancreatitis seems to inhibit activated trypsin in the peritoneal cavity, the treatment has little effect on the balance between proteases and antiproteases. Plasma levels of leukocyte proteases were high in all the patients, indicating leukocyte activation to be an important feature of the pathophysiology of severe acute pancreatitis. A surprise finding was that the patients had higher peritoneal levels of pancreatic secretory trypsin inhibitor (PSTI) after the lavage procedure. Background Although most studies have shown protease inhibitor therapy to have little or no effect on acute pancreatitis, in an earlier study we found that very high doses of the protease inhibitor aprotinin given intraperitoneally to patients with severe acute pancreatitis seemed to reduce the need of surgical treatment for pancreatic necrosis. In the present study we have further analyzed plasma and peritoneal samples from the same patients to ascertain whether the aprotinin treatment affects the balance between proteases and endogenous antiproteases. Methods In a prospective double-blind randomized multicenter trial, 48 patients with severe acute pancreatitis were treated with intraperitoneal lavage. One group (aprotinin group,n=22) was also treated with high doses (20 million KIU given over 30 h) of aprotinin intraperitoneally. The remaining 26 patients made up the control group. The protease-antiprotease balance was studied by measuring immunoreactive anionic trypsin (irAT), cationic trypsin (irCT), complexes between cationic trypsin and alpha 1-protease inhibitor (irCT-α1PI), leukocyte elastase and neutrophil proteinase 4 (NP4), as well as the endogenous protease inhibitors, pancreatic secretory trypsin inhibitor (PSTI), alpha 2-macroglobulin (α 2M), alpha 1-protease inhibitor (α 1PI), antichymotrypsin (ACHY), and secretory leukocyte protease inhibitor (SLPI). Intraperitoneal levels were studied before and after the lavage procedure, and plasma levels were followed for 21 d. Results The control group had lower plasma levels of SLPI and analysis of peritoneal fluid showed the reduction of irCT-α 1PI to be more pronounced in the aprotinin group. None of the other variables measured differed significantly between the two groups. All patients had very high levels of leukocyte elastase and NP4 both in peritoneal exudate and in plasma. Peritoneal levels of PSTI were higher after the lavage procedure in contrast to the other measured variables that all showed lower peritoneal levels after the lavage.     

Influence of continuous veno-venous hemofiltration on the course of acute pancreatitis

AIM: To investigate whether continuous veno-venous hemofiltration (CVVH) in different filtration rate to eliminate cytokines would result in different efficiency in acute pancreatitis, whether the saturation time of filter membrane was related to different filtration rate, and whether the onset time of CVVH could influence the survival of acute pancreatitis. METHODS: Thirty-seven patients were classified into four groups randomly. Group 1 underwent low-volume CVVH within 48 h of the onset of abdominal pain (early CVVH, n = 9). Group 2 received low-volume CVVH after 96 h of the onset of abdominal pain (late CVVH, n = 10). Group 3 underwent high-volume CVVH within 48 h of the onset of abdominal pain (early CVVH, n = 9). Group 4 received high-volume CVVH after 96 h of the onset of abdominal pain (late CVVH, n = 9). CWH was sustained for at least 72 h. Blood was taken before hemofiltration, and ultrafiltrate was collected at the start of CVVH and every 12 h during CVVH period for the purpose of measuring the concentrations of TNPα, IL-1β and IL-6. The concentrations of TNPα, IL-1β and IL-6 were measured by swine-specific ELISA. The Solartron 1 255 B frequency response analyzer (British) was used to observe the resistance of filter membrane. RESULTS: The survival rate had a significant difference (94.44% vs 68.42%, P<0.01) high-volume and low-volume CVVH patients. The survival rate had also a significant difference (88.89% vs 73.68%,P<0.05) between early and late CVVH patients. The hemodynamic deterioration (MAP, HR, CVP) was less severe in groups 4 and 1 than that in group 2, and in group 3 than in group 4. The adsorptive saturation time of filters membranes was 120-180 min if the filtration rate was 1 000-4 000 mL/h. After the first, second and third new hemofilters were changed, serum TNF-α concentrations had a negative correlation with resistance (r: -0.91, -0.89, and -0.86, respectively in group 1; -0.89, -0.85, and -0.76, respectively in group 2; -0.88, -0.92, and -0.82, respectively in group 3; -0.84, -0.87, and -0.79, respectively in group 4). The decreasing extent of TNF-α, IL-1β and IL-6 was significantly different between group 3 and group 1 (TNF-α P<0.05, IL-1β P<0.05, IL-6 P<0.01), between group 4 and group 2 (TNF-α P<0.05, IL-1β P<0.05, IL-6 P<0.01), between group 1 and group 2 (TNP-α P<0.05, IL-1β P<0.05, IL-6 P<0.05), and between group 3 and group 4 (TNF-α P<0.01, IL-1β P<0.01, IL-6 P<0.05), respectively during CVVH period. The decreasing extent of TNF-α and IL-1β was also significantly different between survival patients and dead patients (TNF-α P<0.05, IL-1β P<0.05). In survival patients, serum concentration of TNF-α and IL-1β decreased more significantly than that in dead patients. CONCLUSION: High-volume and early CVVH improve hemodynamic deterioration and survival in acute pancreatitis patients. High-volume CVVH can eliminate cytokines more efficiently than low-volume CVVH. The survival rate is related to the decrease extent of TNF-α and IL-1β. The adsorptive saturation time of filter membranes are different under different filtration rate condition. The filter should be changed timely once filter membrane adsorption is saturated.     

Clinical outcomes of acute pancreatitis in patients with cirrhosis

BackgroundAP outcomes in cirrhotic patients have not yet been studied. We aim to investigate the outcomes of cirrhotics patients with acute pancreatitis.MethodsThe National Inpatient Sample (NIS) database (2003–2013) was queried for patients with a discharge diagnosis of AP and liver cirrhosis. Cirrhosis was further classified as compensated and decompensated using the validated Baveno IV criteria. Primary outcome was inpatient mortality. The analysis was adjusted for age, gender, race, Charlson comorbidity index (CCI), median income quartile, and hospital characteristics.ResultsOver 2.8 million patients with acute pancreatitis were analyzed. Cirrhosis prevalence was 2.8% (80,093). Both compensated and decompensated cirrhosis subjects had significantly higher mortality. Highest odds ratios (OR) were: inpatient mortality (OR 3.4, P < 0.001), Shock (OR 1.5, P = 0.02), Ileus (OR: 1.3, p = 0.02, ARDS (OR 1.2, p = 0.03), upper endoscopy performed (OR 2.0, p < 0.001), blood transfusions (OR 3.1, p < 0.001), gastrointestinal bleed (OR 5.5, p < 0.001), sepsis (OR 1.3, p = 0.005), portal vein thrombosis (PVT) (OR 7.2, p < 0.001), acute cholecystitis (OR 1.3, p < 0.001). Interestingly, cirrhosis patients had lower hospital length of stay, (OR 0.16, p < 0.001), AKI (OR 0.93, p = 0.06), myocardial infarction (OR 0.31, p < 0.001), SIRS (OR 0.62, p < 0.001), parenteral nutrition requirement (OR 0.84, p = 0.002). Decompensated cirrhosis had higher inflation-adjusted hospital charges (+$3896.60; p < 0.001).ConclusionAP patients with cirrhosis have higher inpatient mortality, but it is unlikely to be due to AP severity as patients had lower incidence of SIRS and AKI. Higher mortality is possibly related to complications of cirrhosis and portal hypertension itself such as GI bleed, shock, PVT, AC and sepsis.     

急性胰腺炎病人血浆血栓调节蛋白、D-二聚体变化的研究

目的探讨急性胰腺炎不同阶段血浆血栓调节蛋白（TM）、D-二聚体的变化及其临床意义。方法采用酶联免疫吸附测定法,分析轻症急性胰腺炎患者（20例）、重症急性胰腺炎患者（16例）、正常对照组（15例）的TM、D-二聚体指标,并做APACHEⅡ评分。结果重症急性胰腺炎患者TM、D-二聚体含量升高,与轻症和正常对照组比较差异有显著性（P〈0．05）。伴随APACHEⅡ评分升高,TM、D-二聚体的含量升高。结论急性胰腺炎病人均存在不同程度的血管内皮细胞损伤及凝血和纤溶系统的激活,血浆TM、D-二聚体含量可作为急性胰腺炎病情进展、预后判定的指标之一。     

轻症急性胰腺炎患者血清淀粉酶不降的原因分析及处理对策

目的 探讨轻症急性胰腺炎患者血清淀粉酶不降的原因及防治对策.方法 对我院307例轻症急性胰腺炎患者的临床资料进行回顾性分析.结果 轻症急性胰腺炎患者血清淀粉酶不降的原因主要为急性胰腺炎病因未去除、进食不当、急性胰腺炎病情进展、特殊类型急性胰腺炎及合并其他疾病等.结论 观察并分析轻症急性胰腺炎患者血清淀粉酶不降的原因,采取正确的处理对策,对轻症急性胰腺炎患者的康复至关重要.     

The effect of interleukin-6 on bacterial translocation in acute canine pancreatitis

Summary Background. Bacterial translocation from the gut to mesenteric lymph nodes and other extraintestinal sites is an important source of infection in acute pancreatitis. Impaired host immunity is known to promote bacterial translocation. Interleukin-6 (IL-6) is a multifunctional cytokine that regulates the immune response, acute phase reaction, and hematopoiesis. Methods. Twenty-four mongrel dogs (18–29 kg) were studied in four equal groups. In Groups I and II, acute pancreatitis was induced by direct pressure injection of 4% taurocholate and trypsin into the pancreatic duct at laparotomy. Groups III and IV had only laparotomy. Group I and III dogs were given IL-6 (50 μg/kg/d, sq) daily starting 24 h after operation and Group II and IV dogs received an equal volume of saline administered at similar time. All animals had blood drawn for culture, complete blood count (CBC), platelets, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and amylase on d 0, 1, 4, and 7. On d 7, mesenteric lymph nodes (MLN), spleen, liver, pancreas, and cecum were harvested for pathology study and for cultures of aerobic and anaerobic bacteria. Quantitative cecal cultures of aerobic and anaerobic bacteria were obtained. Results. All Group I and Group II dogs had severe pancreatitis. The increase of plasma CRP in Group I was sustained throughout treatment (1.3±0.3 on d 0 vs 3.1±0.3*, 3.0±0.3*, and 2.9±0.3* and d 1,4, and 7, respectively). Plasma CRP was increased in Group II on d 1 and d 4 (1.3±0.3 mg/dL on d 0 vs 3.6±0.3* mg/dL on d 1, and 3.1±0.3* on d 4, *p<0.05). There were no differences in white blood cell (WBC) count, differential, platelets, and ESR between Groups I and II. Bacterial translocation to MLN was lower in Group I (1/6) than in Group II (6/6) (p<0.05). All 6 dogs in Group II had bacterial spread to distant sites compared to 2 of 6 dogs in Group I (p=0.066). Both MLN and other distant organ cultures were negative in Group III and only 1 of 6 MLN cultures was positive in Group IV. Conclusions. IL-6 treatment decreases bacterial translocation to MLN and may be beneficial in reducing septic complications in acute pancreatitis.     

Elevated level of interleukin-6 predicts organ failure and severe disease in patients with acute pancreatitis

BACKGROUND AND AIM: Cytokines play an important role in the pathogenesis of acute pancreatitis (AP). The aim of the present paper was to study the profile of anti- and proinflammatory cytokines in AP and to determine their predictive value for severity of AP, organ failure and mortality. METHODS: Consecutive patients with AP were included in the study. Cytokines were measured in those patients who presented within the first 72 h of the onset of AP. Plasma levels of proinflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-Ibeta, IL-6 and anti-inflammatory cytokine IL-10 were measured on days 1, 3, 7 and 14 of AP. RESULTS: Of 108 patients, 30 presented within 72 h of the onset (mean age 40.27 +/- 13.89 years; 22 males). Of the 30 patients, 13 (43.3%) had severe and 17 (56.7%) had mild pancreatitis. Eleven (36.7%) patients developed organ failure and three died. The level of IL-6 on day 3 was significantly higher in severe pancreatitis than in mild pancreatitis (146.29 +/- 57.53 pg/mL vs 91.42 +/- 71.65 pg/mL; P = 0.04) and was significantly higher in patients who developed organ failure compared with those who did not (161.59 +/- 53.46 pg/mL vs 88.16 +/- 65.50 pg/mL; P = 0.004). At a cut-off value of 122 pg/mL on day 3, IL-6 predicted organ failure and severe pancreatitis with a sensitivity and specificity of 81.8% and 77.7%, respectively. TNF-alpha and IL-10 were detectable only in one-third of patients and were not related to the severity of pancreatitis, while Il-1beta was not detectable. CONCLUSION: Elevated levels of IL-6 predicted organ failure and severe pancreatitis and suggested its pathophysiological significance in AP.     

Controversial role of toll-like receptors in acute pancreatitis

Acute pancreatitis(AP)is a common clinical condition with an incidence of about 300 or more patients per million annually.About 10%-15%of patients will develop severe acute pancreatitis(SAP)and of those, 10%-30%may die due to SAP-associated complications.Despite the improvements done in the diagnosis and management of AP,the mortality rate has not significantly declined during the last decades.Toll-like receptors(TLRs)are pattern-recognition receptors that seem to play a major role in the development of numerous diseases,which make these molecules attractive as potential therapeutic targets.TLRs are involved in the development of the systemic inflammatory response syndrome,a potentially lethal complication in SAP.In the present review,we explore the current knowledge about the role of different TLRs that have been described associated with AP.The main candidate for targeting seems to be TLR4,which recognizes numerous damage-associated molecular patterns related to AP.TLR2 has also been linked with AP,but there are only limited studies that exclusively studied its role in AP.There is also data suggesting that TLR9 may play a role in AP.     

Relationship between somatostatin and interleukin-6: A cross-sectional study in patients with acute pancreatitis

Objectives

The aim of the analysis is to determine dynamic changes in somatostatin (SS) and interleukin-6 (IL-6) concentrations during in acute pancreatitis (AP).