肝硬变时细胞外基质代谢的血清学研究

目的研究肝纤维化时细胞外基质代谢的血清学变化规律,以及抗肝纤维化治疗的重要性．方法实验对象２６９例分为３个观察组,即正常对照组（ｎ＝３０）ＣｈｉｌｄＡ组（ｎ＝１０３）及ＣｈｉｌｄＢ＋Ｃ组（ｎ＝１６６）．对每例观察对象作血清透明质酸（ＨＡ）,Ⅲ型前胶原肽（ＰⅢＰ）,Ⅳ型前胶原肽（ＰⅣＰ）．层粘蛋白（ＬＮ）水平测定和肝功能有关指标,如ＡＳＴ,ＡＬＴ,甘胆酸（ＣＧ）和吲哚氰绿（ＩＣＧ）潴留率等检测．结果和正常组比较,ＣｈｉｌｄＡ组及ＣｈｉｌｄＢ＋Ｃ组ＨＡ,ＰⅢＰ,ＰⅣＰ,ＬＮ以及ＡＬＴ,ＡＳＴ,ＣＧ,ＩＣＧ潴留率均值呈异常升高（Ｐ＜００１）,但ＣｈｉｌｄＡ组及ＣｈｉｌｄＢ＋Ｃ组间无统计学差异．进一步研究还发现ＰⅢＰ,ＰⅣＰ,ＨＡ以及ＬＮ等血清浓度和ＣＧ,ＩＣＧ潴留率,ＡＳＴ,ＡＬＴ间呈密切正相关,经保肝、利胆等治疗,在血清ＡＳＴ,ＡＬＴ,ＣＧ及ＩＣＧ潴留率好转后ＨＡ,ＰⅢＰ,ＰⅣＰ,ＬＮ的血清水平也呈同向变化．结论部分肝硬变患者,肝纤维化的形成仍很活跃,积极有效的保肝,利胆,抗纤维化治疗十分必要     

急性胰腺炎时细胞外基质代谢的实验研究

机体组织结构的破坏总伴随着修复反应，细胞外基质的增生则是其重要的方面，近年来，细胞外基质的异常增生与一些疾病如肝病关系的研究已较深入，胰腺炎时细胞外基质异常代谢的研究报道尚少。血清透明质酸(HA)及Ⅲ型前胶原(PⅢP)对早期急性重症胰腺炎的诊断及预后判断具有一定的价值^[1]。为深入起见，本文从实验角度，旨在分析急性胰腺炎时细胞外基质代谢的血清学变化，以及这些变化与胰腺病理变化之间的相关性。     

细胞外间质成分与肝病关系的研究

利用固相酶联免疫检测技术（ＥＬＩＳＡ），建立了层粘连蛋白（Ｌａｍｉｎｉｎ，ＬＮ）和透明质酸（Ｈｙａｌｕｒｏｎａｔｅ，ＨＡ）的检测方法，对１３８例肝病患者的血清含量进行了分析。结果发现，ＬＮ和ＨＡ随着肝病程度的加重而逐步升高，急性肝炎时ＨＡ含量轻度高于正常人（Ｐ＜０．０５），ＬＮ变化不显著。慢性肝病时ＬＮ与ＨＡ血清含量均明显升高（Ｐ＜０．０５～０．００１），于肝硬化时达到最高。以慢性活动性肝炎的上限值为界，ＬＮ和ＨＡ联合诊断肝硬化的敏感性、特异性和诊断符合率均为９０％，提示ＬＮ和ＨＡ是判断慢性肝病损伤程度和诊断肝纤维化的良好指标。     

急性胰腺炎中炎症介质的作用

急性胰腺炎中炎症介质的作用王自法潘承恩刘绍诰Ｓｕｂｊｅｃｔｈｅａｄｉｎｇｓｐａｎｃｒｅａｔｉｔｉｓ／ｍｅｔａｂｏｌｉｓｍ；ｐｌａｔｅｌｅｔａｃｔｉｖａｔｉｎｇｆａｃｔｏｒ／ｍｅｔａｂｏｌｉｓｍ；ｐｈｏｓｐｈｏｌｉｐａｓｅｓＡ／ｍｅｔａｂｏｌｉｓｍ...     

急性胰腺炎患者炎性介质变化的意义

急性胰腺炎患者炎性介质变化的意义陆立１周燕１傅由池２Ｓｕｂｊｅｃｔｈｅａｄｉｎｇｓｐａｎｃｒｅａｔｉｔｉｓ／ｍｅｔａｂｏｌｉｓｍ；Ｃｒｅａｃｔｉｖｅｐｒｏｔｅｉｎ／ｍｅｔａｂｏｌｉｓｍ；ｉｎｔｅｒｌｅｕｋｉｎｓ／ｍｅｔａｂｏｌｉｓｍ；ｌｅｕｋｏｃ...     

大鼠急性坏死性胰腺炎脂质代谢的研究

目的 察大鼠急性坏死性胰腺炎时血脂的代谢及其对炎症的影响。方法 36只SD大鼠（250g左右），随机分为对照组和急性坏死性胰腺炎（ANP）3h、6h、12h、24h、48h组，每组6只。除对照组外予胰管内逆行注射5％牛磺胆酸钠复制ANP大鼠模型，观察胰腺组织病理学和透射电镜的改变。检测各组血清淀粉酶、胆固醇、三酰甘油（TG）、游离脂肪酸（FFA）和脂蛋白脂酶（LPL）含量。Rq、-PCR检测硬脂酰基辅酶A脱氢酶（SCD）和脂肪酸转移酶（CD36）mRNA的表达。结果 清淀粉酶和胰腺病理学改变符合大鼠ANP改变特征，在12h组淀粉酶和胰腺病理学改变达峰值。电镜下ANP各组腺泡细胞粗面内质网扩张、酶原颗粒增多。ANP各组血清TG和FFA水平较对照组增高，其中ANP24h组TG为（0．81=0．35）mmol／L与对照组差异显著（P〈0．01）；ANP6h组FFA为（1．32—0．32）mmol／IL；较对照组显著升高（P〈0．05）。但ANP组LPL活性较对照组下降，胰腺组织SCDlmRNA和CD36mRNA表达升高。结论 NP大鼠出现血脂增高、脂质代谢相关酶表达异常、胰腺腺泡细胞内质网扩张等方面改变，提示ANP可诱发机体脂质代谢紊乱。     

TNF-α在急性胰腺炎的实验及临床研究

ＴＮＦ－α在急性胰腺炎的实验及临床研究吕孝东刘根寿陈易人苏州医学院附二院普外科江苏省苏州市２１５００４ＳｕｂｊｅｃｔｈｅａｄｉｎｇｓＴｕｍｏｒｎｅｃｒｏｓｉｓｆａｃｔｏｒ／ｍｅｔａｂｏｌｉｓｍＰａｎｃｒｅａｔｉｔｉｓ／ｍｅｔａｂｏｌｉｓｍ主题词肿...     

大鼠急性坏死性胰腺炎脂质代谢的研究

目的 观察大鼠急性坏死性胰腺炎时血脂的代谢及其对炎症的影响.方法 36只SD大鼠(250 g左右),随机分为对照组和急性坏死性胰腺炎(ANP)3 h、6 h、12 h、24 h、48 h组,每组6只.除对照组外予胰管内逆行注射5%牛磺胆酸钠复制ANP大鼠模型,观察胰腺组织病理学和透射电镜的改变.检测各组血清淀粉酶、胆固醇、三酰甘油(TG)、游离脂肪酸(FFA)和脂蛋白脂酶(LPL)含量.RT-PCR检测硬脂酰基辅酶A脱氢酶1(SCD1)和脂肪酸转移酶(CD36)mRNA的表达.结果 血清淀粉酶和胰腺病理学改变符合大鼠ANP改变特征,在12 h组淀粉酶和胰腺病理学改变达峰值.电镜下ANP各组腺泡细胞粗面内质网扩张、酶原颗粒增多.ANP各组血清TG和FFA水平较对照组增高,其中ANP 24 h组TG为(0.81 ± 0.35)mmol/L,与对照组差异显著(P ＜0.01);ANP 6 h组FFA为(1.32 ± 0.32)mmol/L,较对照组显著升高(P ＜0.05).但ANP组LPL活性较对照组下降,胰腺组织SCD1 mRNA和CD36 mRNA表达升高.结论 ANP大鼠出现血脂增高、脂质代谢相关酶表达异常、胰腺腺泡细胞内质网扩张等方面改变,提示ANP可诱发机体脂质代谢紊乱.     

代谢综合征与急性胰腺炎

代谢综合征与急性胰腺炎的发病、严重程度及预后密切相关,且代谢综合征合并急性胰腺炎的发病率呈逐渐上升的趋势,但其具体发病机制及相关性目前尚未完全阐明,本文将近年来代谢综合征合并急性胰腺炎的相关进展进行了总结,以期为后续临床工作提供参考。     

急性出血坏死性胰腺炎64例

目的观察近8a间治疗急性出血坏死性胰腺炎（AHNP）64例（其中非手术综合治疗9例，先行非手术治疗后再手术24例，早期手术治疗31例）的治疗效果．方法非手术综合治疗为尽早行快速扩容，应用血管活性药物，抑制胰腺分泌（善得定效果较好），有效的抗生素，营养支持和防治并发症的发生．根据有无感染确定手术时机．手术方式根据病情和术中所见，分别采用胰床灌洗引流，坏死组织清除，规则性胰腺切除和肢肿切开引流．结果非手术综合治疗9例，死亡率11．1％，先行非手术综合治疗后再手术24例，死亡率为12．5％，早期手术治疗31例，死亡率为25．8％．结论对AHNP先行非手术治疗可明显降低死亡率，晚期手术较早期手术可提高其治愈率．积极防治并发症是提高治疗效果的重要一环．     

Serum levels of extracellular matrix in acute pancreatitis

BACKGROUND/AIMS: Elevated levels of serum markers of extracellular matrix, i.e., the amino-terminal procollagen-III-peptide, hyaluronic acid and laminin are found in various diseases. The study aims to examine a panel of these parameters in patients with acute pancreatitis and correlate them with the course and severity of the disease. METHODOLOGY: We prospectively examined the time-course of procollagen-III-peptide, hyaluronic acid and laminin in 24 consecutive patients with acute necrotizing (n = 13) or edematous (n = 11) pancreatitis. Patients with chronic pancreatitis with (n = 10) or without (n = 17) acute pain, and 6 patients in complete remission after an episode of acute pancreatitis as well as healthy individuals served as controls. In addition, serum levels of collagen VI and undulin were followed in 10 and 9 patients with acute necrotizing pancreatitis, respectively. RESULTS: The serum concentrations of procollagen-III-peptide, hyaluronic acid and laminin were significantly higher at the onset of acute necrotizing pancreatitis compared to edematous pancreatitis and the controls. They returned to almost normal levels during the course of the disease when the patient recovered, but remained elevated in patients with a lethal course. Laminin allowed us to discriminate between patients with necrotizing pancreatitis from all other forms of pancreatitis on admission (specificity 82%, sensitivity 92%, PPV 86%, NPV 90%). Collagen type VI levels were 2-3-fold higher in sera of patients with acute pancreatitis than in healthy controls, whereas the results for undulin were inconclusive. CONCLUSIONS: Since markers of matrix metabolism (especially laminin) are differently elevated in acute necrotizing versus edematous pancreatitis, we suggest that they might be used as parameters for the outcome.     

Treatment of acute pancreatitis. Comparison of animal and human studies

In this review, we compared the outcome of 25 studies of experimentally induced pancreatitis in animals with 13 studies of human acute pancreatitis in which the same therapeutic agents were used (aprotinin, glucagon, 5-fluorouracil, somatostatin, peritoneal lavage). Whereas 81% of the animal studies had a positive outcome (improvement in survival), only 7.7% of the human studies showed a positive outcome on survival. Most animal studies suffered from a protocol in which treatment was not significantly delayed after induction of acute pancreatitis. Of the 12 human studies that showed no effect of treatment on survival, none had sufficient statistical power (1 - beta error) for the investigators to have confidence in the negative outcomes. This was due to the fact that the studies had too few patients or that the event rates in the untreated populations were too low. Only five of the human studies reported the complication rates of acute pancreatitis in patients who did not die of their disease. Treatment (by any agent) did not improve the complication rate in these studies, but only one of the five reports had sufficient statistical power for the investigators to have confidence in these negative results. Large multicenter studies with sufficient numbers of patients with severe pancreatitis (high mortality and complication rates) are needed to evaluate new therapies in this disease.     

褪黑素干预急性胰腺炎的实验研究进展

褪黑素是一种具有抗氧化作用、免疫调节作用的吲哚类激素,可以下调急性炎症反应过程中炎症介质的表达,减轻急性炎症反应.此文就近年来的褪黑素干预急性胰腺炎的实验研究作一综述.     

Ultrastructure of human acute pancreatitis

Summary Few studies have been published on the ultrastructural changes which accompany human acute pancreatitis, and these have concentrated primarily on parenchyma. The present study concentrates on extraparenchymal changes, compares acute pancreatitis occurring alone with that on a background of chronic pancreatitis, and tests for similarity with observations made previously in an experimental model. Pancreatic tissue came from 16 patients undergoing surgery for pancreatic disease and five subjects without pancreatic disease. Regressive changes in parenchymal cells were consistent with ischemia, and with previously described studies. Polymorphonuclear leukocytes infiltrated into stroma and parenchyma. Platelets accumulated intra- and extravascularly. Fibrin deposits were common in the connective tissue, and could be observed in intercellular spaces at the base of acini, mingled with degenerating acinar cells and secretion product. Microthrombi occurred in blood vessels. These alterations were consistent with those in experimental acute pancreatitis. Similar changes were observed whether or not acute pancreatitis occurred on a background of chronic pancreatitis. The vascular component is important in acute pancreatitis, and altered epithelial barriers allow interaction between blood-borne material and pancreatic exocrine secretions. This paper was presented at the International Symposium on Acute Pancreatitis in Research and Clinical Management held at Schloss Reisensburg, Günzburg, F.R.G., October 31–November 2, 1985.     

Ultrastructure of human acute pancreatitis

Few studies have been published on the ultrastructural changes which accompany human acute pancreatitis, and these have concentrated primarily on parenchyma. The present study concentrates on extraparenchymal changes, compares acute pancreatitis occurring alone with that on a background of chronic pancreatitis, and tests for similarity with observations made previously in an experimental model. Pancreatic tissue came from 16 patients undergoing surgery for pancreatic disease and five subjects without pancreatic disease. Regressive changes in parenchymal cells were consistent with ischemia, and with previously described studies. Polymorphonuclear leukocytes infiltrated into stroma and parenchyma. Platelets accumulated intra- and extravascularly. Fibrin deposits were common in the connective tissue, and could be observed in intercellular spaces at the base of acini, mingled with degenerating acinar cells and secretion product. Microthrombi occurred in blood vessels. These alterations were consistent with those in experimental acute pancreatitis. Similar changes were observed whether or not acute pancreatitis occurred on a background of chronic pancreatitis. The vascular component is important in acute pancreatitis, and altered epithelial barriers allow interaction between blood-borne material and pancreatic exocrine secretions.     

ICAM-1表达在大鼠重症急性胰腺炎肺损伤中的作用

目的研究大鼠重症急性胰腺炎(SAP)肺组织细胞间粘附分子-1(ICAM-1)的表达与肺损伤的关系。方法将30只SD大鼠随机分为假手术组、SAP不同时间点(1 h、4 h、8 h和12 h)各组,用逆行胰胆管注射方法制备SAP模型。采用Western Blot法检测大鼠肺组织中ICAM-1蛋白表达,同时观察肺组织髓过氧化物酶(MPO)及病理改变。结果造模SAP 1 h后大鼠肺组织中ICAM-1的表达水平即比假手术组高(P<0.05),并持续升高达12 h,同时伴有MPO水平升高和肺组织病理损害的加重, ICAM-1表达与肺损伤程度、MPO水平之间以及肺组织MPO水平与与肺损伤程度均呈正相关,相关系数分别为0.88、0.91及0.86(P<0.01)。结论SAP大鼠肺组织中ICAM-1呈过度表达,ICAM-1表达的高低与肺损伤严重程度有关。肺组织中ICAM-1过度表达及中性粒细胞浸润是SAP肺损害发生的原因之一。     

ICAM-1表达在大鼠重症急性胰腺炎肺损伤中的作用

目的研究大鼠重症急性胰腺炎(SAP)肺组织细胞间粘附分子-1(ICAM-1)的表达与肺损伤的关系.方法将30只SD大鼠随机分为假手术组、SAP不同时间点(1 h、4 h、8 h和12 h)各组,用逆行胰胆管注射方法制备SAP模型.采用Western Blot法检测大鼠肺组织中ICAM-1蛋白表达,同时观察肺组织髓过氧化物酶(MPO)及病理改变.结果造模SAP 1 h后大鼠肺组织中ICAM-1的表达水平即比假手术组高(P ＜ 0.05),并持续升高达12 h,同时伴有MPO水平升高和肺组织病理损害的加重,CAM-1表达与肺损伤程度、MPO水平之间以及肺组织MPO水平与与肺损伤程度均呈正相关,相关系数分别为0.88、0.91及0.86(P ＜ 0.01).结论 SAP大鼠肺组织中ICAM-1呈过度表达,CAM-1表达的高低与肺损伤严重程度有关.肺组织中ICAM-1过度表达及中性粒细胞浸润是SAP肺损害发生的原因之一.     

生物学标志物对急性胰腺炎严重程度预测的研究进展

急性胰腺炎(AP)是由多种病因导致胰酶激活,继以胰腺局部炎症反应为主要特点,根据有无胰腺局部并发症和器官功能衰竭的出现及持续时间将急性胰腺炎分为轻、中重度、重度3级[1].临床上约80％是轻中度急性胰腺炎,通常经过对因治疗和保守治疗后通常预后良好,然而约20％会进展为重症急性胰腺炎(SAP).SAP病程早期是由于多种病...