急性胰腺炎合并肝损害临床分析

目的分析急性胰腺炎合并肝损害的临床特点。方法回顾性分析2009年2月至2012年8月西安市中心医院收治的116例急性胰腺炎患者的临床资料。结果67％（78／116）的急性胰腺炎患者合并肝损害。按病因分类,胆源性胰腺炎合并肝损害者的发病率为79％（38／48）,胰胆手术后（含胆囊切除术后及经内镜逆行性胰胆管造影术后）所致的急性胰腺炎合并肝损害的发病率为68％（15／22）,暴饮暴食所致的急性胰腺炎合并肝损害的发病率为67％（20／30）,其他因素所致的急性胰腺炎合并肝损害的发生率低。胆源性胰腺炎较非胆源性胰腺炎肝功能损害更明显,总胆红素、直接胆红素、谷丙转氨酶、谷草转氨酶、γ-谷氨酰转肽酶、碱性磷酸酶浓度差异均有统计学意义（t值分别为3．16、3．72、4．12、3．26、3．64、3．25,P均〈0．01）。结论胆源性胰腺炎患者大多合并肝损害。     

急性胰腺炎合并肝脏损害156例临床分析

目的分析急性胰腺炎合并肝脏损害的临床特点．方法对我院近3a收治的238例急性胰腺炎患者的临床资料进行分析，其中男112例，女126例，年龄6岁～83岁，平均年龄48．5岁．水肿型218例，坏死型20例．分析内容包括一般资料、诊断标准、病因、临床表现、实验室检查指标、B超、CT、病理类型及并发症等．全部数据都进行了统计学处理．结果在全部238例急性胰腺炎患者中，发现156例（占65．5％）合并不同程度的肝脏损害，女性明显多于男性．不同病因所致急性胰腺炎合并肝脏损害者无直接相关性，重症急性胰腺炎，较轻症者肝脏损害发生率高，损害程度严重，呈正相关系，肝功能异常多属可逆性．平均住院天数较同期无肝脏损害者明显延长．并发症多，预后差．结论肝脏损害的发生率及损害程度与急性胰腺炎的严重程度呈正相关性．     

207例急性胰腺炎合并肝功能损害的临床观察

目的研究急性胰腺炎（AP）合并肝功能损害的临床特点、发病机制及对预后的预测。方法对207例合并肝功能损害AP患者按照病因、严重程度、年龄分组。分别比较各组患者肝功能损害的严重程度、预后及转归，分析对AP严重程度预测灵敏度、特异度较显著的肝功能变化指标。结果重症急性胰腺炎（SAP）肝功能损害的严重程度明显高于轻症急性胰腺炎（MAP）（P〈0．05）。胆源性AP肝功能指标中ALT、ALP、LDH比非胆源性AP损害程度重（P〈0．05）；胆源性AP比非胆源性AP符合SAP人数、转手术率、死亡率均较高．住院天数较长。不同年龄AP患者肝功能损害的严重程度无显著差异（P〉0．05）。各肝功能指标中ALT、AST、LDH对AP严重程度预测灵敏度、特异度较显著。结论胆源性AP合并肝功能损害明显。ALT、AST、LDH等肝功能变化指标可作为对AP严重程度预测的参考指标。     

急性胰腺炎并肝损害（附201例临床分析）

目的 观察急性胰腺炎(AP)时肝功能的损害和损害程度及预后。方法 对我院2001-01／2003-07收治的急性胰腺炎进行了回顾性调查和分析。结果 在201例AP中有135例合并不同程度的肝功能损害。重型AP较轻型AP肝功能损害发生率高，损害程度也严重。胆源性AP比非胆源性AP肝功能损害发生率高，损害程度也明显。结论 肝功能损害是AP的常见临床表现，肝功能损害程度与胰腺炎的轻重程度呈正相关。肝脏的损害不仅加重AP的病情，还影响其预后。     

血浆花生四烯酸代谢紊乱在大鼠急性胰腺炎肝脏损害发病机理中的作用

目的探讨急性胰腺炎肝脏受损与血浆花生四烯酸紊乱的关系．方法同时观察不同程度急性胰腺炎大鼠（ｎ＝１４０）肝脏受损情况和血浆花生四烯酸代谢产物血栓素Ｂ２（ＴＸＢ２）和６酮前列腺素Ｆ１α（６ｋｅｔｏＰＧＦ１α）的变化关系，并对急性胰腺炎时大鼠胰腺和肝脏组织病理学观察．结果发现急性出血坏死性胰腺炎大鼠肝脏发生明显病变，其程度与胰腺病理程度一致，急性出血坏死性胰腺炎时血浆ＴＸＢ２从对照组的１２１ｎｇ／Ｌ±２７ｎｇ／Ｌ上升至ＡＰ后２ｈ的３９９ｎｇ／Ｌ±１３１ｎｇ／Ｌ和４ｈ的６０７ｎｇ／Ｌ±１７４ｎｇ／Ｌ（Ｐ＜００１），ＴＸＢ２／６ｋｅｔｏＰＧＦ１α异常（Ｐ＜００１），而ＴＸＢ２／６ｋｅｔｏＰＧＦ１α比值变化与肝脏病理变化呈正相关（ｒｓ＝０８８９７，Ｐ＜００１）．通过异搏定治疗可明显改善胰腺病理损害和稳定血浆花生四烯酸代谢，明显减轻肝脏的损害．结论急性胰腺炎伴发的肝脏损害的发生发展与血浆花生四烯酸代谢紊乱有关     

急性胰腺炎并发呼吸系统损害52例临床分析

目的 探讨急性胰腺炎并发呼吸系统损害的临床特点及发病机理。方法回顾性总结分析52例急性胰腺炎并发呼吸系统损害病人的临床资料。结果52例急性胰腺炎并发呼吸系统损害的病人，临床上主要表现为呼吸急促或困难(39例，占75％)、发生ARDS(6例，占．11．54％)、体检肺部有湿罗音、PaO2降低(11例，21．15％)。胸片发现有问质性肺炎(18例，34．62％)、肺不张(7例，13．46％)、斑片状阴影或毛玻璃样改变(6例，11．54％)、胸腔积液(20例，38．46％)；其病因主要为胆源性胰腺炎(25例，48．08％)、酒精性胰腺炎(6例，11．54％)、饮食不当(16例，30．77％)、特发性胰腺炎；其病变程度水肿型胰腺炎9例，坏死型胰腺炎43例。结论急性胰腺炎并发呼吸系统损害的病因主要为胆源性者，重症急性胰腺炎的呼吸系统损害发生率高、病情重，重度损害表现为ARDS，因而防治ARDS成为治疗的关键。     

经内镜治疗急性胆源性胰腺炎的临床价值

目的探讨治疗性ERCP在急性胆源性胰腺炎（acute biliary pancreatitis，ABP）治疗及减少复发中的临床价值。方法将ABP患者依据其治疗方式，分为内镜组行ERCP治疗和对照组行常规治疗，比较其腹痛缓解时间及血、尿淀粉酶降至正常时间及肝功能恢复时间和住院天数。随访所有ABP患者，比较两组患者复发率。结果117例ABP患者中急性轻症胆源性胰腺炎患者99例（84．6％），急性重症胆源性胰腺炎患者18例（15．4％）。内镜组和对照组总例数分别为49例和68例。内镜组与对照组比较，急性轻症胆源性胰腺炎和急性重症胆源性胰腺炎的腹痛缓解时间、肝功能恢复时间、住院天数均明显缩短（P〈0．05或P〈0．01）。血、尿淀粉酶恢复时间两组比较差异无统计学意义。内镜组无明显内镜治疗相关并发症发生。所有患者平均随访时间20个月（5—37个月）；7例失访，随访率94．0％。内镜组的复发率0（0／46）明显低于对照组46．8％（29／62）（P〈0．01）。结论与常规治疗比较，ERCP治疗ABP是较好方法之一，不仅疗效好、恢复较快，而且安全，并能减少胆源性胰腺炎的复发。     

急性胰腺炎呼吸困难发病因素与临床特征探讨

作者报道经手术确诊的急性胰腺炎并发呼吸，呼吸频率≥３０次／分与＜３０次／分的急性胰腺炎患者二组的临床资料并进行比较，前者的临床特征为：出血死型为主，占９５．７％休克率高达５６．５％，低氧自症（ＰＯ２＜８ｋＰａ）多，占７２．２％，１００％有胰性腹水发生，而对照组依次为７２％、１２％、２３。．５％及１８％，各项之间相比较差异均有显著性（Ｐ＜０．０５）。呼吸困难组病死率为７３．９％，多器官损害者占６９．     

急性水肿型胰腺炎合并胃损害45例分析

总结分析７２例急性水肿型胰腺炎合并胃损害的情况。结果显示６２５％（４５／７２）的患者伴有活动性胃炎和消化性溃疡，前者的发生率为４８６％，后者为１３８％。胆源性和酒精源性胰腺炎合并胃损害的发生率分别为６８３％和６０７％，无显著性差异。轻度胰腺炎合并胃损害的发生率低于中、重度的发生率。血清胃泌素无明显变化，幽门螺杆菌（Ｈｐ）的感染率为３７８％。结果表明急性水肿型胰腺炎合并胃损害的发生可能主要与胰蛋白酶、溶血磷脂活性增加，使胃粘膜血流减少，从而导致胃粘膜抗力下降等因素有关，而与胃泌素、酒精刺激及Ｈｐ的感染关系不大。此外，合并的胃损害可能是急性水肿型胰腺炎腹痛消失较慢的原因。     

急性胰腺炎并肝脏损害的临床分析

急性胰腺炎并肝脏损害临床上比较常见，它不仅与急性胰腺炎程度相关，还可影响其预后，甚至引起肝功能衰竭，导致患者死亡。我们就1996年以来收治的48例急性胰腺炎并肝脏损害的病例进行分析，旨在探讨其病因和发病机制，现总结报告如下。     

The effect of pancreatitis associated ascitic fluid on some functions of rat liver mitochondria. A possible mechanism of the damage to the liver in acute pancreatitis

The damage to the liver during acute pancreatitis (AP) could be partly dependent on depressive action of pancreatitis associated ascitic fluid (PAAF) on the energy metabolism of hepatocytes. The aim of the study was to assess the effect of PAAF from dogs with acute experimental pancreatitis (AEP) and from humans with AP on the respiratory function of isolated rat liver mitochondria (RLM). The mitochondrial oxygen consumption rate in state 3 respiration (with ADP) and in state 4 (without ADP) using sodium succinate as substrate and oxygen Clark's electrode was estimated. Respiratory control ratio (RCR) and P/O ratio were calculated. PAAF was collected after 6 h of AEP induced by Elliott's method in 8 dogs, and from 4 patients with AP, intraoperatively. Both animal and human PAAFs increase the oxygen consumption rate by RLM in state 4 dose dependently (by 65% with 50 microL to 150% with 200 microL of canine PAAF). This uncoupling effect of human PAAF was twice more potent than the canine. Dialysis of PAAF reduced this effect almost completely. The mitochondrial ATPase activity in RLM treated with PAAF was stimulated and this effect was also reduced by dialysis. The conclusion was that the damage to the liver in AEP could be partly dependent on the toxicity of dializable component(s) of PAAF on the energy metabolism of mitochondria. These findings may partly explain the beneficial effects of peritoneal lavage in acute pancreatitis.     

急性胰腺炎合并肝损害的临床分析

目的探讨急性胰腺炎时肝损害的临床特点。方法对81例急性胰腺炎病人的肝功能进行分析,以了解肝损害的发生率、肝损害程度和对病程的影响。结果81例急性胰腺炎中合并肝损害者46例(56.8%),重症急性胰腺炎(SAP)较轻症急性胰腺炎(MAP)肝损害发生率高(100%对48.5%,P<0.01)。胰腺炎的诱因与肝损害程度无关(P>0.05)。SAP肝损害者比MAP肝损害者住院天数明显延长(P<0.01)。结论急性胰腺炎肝损害的程度与病情严重性呈正相关。     

99mTc-hexamethylpropylene amineoxime leukocyte scintigraphy in acute pancreatitis: an alternative to contrast-enhanced computed tomography?

OBJECTIVE: Contrast-enhanced computed tomography (CECT) is the most efficient imaging technique for the diagnosis and staging of acute pancreatitis (AP); its use, however, may be unfeasible in some patients as a consequence of the drawbacks of intravenous (IV) contrast material. The aim of this study was to test the utility of labeled leukocyte scintigraphy (LLS) as an alternative imaging technique to CECT for the staging of AP. METHODS: Sixty-six patients with AP were prospectively studied. All patients underwent CECT and pancreatic LLS using (99m)Tc-hexamethylpropylene amineoxime as leukocyte label within a time interval of 2 days, in the early phase of AP. In addition, all patients had their serum C-reactive protein (CRP) concentration measured within 48-72 h after admission. CECT images were analyzed for Balthazar's grade of pancreatitis and for the presence or absence of pancreatic necrosis. Scintigraphic activity of 3-4 h planar images was scored on a 0-2 scale in relation to physiological liver uptake. RESULTS: LLS score was significantly related (p < 0.001) to both components of CECT (grade of pancreatitis and pancreatic necrosis). LLS and serum CRP showed similar results for detecting the most severe pancreatic damage as showed by their respective receiver operating characteristic (ROC) curves. Sensitivities and specificities of LLS score of 2 were, respectively, 62% and 96% for the detection of grade D-E pancreatitis and 90% and 89% for the detection of pancreatic necrosis. Scintigraphic score of 2 increased the likelihood of grade D-E pancreatitis from 32% (pretest probability) to 87% (posttest probability) (likelihood ratio: 13.9) and that of pancreatic necrosis from 16% to 60% (likelihood ratio: 8.4). CONCLUSIONS: Our results show that leukocytes are related to the severity of local pancreatic damage in AP. Thus, LLS is a potential alternative technique to CECT for staging AP.     

The dynamics of the oxidant-antioxidant balance in the early phase of human acute biliary pancreatitis.

BACKGROUND/AIM: Reactive oxygen species play an important role in the pathogenesis of acute pancreatitis (AP) in animal models. Data on the oxidant-antioxidant balance in humans are scanty. The present study was undertaken to evaluate the dynamics of changes in the oxidant-antioxidant balance in the early phase of human AP. METHODS: 74 consecutive patients with acute biliary pancreatitis (16 with severe, 58 with mild pancreatitis), treated endoscopically, were included in the study. Serum concentrations of sulfhydryl groups (SH; main nonenzymatic antioxidant; 73 patients) and thiobarbituric acid reactive substances (TBARS; markers of reactive oxygen species-mediated tissue damage; 56 patients) were determined on admission and on each of 10 successive days. The analysis comprised the comparison of results in patients with mild and severe outcome of pancreatitis. RESULTS: Serum SH dropped by 27%, reaching the trough level on day 4 of hospitalization, whereas serum TBARS rose by 28%, reaching a peak 1 day later. Neither SH nor TBARS returned to initial values at the end of observation. The most dynamic changes in both SH and TBARS concentrations occurred in the first 3 days of hospitalization. The changes were significantly greater in patients with complicated pancreatitis in comparison to patients with mild disease, and were most pronounced in patients who developed infected pancreatic necrosis and who subsequently died. CONCLUSIONS: The oxidant-antioxidant balance changes rapidly in the early phase of human AP, confirming the role of oxidative stress in the pathogenesis of AP. The degree of changes correlates with the clinical severity of pancreatitis.     

Macrophage migration inhibitory factor is a critical mediator of severe acute pancreatitis

BACKGROUND & AIMS: Macrophage migration inhibitory factor (MIF), originally described as an inhibitor of the random migration of macrophages, has been shown recently to be involved in the pathogenesis of several inflammatory diseases such as sepsis. The aim of this study was to clarify the role of MIF in acute pancreatitis (AP). METHODS: Hemorrhagic necrotizing pancreatitis and edematous pancreatitis were induced by the injection of taurocholic acid (TCA pancreatitis) and cerulein (cerulein pancreatitis), respectively, on male Wistar rats. MIF levels in ascitic fluids, serum, and the organs were determined. The effects of anti-MIF antibody were examined on the prognosis of rats with TCA pancreatitis and of female CD-1 mice with choline-deficient, ethionine-supplemented, diet-induced model of severe AP. In addition, serum MIF levels in AP patients and in healthy controls were measured. RESULTS: Serum and ascitic MIF levels in TCA pancreatitis were increased rapidly and decreased gradually thereafter. Ascitic MIF levels were also increased in cerulein pancreatitis, but to a lesser degree. MIF level was increased in the lung in TCA pancreatitis, but not in the pancreas and the liver. Prophylactic (1 hour before and immediately after induction) administration of anti-MIF antibody significantly improved the survival rate of rats with TCA pancreatitis. The survival rate of mice with severe AP was also improved significantly by the antibody treatment. Serum MIF levels were higher in severe AP patients than mild AP patients and healthy controls. CONCLUSIONS: These results suggest a role of MIF in the pathogenesis of severe AP.     

抑制JAK／STAT信号通路对实验性急性胰腺炎大鼠肝损伤的保护作用

背景：JAK／STAT细胞内信号通路广泛参与细胞的增殖、分化、凋亡以及炎症、肿瘤的发生等多种生理、病理生理过程，然而关于其在重症急性胰腺炎（SAP）急性肝损伤中作用的研究尚少。目的：观察抑制JAK〈STAT通路对实验性急性胰腺炎（AP）大鼠肝损伤的保护作用。方法：56只Sprague-Dawley大鼠随机分为正常对照组、3组AP模型组和3组JAK特异性抑制剂AG490干预组。以4％牛磺胆酸钠胰胆管逆行注射诱导AP模型。分批处死各组大鼠，动态测定血清丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）水平，观察肝脏大体和组织学表现，以免疫组化染色和蛋白质印迹法检测肝组织中JAK2的定位和表达。结果：与正常对照组相比，AP模型组各时间点血清ALT、AST水平均显著升高；肝组织大体和组织学损伤随病情进展而逐渐加重；肝组织JAK2表达逐渐增强，于18h时达高峰。经AG490预处理的大鼠，上述各项指标均较同时间点AP模型组显著改善。结论：JAK2参与了大鼠实验性AP肝损伤的病理过程，抑制肝组织JAK／STAT通路活化有助于SAP急性肝损伤的防治。     

Hepatic mitochondrial and lysosomal alterations in acute experimental pancreatitis with ethanolic coetiology in rats

In order to assess the cumulative effects of antecedent acute ethanol intake and acute pancreatitis on the liver, the mitochondrial respiratory functions and lysosomal membrane integrity of the liver were evaluated in taurocholate pancreatitis (AP) in rats, induced 6 hr after intragastric ethanol 40% (5 g/kg body wt). The oxygen consumption rate. RCR (respiratory control ratio), and ADP/O ratio were measured according to Estabrook. Fractional free activity of lysosomal hydrolases was assayed. RCR with glutamate+malate was most decreased at 12 hr of AP with partial improvement after 18 hr. The ADP/O ratio dropped maximally after 18 hr of AP. The fragility of lysosomal membranes increased significantly at 18 hr of AP. The antecedent ethanol intake abolished the partial restoration of RCR after 18 hr; however, it did not affect the ADP/O ratio or the integrity of lysosomal membranes impaired in AP at this time. In conclusion, the antecedent acute ethanol abuse could aggravate the liver mitochondrial deterioration, but not the lysosomal membrane labilization seen in AP.Sponsored by Polish Committee for Scientific Research (KBN) grant 4 0435 91 01.     

Resistin is not an appropriate biochemical marker to predict severity of acute pancreatitis: A case-controlled study

AIM: To assess levels of serum resistin upon hospital admission as a predictor of acute pancreatitis (AP) severity.METHODS: AP is both a common and serious disease, with severe cases resulting in a high mortality rate. Several predictive inflammatory markers have been used clinically to assess severity. This prospective study collected data from 102 patients who were diagnosed with an initial acute biliary pancreatitis between March 2010 and February 2013. Measurements of body mass index (BMI) and waist circumference (WC) were obtained and serum resistin levels were analyzed at the time of hospital admission using enzyme-linked immunosorbent assay. Additionally, resistin levels were measured from a control group after matching gender, BMI and age.RESULTS: A total of 102 patients (60 females and 42 males) were diagnosed with acute gallstone-induced pancreatitis. The mean age was 45 years, and mean BMI value was 30.5 kg/m² (Obese, class I). Twenty-two patients (21.6%) had severe AP, while eighty-eight patients had mild pancreatitis (78.4%). Our results showed that BMI significantly correlated with pancreatitis severity (P = 0.007). Serum resistin did not correlate with BMI, weight or WC. Furthermore, serum resistin was significantly higher in patients with AP compared to control subjects (P < 0.0001). The mean resistin values upon admission were 17.5 ng/mL in the severe acute biliary pancreatitis group and 16.82 ng/mL in the mild AP group (P = 0.188), indicating that resistin is not an appropriate predictive marker of clinical severity.CONCLUSION: We demonstrate that obesity is a risk factor for developing severe AP. Further, although there is a correlation between serum resistin levels and AP at the time of hospital admission, resistin does not adequately serve as a predictive marker of clinical severity.     

Hyperlipidemia in acute pancreatitis. Relationship with etiology, onset, and severity of the disease.

Serum lipid (triglycerides and cholesterol) concentrations were studied in 49 patients with acute pancreatitis (AP). The aims of the study were to investigate the prevalence of hyperlipidemia (HL) in patients with AP according to etiology and to evaluate whether HL precedes or is a consequence of AP. Moreover, we analyzed the relationship between HL and the development of pancreatic necrosis. At admission, 23 patients (47%) had HL: 9 of 19 patients with alcoholic pancreatitis, 5 of 18 patients with biliary pancreatitis, and 9 of 12 patients with AP of miscellaneous etiologies (p less than 0.05). Severe HL (serum triglycerides greater than 20 mmol/L) was observed in five patients. Serum lipid levels in patients with AP and HL decreased markedly during the first 72 h of evolution, but remained slightly above the upper normal limit in most of them after 15 d. The prevalence of HL was similar in edematous and necrotizing pancreatitis. Necrotizing pancreatitis was significantly associated with the presence of hypertriglyceridemia in conjunction with hypercholesterolemia (p less than 0.05). The observations that a) hyperlipidemia is an early event in acute pancreatitis, (b) serum lipid values decrease during the acute phase of the disease, (c) hyperlipidemia has a different prevalence in different etiologies, and (d) high serum lipid levels are not always associated to pancreatic necrosis suggest that HL is a preexistent metabolic abnormality with respect to AP. On the other hand, HL may play a role in aggravating AP.