急性坏死性胰腺炎生长抑素和生长激素联合治疗对多器官损伤的保护作用

目的研究生长抑素和生长激素联合应用防治急性坏死性胰腺炎（ANP）的全身炎症反应综合征和多器官功能障碍综合征及其治疗策略．方法经胰胆管逆行注射35g／L牛磺胆酸钠2．5mL／kg建立鼠ANP模型．测定血清IL-8，IL-6，TNFα,淀粉酶、内毒素和清蛋白．胰腺、肝、心、肺和肾病理观察及细胞超微结构观察，TNFαmRNA分子转录水平的RT－PCR分析及TNFα的免疫组化原位观察，探讨生长抑素和生长激素治疗作用．结果ANP的发生和发展伴有炎性递质的明显升高，与ANP和MODS的发展呈正相关．生长抑素和生长激素对抑制炎性递质的释放和TNFarnRNA过度表达有协同作用，同时亦表明肝脏在ANP中对预防宿主多器官衰竭有重要作用结论TNFαmRNA的高度表达在ANP的进展中至关重要，生长抑素和生长激素的联合治疗时防治ANP的MODS的发生和防治有重要作用.     

生长抑素对重症急性胰腺炎患者血小板参数的影响

目的　探讨重症急性胰腺炎患者血小板参数的变化特点及生长抑素治疗对其的影响。方法　应用血细胞自动分析仪检测轻症急性胰腺炎 (MAP)和重症急性胰腺炎 (SAP)患者不同时期血小板计数 (PLT)、血小板容积 (PCT)、平均血小板体积 (MPV)和血小板分布宽度 (PDW )。结果　与MAP组比较 ,SAP患者入院时外周血PLT、PCT明显下降 (P <0 .0 0 1) ,MPV和PDW显著升高 (P <0 .0 5 ) ;SAP患者死亡组与存活组比较 ,PLT、PCT明显下降 (P <0 .0 1) ,MPV和PDW明显升高 (P <0 .0 1) ;与常规治疗组比较 ,生长抑素治疗组SAP患者PLT和PCT明显上升 (P <0 .0 1) ,MPV和PDW明显下降 (P <0 .0 5 )。结论　SAP与MAP患者血小板参数的变化程度明显不同。生长抑素治疗后PLT和PCT升高 ,血小板的活性降低 ,提示生长抑素对SAP患者具有一定的治疗和预防作用。     

生长抑素对急性胰腺炎患者血小板参数的影响

目的：研究血小板参数在急性水肿型胰腺炎（ＡＥＰ）和出血坏死型胰腺炎（ＡＨＮＰ）中的变化特点及生长抑制（ＳＳ）治疗后对其影响。方法;血细胞自动分析仪检测血小板计数（ＰＬＴ）、平均血小板体积（ＭＰＶ）和血小板分布宽度（ＰＤＷ）。结果：ＡＥＰ患者血小板参数无明显变化。１周后,ＰＬＴ无明显升高,ＭＰＶ和ＰＤＷ有显著性升高;常规治疗后,对血小板参数无影响;ＳＳ治疗后,ＭＰＶ和ＰＤＷ有显著性升高。而ＡＨＮＰ患     

综合治疗重症急性胰腺炎119例

目的分析综合治疗重症急性胰腺炎的效果方法119例重症急性胰腺炎采用综合治疗，即在西医常规治疗的基础上加用中药腹腔排脓汤．其中Ⅰ级35（29．41％），Ⅱ级84例（70．59％）；119例中男66例，女53例．结果119例采用综合治疗，其中102例治愈（85．71％），16例好转（13．45％）；1例无效（0．84％）．总有效率为99．16％．结论重症急性胰腺炎应采用综合治疗为主．     

生长抑素对急性胰腺炎患者血小板相关指标与消化功能影响的研究

目的探讨生长抑素对急性胰腺炎患者血小板相关指标与消化功能影响的程度。方法选取2011年10月-2013年11月淄博矿业集团有限责任公司中心医院收治的68例急性胰腺炎患者为研究对象,将其随机分为对照组和观察组各34例,对照组接受常规治疗,观察组则在对照组的基础上加用生长抑素,比较两组患者治疗前后的血小板相关指标与消化功能相关指标。结果观察组治疗后1 d、3 d及7 d血小板相关指标均低于对照组,血清胰腺消化酶均低于对照组,其他消化功能相关指标也均优于对照组,差异有统计学意义(P0.05)。结论生长抑素对急性胰腺炎患者血小板相关指标与消化功能的影响较大,有助于改善患者的微循环及消化功能状态。     

前列腺素E1治疗急性胰腺炎

前列腺素Ｅ１治疗急性胰腺炎张弘迟景宏齐齐哈尔铁路中心医院黑龙江省齐齐哈尔市１６１０００ＳｕｂｊｅｃｔｈｅａｄｉｎｇｓＡｌｐｒｏｓｔａｄｉｌ／ｔｈｅｒａｐｅｕｔｉｃｕｓｅＰａｎｃｒｅａｔｉｔｉｓ／ｄｒｕｇｔｈｅｒａｐｙＡｃｕｔｅｄｉｓｅａｓｅ主题...     

14肽生长抑素治疗急性重症胰腺炎16例

目的观察14肽生长抑素（施他林，stilamin）治疗急性重症胰腺炎的疗效．方法1994－01／1998－03共收治急性重症胰腺炎36例，其中1994－01／1996－09收治的20例，采用常规治疗为对照组，1996－10／1998．03收治的16例在常规治疗的基础上加用14肽生长抑素持续静脉点滴sd～7d为治疗组，通过血淀粉酶下降程度，转手术治疗率，并发症、住院日等指标观察两组疗效差异．结果治疗组入院后10d血淀粉酶100％降至正常；对照组50％降至正常P＜0．01．治疗组无1例手术治疗，对照组9例45％转手术治疗．治疗组出现并发症14例次，对照组20例次．住院日：治疗组23．93d±11．37d，对照组42．28d±24．52d，P＜0．05．结论14肽生长抑素能有效地抑制胰液、胰酶的分泌，在发病初期开始应用，能在一定程度上控制病情发展，减少手术治疗及并发症的发生，缩短住院日．     

血小板活化因子与急性胰腺炎

血小板活化因子(PAF)是多种细胞产生的生物活化因子,在急性胰腺炎的炎症反应中,起到微循环障碍,氧自由基活化,细胞内领导转导异常,增强其他细胞因子的作用,介导胰腺形态和机能的改变,并在急性胰腺炎并发多器官功能衰竭中起关键作用。血小板活化因子拮抗剂有潜在治疗急性胰腺炎的作用。     

奥曲肽治疗急性胰腺炎的临床研究

目的探讨（SS）治疗急性胰腺炎的临床效果方法应用人工合成的SS类似物-奥曲肽（Octreotide,Oct）治疗38例和非OCt治疗59例急性胰腺炎（acutepancreatitis，AP）．观察了两组以及Oct治疗用药前后血清淀粉酶及胰液淀粉酶的含量，比较了两组并发症的发生率。结果Oct能有效降低血清淀粉酶和胰液淀粉酶的活性，改善临床症状和体征，降低并发症的发生．结论Oct有助于AP的治疗.     

生长抑素治疗重症急性胰腺炎40例

[目的]观察在中西医结合治疗重症急性胰腺炎（SAP）的基础上，早期应用生长抑索的临床疗效。[方法]将72例SAP患者随机分为生长抑素治疗组40例和对照组32例，两组均予中西医结合治疗，治疗组加用生长抑素250μg／h持续微泵泵人，持续5～7d，对两组之间腹痛及压痛缓解、多项实验室指标、腹水消失、住院时间以及并发症发生率、转手术率、病死率进行分析。[结果]治疗组腹痛及压痛缓解时间、实验室指标恢复时间、腹水消失、住院时间等明显优于对照组（P〈0．05，〈0．01），并发症发生、转手术率及病死率低于对照组（P〈0．05）。[结论]早期中西医结合联合生长抑素对SAP治疗有重要价值。     

清胰汤治疗重症急性胰腺炎42例

目的评估清胰汤中西医结合治疗重症急性胰腺炎（ＳＡＰ）的疗效．方法１９８６／１９９６收治重症急性胰腺炎８０例，随机分成两组，治疗组４２例，采用清胰汤中西医结合治疗；对照组３８例，仅给予单一西医治疗，将两组疗效进行对比分析．结果治疗组治愈３６例，治愈率８５７％，对照组治愈２４例，治愈率６４７％，经卡方检验χ２＝５４４，Ｐ＜００５．结论中西医结合治疗ＳＡＰ较单一西医治疗效果为佳．     

血小板异常评估急性胰腺炎严重程度的临床价值

目的 探讨血小板在急性胰腺炎（AP）患者中的变化及与AP严重程度和预后的关系.方法 比较重症急性胰腺炎（SAP）组和轻症急性胰腺炎（MAP）组血小板的计数变化.SAP组进一步分为血小板降低组和血小板正常组,比较两组局部并发症和多器官功能不全综合征（MODS）的发生率、病死率以及胰腺坏死程度与血小板计数（PLT）之间的关系,并分析差异有无统计学意义.分析血小板与APACHEⅡ评分系统、BISAP评分系统、CT评分系统、Ranson评分系统之间的相关性.结果 AP患者重症组与轻症组相比,PLT下降,血小板平均体积（MPV）升高,两组比较差异有统计学意义（P＜0.05）,PDW及PCT差异无统计学意义（P＞0.05）;SAP患者发病前3d首次PLT计数（＜100×109/L）的比例明显多于MAP组,差异有统计学意义（P＜0.001）;血小板降低组中局部并发症患者、MODS患者及病死率明显高于血小板正常组,两者相比差异有统计学意义（P ＜0.05）;SAP中胰腺坏死程度与血小板计数水平呈负相关性（P＜0.05）;血小板计数水平与CTSI评分标准相关性最强,其次是APACHEⅡ评分系统,而与Ranson评分系统无明显相关性.结论 血小板计数能够比较准确地反映AP的严重程度和预后,尤其在预测SAP局部并发症、MODS、坏死程度中有较高的临床价值.     

Effect of somatostatin on immune inflammatory response in patients with severe acute pancreatitis

OBJECTIVE: Somatostatin regulates immune inflammatory response via apoptosis and adhesion of leukocytes in many diseases. This article reported a study that aimed to observe the mechanism and effect of somatostatin on the immune inflammatory response through apoptosis and adhesion of leukocytes in severe acute pancreatitis. METHODS: Thirty‐eight patients with severe acute pancreatitis, that fulfilled the guidelines for the treatment of severe acute pancreatitis of China and Balthazar computed tomography severity index (≥5) were enrolled consecutively. Nineteen of these patients received our routine treatment and 19 received additional somatostatin. In all patients the expressions of CD₄, CD₈, CD₉₅/CD₉₅ ligand and CD₁₈/CD₆₂ ligand on leukocytes were determined by flow cytometry, both upon admission and on the fourth day. Thirty healthy volunteers constituted the normal healthy group. RESULTS: In the treatment group, CD₄, CD₄ : CD₈ ratio and CD₆₂ ligand on leukocytes increased from 11.4 ± 8.2, 0.47 ± 0.10 and 25.5 ± 9.2 to 22.1 ± 9.7, 0.68 ± 0.11 and 36.2 ± 11.7 (P < 0.05) respectively, while CD₉₅ ligand on both lymphocyte and polymorphonuclear cells increased from 0.65 ± 0.21 and 0.76 ± 0.29 to 1.18 ± 0.32 and 1.58 ± 0.43 after treatment with somatostatin (P < 0.05). Furthermore, lactate dehydrogenase, aspartate aminotransferase, amylase, C reactive protein and acute physiology and chronic healthy evaluation (APACHE II) score in the treatment group reduced faster than those in the control group (P < 0.05), though there was no difference in mortality (15.7%vs 5.3%) between the two patient groups (P > 0.05). CONCLUSION: Somatostatin can modulate the immune inflammatory response and the severity of severe acute pancreatitis through apoptosis and adhesion of leukocytes, but this modulatory effect by itself is not strong enough to improve the final.     

Extensive hemorrhagic erosive gastritis associated with acute pancreatitis successfully treated with a somatostatin analog

In massive hemorrhage from acute gastric mucosal lesions, it is occasionally difficult to control the bleeding with nonsurgical therapy. We used the somatostatin analog, octreotide, which suppresses gastric and pancreatic function, to treat severe hemorrhagic erosive gastritis in a patient with acute pancreatitis. A 22-year-old man presented with epigastralgia and melena. Blood levels of pancreatitis markers were elevated. Computed tomography revealed diffuse enlargement of the pancreas, without fluid collection around the organ. An endoscopic examination showed extensive hemorrhagic erosions over almost the whole gastric mucosa. We diagnosed extensive hemorrhagic erosive gastritis with acute pancreatitis. A protease inhibitor (nafamostat mesilate 50 mg/day) and an H₂ receptor antagonist (famotidine 40 mg/day) were administered by injection for 6 days; the patient's serum and urine amylase levels fell, but the gastric erosions with hemorrhage were not attenuated. Octreotide was given subcutaneously, at a daily dose of 100 μg for 5 days, without famotidine administration. His melena disappeared, and the gastric erosions were markedly decreased. Administration of the somatostatin analog, octreotide, proved to be effective treatment in a patient with severe hemorrhagic erosive gastritis associated with acute pancreatitis. Received: February 20, 2001 / Accepted: May 25, 2001 Reprint requests to: K. Yabuki     

加倍生长抑素联合早期肠内营养对重症急性胰腺炎炎症因子和肠通透性的影响

目的研究加倍生长抑素（SS）联合早期肠内营养对重症急性胰腺炎炎症因子和肠通透性的影响。方法将60例重症急性胰腺炎患者随机分成三组：SS组、加倍SS组（DSS组）和加倍SS联合早期肠内营养组（DSEN）。在第1、3、6、9天分别检测炎症介质（TNF-α、IL-1）和肠屏障通透性指标（D-乳酸及二胺氧化酶）。结果第3、6天DSS组和DSEN组的TNF-α、IL-1水平低于SS组;第9天DSEN组的TNF-α、IL-1水平低于SS组、DSS组,DSEN组D-乳酸及二胺氧化酶水平低于SS组、DSS组（P〈0.05或0.01）。而SS组D-乳酸及二胺氧化酶水平与DSS组比较无统计学差异（P〉0.05）。结论加倍SS早期能减少炎症因子生成,同时可能影响肠黏膜的通透性,而联合早期肠内营养能减少肠黏膜的通透性,达到保护肠黏膜屏障的作用。     

Effects and mechanisms of somatostatin analogs on apoptosis of pancreatic acinar cells in acute pancreatitis in mice

AIM: To investigate the effects of somatostatin analogs (SSa) on apoptosis of pancreatic acinar cells and apoptosis-regulated gene bax, and p53 in treating acute pancreatitis in mice. METHODS: In cerulein-induced pancreatitis, with or without treatment of somatostatin, analogs (Octreotide) in CD-1 (BALB/c x DBetaAlpha/1) mice, apoptosis of pancreatic acinar cells was detected by using the TdT-mediated dUTP nick-end labeling (TUNEL) method, and the expression of apoptosis-regulated gene bax and p53 was determined by using the streptavidin-peroxidase immunohistochemical technique and the RT-PCR method, respectively. RESULTS: On HE staining, acinar cells in the pancreas showed pyknotic nuclei and the formation of apoptotic bodies, which are the typical morphological features of apoptosis. Regarding TUNEL use, the apoptotic index of pancreatic acinar cells in the non-treated group at 5 and 14 h after induction of acute pancreatitis was significantly lower than those of the SSa-treated group, respectively (P < 0.01). On immunohistochemistry and RT-PCR, there was an expression of neither bax nor p53 in normal pancreatic tissues. The expression of bax in the SSa-treated group at 5 and 14 h after treatment of SSa was markedly higher than those of the non-treated group, respectively (P < 0.01), but there was no significant difference in the expression of p53 between the SSa-treated group and the non-treated group. CONCLUSIONS: The induction of apoptosis in pancreatic acinar cells injury to reduce inflammatory reaction might be one of the mechanisms of SSa in treating acute pancreatitis in mice, and the mechanisms of apoptosis probably correlated with the expression of apoptosis-regulated gene bax, but have no relationship with the expression of p53.     

Therapy of acute severe pancreatitis awaits further improvement

ＴｈｅｒａｐｙｏｆａｃｕｔｅｓｅｖｅｒｅｐａｎｃｒｅａｔｉｔｉｓａｗａｉｔｓｆｕｒｔｈｅｒｉｍｐｒｏｖｅｍｅｎｔＷＵＸｉａｎＺｈｏｎｇＳｕｂｊｅｃｔｈｅａｄｉｎｇｓｐａｎｃｒｅａｔｉｔｉｓ／ｔｈｅｒａｐｙ;ｐａｎｃｒｅａｔｉｔｉｓ／ｄｒｕｇｔｈｅｒ...