乌司他丁治疗急性胰腺炎临床分析

随着人们生活水平的提高,急性胰腺炎的发病率呈上升趋势,奥曲肽是目前治疗急性胰腺炎公认有效的药物,但由于其价格昂贵,限制了其临床广泛使用,乌司他丁是从人尿中提取的精制糖蛋白,有抑制胰蛋白酶、弹性蛋白酶、纤溶酶等蛋白水解酶及透明质酸酶、淀粉酶、脂肪酶等糖类和脂类水解酶的作用.我院2002～2006年对乌司他丁和奥曲肽治疗急性胰腺炎进行临床分析,总结如下.     

多层CT联合血清淀粉酶、脂肪酶浓度检测在急性胰腺炎诊断中的应用

目的 观察分析多层CT联合血清淀粉酶、脂肪酶浓度检查在急性胰腺炎诊断中的应用.方法 选取2010年3月至2015年8月收治的急性胰腺炎患者共计237例,根据患者病情分为轻型胰腺炎组(n =160)和重性胰腺炎组(n=77),另选取体检正常组患者98例作为对照组.比较患者的胰腺CT表现、应用不同检测方法对胰腺的检出率情况、血清中淀粉酶和脂肪酶含量以及体征和临床症状的缓解情况.结果 应用多层CT检查对胰腺的检出率(96.31％)明显高于应用超声影像检查对胰腺的检出率(83.87％),差异有统计学意义(P＜0.05).重型胰腺炎组和轻型胰腺炎组患者的血清淀粉酶和脂肪酶含量均显著高于对照组患者,且重型胰腺炎组患者的水平又明显高于轻型胰腺炎组患者,差异有统计学意义(P＜0.05).两项指标联合检测的特异性、灵敏性和准确度明显高于单独一项指标检测,差异有统计学意义(P＜0.05).重型胰腺炎组患者的症状体征恢复时间均长于轻型胰腺炎组患者,差异有统计学意义(P＜0.05).结论 多层CT、血清淀粉酶以及脂肪酶联合检测不仅能够提高诊断的准确度和阳性率,而且检查时间较短,有利于临床诊断.     

血清淀粉酶和脂肪酶联合检测对急性胰腺炎的诊断价值

目的探讨血清淀粉酶和脂肪酶联合检测对急性胰腺炎的诊断价值。方法对33例型胰腺炎患者、7例重型胰腺炎患者及40例健康体检者进行血清淀粉酶和脂肪酶检测。结果胰腺炎患者的血清淀粉酶和脂肪酶水平明显高于健康人(P <0.05),重型胰腺炎明显高于轻型胰腺炎(P <0.05)。血清脂肪酶诊断急性胰腺炎的灵敏度、特异度、准确度分别为62.3%、60.2%、61.9%;淀粉酶分别为63.5%、64.4%、65.1%,联合检测分别为85.3%、85.3%、85.3%。结论在急性胰腺炎的检测中,联合血清脂肪酶、淀粉酶可以提高诊断的准确性,为临床提供更为科学的依据。     

流行性腮腺炎并发急性胰腺炎28例临床分析

目的流行性腮腺炎并发急性胰腺炎的早期诊断和治疗初探。方法回顾性分析28例小儿流行性腮腺炎并发急性胰腺炎的临床资料。全部病例检查血、尿淀粉酶、血脂肪酶和胰腺B超。结果全组血、尿淀粉酶增高，血脂肪酶异常23例，占82．1％，胰腺B超检查异常24例，占85．7％。28例患儿均为腮腺炎并发急性水肿性胰腺炎，给予保守治疗，全部治愈。结论流行性腮腺炎如出现腹痛、呕吐和发热，应尽早行血尿淀粉酶和胰腺B超检查，以早期诊断治疗。流行性腮腺炎并发急性胰腺炎并不少见。保守治疗效果良好。     

胰腺疾病检查及治疗方面的进展

检查胰腺的方法一、酶的测定: 1.血清淀粉酶与脂肪酶是人们最熟悉的测定急性和亚急性胰腺炎的直接而迅速的方法。它们浓度的升高是由于腺泡细胞所产生的酶经过各级胰管向十二指肠的排出受干扰所致,这是水肿、炎细胞浸润等变化压迫的后果。有足够的腺泡细胞是胰腺酶升高的必需前提。     

急性胰腺炎早期严重程度的预测因子研究现状

<正>急性胰腺炎(AP)是指胰腺的急性炎症过程,是伴有剧烈腹痛、氧化应激、自由基生成的炎症性疾病[1]。其发病过程伴随组织损伤和炎症介质的释放,从而导致血小板活化,引起全身严重反应[2]。大多数为轻型急性胰腺炎,有10%~20%为重症急性胰腺炎(SAP),其病死率高达20%~30%[3]。腹痛和血胰酶水平(即胰腺细胞受损释放的淀粉酶和脂肪酶)为诊断急性胰腺炎的基础指标[4]。然而,在     

急性胰腺炎血清脂肪酶和淀粉酶的对比研究

目的：探讨脂肪酶、淀粉酶同时测定对急性胰腺炎的敏感度特异性。方法：采用酶法水解消浊法和动力学法，结果：血清脂肪酶诊断急性胰腺炎的灵敏度为91．3％，特异性为93．6％；血清淀粉酶分别为89．6％和89．4％。结论：二酶联合测定有互补作用，可提高灵敏度和特异性。     

替加环素相关急性胰腺炎

替加环素(tigecycline)是一种新型广谱抗生素,为甘氨酰环素类(glycyclines)抗生素的首个药物,其化学结构与四环素相似.替加环素对革兰阳性菌和革兰阴性菌具有抗菌活性,用于治疗复杂皮肤、软组织感染和复杂腹腔内感染.通常,替加环素偶致急性胰腺炎,但近年资料表明,替加环素致急性胰腺炎有所增加.临床表现主要为恶心、呕吐、腹痛、腹胀以及血清脂肪酶和淀粉酶水平升高.替加环素致胰腺炎的机制尚不明确,但由于替加环素的结构与四环素结构相似,推测替加环素是通过四环素致胰腺炎的同样机制引起急性胰腺炎.替加环素若引起胰腺炎,应立即停药,保持患者禁食状态,静脉给予足量液体,并给予其他对症治疗.替加环素使用期间,临床医师应密切观察患者有无胰腺炎的症状和体征,监测患者的血清脂肪酶和淀粉酶水平.     

糖尿病酮症酸中毒合并胰酶升高36例分析

目的 探讨糖尿病酮症酸中毒(DKA)患者血淀粉酶、脂肪酶升高的程度及其与急性胰腺炎(AP)的关系.方法 将36例糖尿病酮症酸中毒合并胰酶升高患者根据腹部CT结果分为非胰腺炎组20例和胰腺炎组16例.测定并比较两组患者血淀粉酶、尿淀粉酶、血脂肪酶水平.结果 血淀粉酶非胰腺炎组为(275.0±10.5)U/L,胰腺炎组为(615.4±17.8)U/L,两组差异有统计学意义(P＜0.01),而血脂肪酶非胰腺炎组为(2125.0±50.4)U/L,胰腺炎组为(2021.0±19.8)U/L,两组差异无统计学意义(P＞0.05),血淀粉酶与腹CT结果符合性高.结论 单纯糖尿病酮症酸中毒可引起胰酶升高,在诊断急性胰腺炎的胰酶检查中,血淀粉酶的特异性较脂肪酶高.     

彩色多普勒超声检查对急性胰腺炎的诊断价值

急性胰腺炎是一种急腹症．一般认为是胰腺消化酶被激活后对胰腺自身和周围组织消化所引起的急性炎症。其具有发病急、进展快、并发症多、病死率高的特点,国内外报道的死亡率均在10％以上。临床对急性胰腺炎的及时正确诊断至关重要,常规的实验室检查显示白细胞及中性粒细胞增多,血尿淀粉酶及血清脂肪酶升高,但这些都不能作为临床的确诊指标,必须加以影像学检查。     

Acute pancreatitis in patients with type 2 diabetes mellitus treated with dipeptidyl peptidase-4 inhibitors

Dipeptidyl peptidase (DPP)-4 inhibitors are approved for use in monotherapy or in combination therapy for patients with type 2 diabetes mellitus for <1 decade. However, numerous reports of DPP-4 inhibitors induced acute pancreatitis were made through the US Food and Drug Administration Adverse Event Reporting System, and this led to a revision in the prescribing information for these drugs. Therefore, this study is designed to evaluate DPP-4 inhibitors induced acute pancreatitis via the spontaneous adverse drug reactions (ADRs) reporting system in a medical center. In four of 2305 ADR cases, it is suspected that DPP-4 inhibitors induced moderate to serious acute pancreatitis. Beyond drugs, other factors also contribute to acute pancreatitis and affect the possibility of ADRs assessed using the Naranjo algorithm. Finally, our results indicate that the incidence of DPP-4 inhibitors induced acute pancreatitis is low.     

Prevention effects of ND-07, a novel drug candidate with a potent antioxidative action and anti-inflammatory action, in animal models of severe acute pancreatitis

Oxidative stress and inflammation both play major roles in the development of the acute pancreatitis. Currently, a pancreatic enzyme inhibitor with limited efficacy is only clinically available in a few countries, and antioxidants or non-steroidal anti-inflammatory drugs (NSAIDs) provide only partial tissue protection in acute pancreatitis animal models. Here, we introduce a new drug candidate for treating acute pancreatitis named ND-07 [chemical name: 2-acetoxy-5-(2-4-(trifluoromethyl)-phenethylamino)-benzoic acid] that exhibits both potent antioxidative and anti-inflammatory activities. In an electron spin resonance (ESR) study, ND-07 almost blocked hydroxyl radical generation as low as 0.05 μM and significantly suppressed DNA oxidation and cell death in a lipopolysaccharide (LPS)-stimulated pancreatic cell line. In a cerulein plus LPS-induced acute pancreatitis model, ND-07 pretreatment showed significant tissue protective effects, with reductions of serum amylase and lipase levels and pancreatic wet weights. ND-07 not only diminished the plasma levels of malondialdehyde (MDA) and nitric oxide but also significantly decreased prostaglandin E? (PGE?) and expression of tumor necrotizing factor-alpha (TNF-α) in the pancreatic tissue. In a severe acute necrotizing pancreatitis model induced by a choline deficient, ethionine-supplemented (CDE) diet, ND-07 dramatically protected the mortality even without any death, providing attenuation of pancreas, lung, and liver damages as well as the reductions in serum levels of lactate dehydrogenase (LDH), amylase and lipase, MDA levels in the plasma and pancreatic tissues, plasma levels of TNF-α, and interleukin-1 (IL-1β). These findings suggest that current dual synergistic action mechanisms of ND-07 might provide a superior protection for acute pancreatitis than conventional drug treatments.     

The effects of a new human leukocyte elastase inhibitor (recombinant guamerin) on cerulein-induced pancreatitis in rats

BACKGROUND: Pancreatic and neutrophil elastase can aggravate or induce acute pancreatitis. Although increased elastase levels in the plasma of pancreatitis patients and animal models have been reported, the mechanism by which elastase is involved in the pathogenesis of acute pancreatitis has not yet been elucidated. We aimed to investigate the effects and the possible mechanism of a new human leukocyte elastase inhibitor (recombinant guamerin) in the treatment of cerulein-induced acute pancreatitis in rats. METHODS: Fifty Sprague-Dawley rats were divided into three groups: a saline-infused control group (I), a cerulein-induced acute pancreatitis group (II), and a cerulein plus guamerin infusion group (III). Guamerin (1-2 micromol/kg/h) was infused continuously in group III. The severity of pancreatitis was determined biochemically, histologically, and by cytokine changes between groups I, II and III. RESULTS: Significant differences in serum amylase, lipase, and pancreatic wet weight were observed in each group, respectively (group I; 2346.2 IU/L, 9.9 IU/L, 1.4+/-0.3 g, group II; 13,596.8 IU/L, 7439.4 IU/L, 2.2+/-0.5 g, group III; 9443.2 IU/L, 4516.3 IU/L, 1.7+/-0.6 g). Serum IL-6 and TNF-alpha [AU1]level peaked 1-4 h and 1-2 h. After the induction of pancreatitis, IL-6 and TNF-alpha levels were decreased in group III than group II, (group I; 13.1/4.0 pg/mL, group II; 198.5/63.2 pg/mL, group III; 102.1/13.1 pg/mL), but no significant difference in IL-1beta was observed. Histologic gradings and severity, such as vacuolization, inflammation, lobular disarray, and edema of the pancreas, were significantly lower in the cerulein plus guamerin infusion group III. CONCLUSIONS: Recombinant guamerin, a new human leukocyte elastase inhibitor, may decrease the severity of pancreatitis and diminish pancreatic acinar cell injury by inhibition of neutrophilic infiltration and cytokine activation in the initial stage of cerulein-induced acute pancreatitis in rats.     

基于美国FDA不良事件报告系统评价钠-葡萄糖共转运蛋白2抑制剂致急性胰腺炎的风险

目的:评价钠葡萄糖共转运蛋白2抑制剂致急性胰腺炎的风险.方法:检索美国FDA不良事件报告系统中2013年1月1日至2020年10月31日的数据,采用报告比值比法(ROR)分析钠-葡萄糖共转运蛋白2(SGLT-2)抑制剂与急性胰腺炎的相关性.结果:共检索到SGLT-2抑制剂致急性胰腺炎报告264份,整体SGLT-2抑制剂...     

Effects of 3-aminobenzamide, an inhibitor of poly (ADP-ribose) polymerase, in a mouse model of acute pancreatitis induced by cerulein

Poly (ADP-ribose) polymerase (PARP), a nuclear enzyme activated by strand breaks in DNA, plays an important role in the colon injury associated with experimental colitis. The aim of the present study was to examine the effects of 3-aminobenzamide (3-AB), an inhibitor of PARP activity, in the development of acute pancreatitis caused by cerulein in mice. Intraperitoneal injection of cerulein in mice resulted in severe, acute pancreatitis characterized by oedema, neutrophil infiltration and necrosis and elevated serum levels of amylase and lipase. Infiltration of pancreatic and lung tissue with neutrophils (measured as increase in myeloperoxidase activity) was associated with enhanced expression of the intercellular adhesion molecule-1 (ICAM-1) and P-selectin. Immunohistochemical examination demonstrated a marked increase in the staining (immunoreactivity) for transforming growth factor-beta (TGF-beta) and vascular endothelial growth factor (VEGF) in the pancreas of cerulein-treated mice in comparison to sham-treated mice. Acute pancreatitis in vehicle-treated mice was also associated with a significant mortality (40% survival at 5 days after cerulein administration). In contrast, (1) the degree of pancreatic inflammation and tissue injury (histological score), (2) upregulation/formation of ICAM-1 and P-selectin, (4) neutrophils infiltration and (5) the expression of TGF-beta and VEGF was markedly reduced in pancreatic tissue obtained from cerulein-treated mice which have been treated with 3-AB. These findings provide the evidence that PARP inhibition reduce the degree of pancreas injury caused by acute pancreatitis induced by cerulein administration.     

Different effects of dexamethasone and the nitric oxide synthase inhibitor L-NAME on caerulein-induced rat acute pancreatitis, depending on the severity

Effects of dexamethasone and N^G-nitro-L-arginine methyl ester (L-NAME), the nitric oxide (NO) synthase inhibitor, on caerulein-induced acute pancreatitis were examined in rats. Acute pancreatitis was induced by caerulein (20 μg/kg, s.c.) given repeatedly 2 or 4 times every hour, and serum amylase levels, pancreas weight and myeloperoxidase (MPO) activity were measured 6 h after the first injection of caerulein. Dexamethasone (3 mg/kg) and L-NAME (30 mg/kg) were administered p.o. 30 min before the first injection of caerulein. Caerulein caused moderate or severe pancreatitis, depending on the times of injections, resulting in different degrees of increase in serum amylase levels and pancreas weight, and the marked elevation of MPO activity was observed only after injections of caerulein given 4 times per hour. Both dexamethasone and L-NAME suppressed the severity of pancreatits, yet the effect of L-NAME as compared with dexamethasone was more potent against mild pancreatitis but less potent against severe pancreatitis. These results suggest that caerulein-induced acute pancreatitis shows different responsiveness to L-NAME and dexamethasone, depending on the severity; the former is more effective against pancreatitis with less inflammation, while the latter is more effective against pancreatitis with severe inflammation. It is assumed that endogenous NO may be involved in oedema formation as the early event in the development of acute pancreatitis.     

The prevalence of pancreatitis in organophosphate poisonings

OBJECTIVE: The aim of this study was to evaluate the prevalence of pancreatitis in cases of organophosphate (OP) poisonings admitted to Yüzüncü Yil University Teaching Hospital over an 18-month period. MATERIALS AND METHODS: A total of 47 patients of acute poisoning with OP insecticides attended the Emergency Department of the Yüzüncü Yil Medical School Hospital, from May 1999 to December 2000, and were prospectively studied. Serum amylase and lipase levels were studied with colorimetric assay. Serum SGOT, SGPT, LDH, CPK, K levels, leukocyte count and total hospitalization days were also evaluated. RESULTS: Four of 47 patients had obviously elevated amylase and lipase levels (amylase >300 U/L, lipase >60 U/L). Only two of the patients with amylase levels between 100 and 300 U/L had also elevated levels of lipase. None of the patients with normal amylase levels had elevated levels of lipase. A total of 12.76% was diagnosed as acute pancreatitis. CONCLUSION: Acute pancreatitis as a complication of OP intoxication is not a rare condition. In order to improve the outcome of OP poisoning, early diagnosis of acute pancreatitis is important and serum levels of amylase and lipase should be routinely considered carefully. In acute pancreatitis, serum levels of SGOT, SGPT, LDH and leukocyte counts may also be found to be elevated. However, serum K levels are only slightly decreased.     

Tyrosine kinase inhibitors, pancreatic hyperenzymemia and acute pancreatitis: a review

The advent of new drugs can rapidly increase the number of substances causing acute pancreatitis. This is the case of tyrosine kinase inhibitors; these drugs are currently used for chronic myeloid leukemia, gastrointestinal stromal tumors, unresectable hepatocellular carcinomas and advanced renal cell carcinomas that and they have been reported to cause acute pancreatitis or asymptomatic elevations of serum pancreatic enzymes. Of the classes of drugs capable of inducing acute pancreatitis, we aimed to evaluate, in which class tyrosine kinase inhibitors can be allocated. A search was carried out using the MEDLINE database in order to select the data existing in the literature on pyrimidines and acute pancreatitis or serum lipase/amylase elevation covering the period from January 1966 to January 2010; thirteen papers were found and utilized for this review. Based on the data in the literature, we found that tyrosine kinase inhibitors may often cause an increase in pancreatic enzymes in plasma and patients treated with these drugs, especially those who are treated with sorafenib, might be at risk of developing acute pancreatitis. Whether acute pancreatitis due to tyrosine kinase inhibitors is associated only with sorafenib or may also be caused by other drugs of the same class remains an open question. Recent patents on tyrosine kinase inhibitors and acute pancreatitis are pointed out in this review.     

Effects of the bradykinin antagonist,icatibant (Hoe 140), on pancreas and liver functions during and after caerulein-induced pancreatitis in rats

It has been found earlier that the bradykinin antagonist, icatibant (Hoe 140), prevents the pancreatic oedema and the ensuing hypotension and haemoconcentration, and facilitates the removal of activated enzymes from the tissue during caerulein-induced acute pancreatitis. For a potential therapeutic use of the compound in clinical situations it is essential to investigate whether the associated increase in enzyme activities in the blood serum has any adverse effects on the pancreas itself or on other organs.Normal amylase secretion into the biliopancreatic duct stimulated by a low dose of caerulein (0.4 nmol kg^–1 h^–1, i.v.) was not affected by icatibant (100 nmolkg^–1, s.c.). Acute pancreatitis, induced by a high dose of caerulein (4 nmol kg^–1 h^–1 for 2 h, i.v.), resulted in elevations in the activities of amylase and lipase in the pancreatic tissue and in the blood serum lasting for at least 4 h after the end of the caerulein infusion. While the rise in enzyme activities in the blood serum was augmented in icatibant-treated rats only at the end of the caerulein-infusion, the enzyme accumulation in the pancreas was significantly reduced by icatibant for at least 4 h after the end of the caerulein infusion. The secretion of amylase and lipase into the biliopancreatic duct was significantly increased only during the first 20 min of acute pancreatitis; in rats pre-treated with icatibant, no significant increase could be observed. Twenty-four hours after induction of pancreatitis, a low-dose caerulein stimulation of the exocrine function of the pancreas led to a reduced but sustained secretion of amylase regardless of whether the animals had received icatibant or not. During the first 45 min of pancreatitis, blood glucose concentrations were significantly reduced, but returned to values not different from those obtained in saline-infused controls. This effect was not affected by icatibant. No changes in the response to an i.v. glucose tolerance test were found on the day after induction of acute pancreatitis. The serum activities of glutamic pyruvic transaminase and -glutamyl transpeptidase determined up to 24 h after induction of pancreatitis were not different from saline controls. Icatibant had no effect on the activities of these enzymes.It is concluded that during caerulein-induced acute pancreatitis normal exocrine secretion of pancreatic enzymes into the pancreatic duct ceases almost immediately. Pre-treatment with icatibant significantly reduces the accumulation of activated enzymes in the pancreatic tissue for several hours after induction of pancreatitis while a concomitant augmentation in enzyme activities in the blood serum lasts much shorter. There is no indication of adverse effects on the function of the endocrine or exocrine pancreas and that of the liver, either during the acute stages of pancreatitis or during the recovery period.     

Protective effect of the combined treatment of pancreatic and neutrophil elastase inhibitors on acute pancreatitis elicited by lipopolysaccharide in rats given intraductal injection of taurocholate plus trypsin

A severe acute pancreatitis was produced by intraperitoneal injection of lipopolysaccharide (LPS) in rats with preexisting hemorrhagic and necrotizing pancreatitis induced by retrograde injection of a 5% taurocholate plus 1% trypsin solution into the pancreatic duct. Mortality and time-course changes in pancreatic, hepatic, renal and pulmonary functions, and organ myeloperoxidase (MPO) levels were examined in this model. LPS at an intraperitoneal dose of 30 mg/kg, which scarcely caused death and had no marked effect on serum parameters and organ MPO levels in rats without pancreatitis, increased the mortality in rats with taurocholate plus trypsin-induced pancreatitis. Pancreatic weight and ascitic volume increased in rats with taurocholate plus trypsin-induced pancreatitis regardless of the presence or absence of LPS. Serum amylase and lipase levels were also significantly increased in rats with induced pancreatitis, but was higher in the group given LPS. Serum glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN) and creatinine levels were significantly elevated in LPS-treated rats with induced pancreatitis, whereas levels in rats with induced pancreatitis not given LPS were only slightly elevated. Renal weight was also significantly increased in rats with induced pancreatitis despite the presence or absence of LPS. In LPS-treated rats with induced pancreatitis, the arterial oxygen pressure, pulmonary weight and pulmonary MPO level were significantly elevated. However, the MPO level in the kidney in these rats was not different from that in control rats, indicating that the renal dysfunction was not produced by the infiltration of neutrophils into the kidney. Increase in the pancreatic MPO level was observed in rats with induced pancreatitis, but combination treatment with LPS did not raise it. Protective effects of prophylactic treatment of 2-(3-methylsulfonylamino-2-oxo-6-phenyl-1,2-dihydro-1-pyridyl)-N-(3,3,3-trifluoro-1-isopropyl-2-oxopropyl)acetamide (compound 1), a neutrophil elastase inhibitor, and trifluoroacetyl-L-lysyl-L-alaninanilide hydrochloride (compound 2), a pancreatic elastase inhibitor, on mortality were also examined in this model. Results were compared with that of the combined treatment of compound 1 and compound 2. In LPS-treated rats with taurocholate plus trypsin-induced pancreatitis, the combined treatment of compound 1 (2 mg/kg/h) and compound 2 (30 mg/kg/h) significantly reduced mortality, whereas single treatment of compound 1 or compound 2 did not show the beneficial effect. These results suggest that marked hepatic and renal dysfunction accompanies pancreatitis in this pancreatitis model rats, which may be good models for acute pancreatitis in humans. It is also suggested that neutrophil and pancreatic elastases may be synergistically involved in the pathogenesis of acute pancreatitis in this model. Received: 24 November 1997 / Accepted: 10 February 1998