Hyperamylasemia and acute pancreatitis following anticholinesterase poisoning

A prospective study was undertaken to find the incidence of hyperamylasemia and acute pancreatitis in patients with anticholinesterase poisoning. This was done by serial estimation of total serum amylase and pancreatic imaging by ultrasonography and confirmed, if necessary, by computerized tomography. Anticholinesterase poisoning was caused by either ingestion or accidental exposure to organophosphates or carbamates; it was diagnosed when patients presented with features of cholinergic crisis, depressed serum butyrylcholinesterase activity of >50% and showed improvement following administration of atropine alone or atropine and 2-PAM. All the patients admitted with anticholinesterase poisoning between July 2001 and June 2005 were prospectively studied for elevated serum amylase. The serum amylase levels were estimated daily up to 10 days in survivors and in nonsurvivors till they survived. Ultrasonography of the abdomen was carried out in all to find swelling of the pancreas. Computerized tomography was undertaken in those who had a swollen pancreas or whose serum amylase levels were elevated significantly (> or =800 S.U). Of the 86 patients enrolled, 79 were taken up for analysis as data were incomplete in 7. Of the 79 patients, serum amylase was found to be elevated that is, >200 S.U. in 37 patients (46.95%). In three patients it was 800 S.U. One of them showed swollen pancreas on ultrasonography, which was confirmed by computerized tomography. This patient had ingested propoxyfur. In the other two patients, evidence of acute pancreatitis was not observed (on autopsy in one who died and on imaging in the other who survived). They had ingested chlorpyrifos. There was no significant correlation between the nature of the compounds (organophosphate or carbamates), inhibition of serum BUChE at admission, duration and severity of cholinergic syndrome and increase and time course of increase in serum amylase. Except for fenthion, significant persistent increase in serum amylase was not observed with individual compounds. The other associated abnormalities were polymorphonuclear leukocytosis (TLC >11,000/cumm) in all 37 patients who had elevated amylase, hyperglycemia (6/37) and, elevated transaminases (6/37). Mild elevation of serum amylase is common in patients with anticholinesterase poisoning. However, acute pancreatitis is rare.     

Hyperamylasaemia and acute pancreatitis in paracetamol poisoning

BACKGROUND: Hyperamylasaemia and even acute pancreatitis have been reported in patients with paracetamol poisoning. AIMS: To describe the incidence, clinical characteristics, and prognostic implications of hyperamylasaemia in paracetamol poisoning. PATIENTS: Six hundred and two patients transferred to a specialized unit with severe paracetamol poisoning and 212 unselected patients admitted from the local region. METHODS: Retrospective study based on hospital charts. The optimum threshold of serum amylase to discriminate non-survivors was identified. RESULTS: An elevated serum amylase (>100 U/L) occurred in 28 of the unselected patients (13%), in 218 of the transferred patients (36%), and in 118 of 148 patients (80%) with fulminant hepatic failure. Only 33 cases of paracetamol-associated acute pancreatitis were diagnosed. A threshold serum amylase of 150 U/L to discriminate non-survivors had sensitivity 76%, specificity 85%, positive predictive value 33%, and negative predictive value 97%. In a logistic regression analysis, a serum amylase > 150 U/L was associated with an excess mortality (odds ratio 5.0, 2.6-9.7). CONCLUSIONS: Hyperamylasaemia is frequent in patients with paracetamol poisoning, whereas clinical acute pancreatitis occurs rarely. The incidence of hyperamylasaemia increases with the degree of hepatic dysfunction. A serum amylase exceeding 1.5 times the upper normal limit indicates a poor prognosis.     

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.     

Parotitis due to organophosphate intoxication

Acute pancreatitis due to pancreatic exocrine over-secretion induced by organophosphate poisoning has been previously reported but parotid gland involvement has not. This paper describes a case of acute organophosphate-induced parotitis in a patient with pre-existing sialolithiasis. The patient developed bilateral facial swelling in the pre-auricular area extending to the angle of the jaw and also developed elevated serum amylase on the second day of the poisoning. Serum lipase remained normal. Autopsy confirmed parotid gland inflammation and pre-existing ductal lithiasis. This case illustrates that organophosphate-induced parotitis can occur and should be considered in patients with organophosphate poisoning who have hyperamylasemia without elevation in serum lipase.     

二肽基肽酶Ⅳ抑制剂与急性胰腺炎

二肽基肽酶IV（DPP-4）抑制剂是新型口服降糖药物,该类药物能有效降低糖化血红蛋白,耐受性与安全性较好,急性胰腺炎是其少见而严重的不良反应。DPP-4抑制剂致急性胰腺炎潜伏期为14～515d,临床表现为上腹部疼痛,实验室检查可见血清淀粉酶、脂肪酶和弹性蛋白酶水平显著升高。病理学检查可见胰腺和胰周组织水肿和坏死。DPP-4抑制剂致急性胰腺炎的机制主要涉及变态反应和药物或代谢产物对胰腺的直接毒性。有胰腺炎病史者应慎用DPP-4抑制剂。密切注意患者用药情况并监测血清淀粉酶、脂肪酶和弹性蛋白酶水平,是预防DPP-4抑制剂致急性胰腺炎发生和发展的有效措施。     

Sociodemographic factors in organophosphate poisonings: a prospective study

The sociodemographic features of organophosphate poisonings (OPPs) in the east Anatolian region of Turkey were investigated in this study. All OPPs admitted to the Emergency Department of Yüzüncü Yil University Medical Faculty Hospital in Turkey from 1 April 1999 to 31 August 2001 were prospectively studied. Data collected included age, gender, education, employment and marital status, socioeconomic levels, time and route of exposure of the toxic agents, treatment before admission, duration of hospitalization and complications. The proportion of OPPs was 15.1% among 564 poisonings. Fifty-seven (67.1%) patients were female, 28 (32.9%) were male. Fifty-six (65.9%) cases were attempted suicides and 29 cases (34.1%) were due to accidental events. Mean age was 22.1 +/- 9.2 years in the suicidal cases and 43 (76.8%) of them were less than 24 years (P = 0.001). Among the suicide attempts, 29 (51.8%) patients were unmarried and 43 (76.8%) patients were female. The attempted suicide proportion was 46.4% in men and 75.4% in women (P = 0.008). Eighty per cent of cases had a primary education level or were illiterate and 78.8% of the patients were in the lower socioeconomic status. The patients' mean arrival time to the hospital after poisoning was 4.4 +/- 3.7 (1-15) hours and mean hospitalization duration was 4.9 +/- 4.1 (1-32) days. Exposure routes were gastrointestinal in 75 (88.2%), respiratory in five (5.9%), dermal in four (4.7%) and both dermal and respiratory in one case (1.2%). Seventeen patients (23.5%) were admitted to the ICU and four (4.7%) of them died. In conclusion, OPPs especially affected young unmarried females, and most of them were due to attempted suicide. As OPP is the important cause of morbidity and mortality in the region, therapy should be started as early as possible so undesirable consequences can be avoided.     

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.     

塞来昔布致急性胰腺炎

1例43岁女性患者因肩周炎服用塞来昔布胶囊0．2g,2次／d,共服用2周。末次服药后2h上腹出现持续性钝痛,伴腹胀、恶心、呕吐。实验室检查示血清淀粉酶1822U／L,胰淀粉酶1529U／L,脂肪酶1410U／L,白细胞计数12．7×10^9／L,中性粒细胞0．74,淋巴细胞0．16。腹部超声检查和磁共振胰胆管造影示胰腺弥漫性增大、胰腺周围有液性渗出,诊断为急性胰腺炎。停用塞来昔布,禁食,给予营养支持和抑酶、抑酸、抗感染治疗13d,患者腹痛、腹胀消失,实验室检查示淀粉酶86U／L,胰淀粉酶48U／L,脂肪酶55U／L,白细胞计数7．2×10^9／L,中性粒细胞0．65,淋巴细胞0．32。胰腺CT示胰头、胰体和胰尾位于同一层面,形态及大小基本正常。     

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.     

尿胰蛋白酶原-2、血脂肪酶、血淀粉酶在急性胰腺炎早期断中的应用比较

目的本实验旨在探讨尿胰蛋白酶原-2、血淀粉酶、血脂肪酶检测对急性胰腺炎的早期诊断意义。方法对70例急性胰腺炎患者、70例非急性胰腺炎患者,70例正常健康体检者测定尿胰蛋白酶原-2,血淀粉酶及血脂肪酶,比较其对诊断胰腺炎的敏感性及特异性。结果尿胰蛋白酶-2诊断急性胰腺炎的敏感性为96．0％;特异性为94．3％,血脂肪酶分别为78．0％、76．0％;血淀粉酶分别为80．0％、80．0％。结论胰蛋白酶原-2较之常规的血淀粉酶、血脂肪酶检测,在急性胰腺炎早期诊断中具有更高的价值。     

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.     

Effect of flickering light stress on certain biochemical parameters in rats

The acute effects of flickering light of 80 Lux intensity for thirty minutes duration, on plasma corticosterone, total serum cholesterol, serum triglycerides, serum glutamic pyruvic transaminase (SGPT) and serum glutamic oxaloacetic transaminase (SGOT) levels were studied in albino rats. Statistically significant increase was observed in the corticosterone, cholesterol, SGOT and SGPT, while a marked reduction was seen in the serum triglyceride level, indicating that the flickering light is a potent stressor to these animals causing alterations in the biochemical parameters studied.     

Capecitabine-induced pancreatitis

A 47-year-old woman with metastatic breast cancer developed acute pancreatitis while receiving capecitabine. She had been receiving capecitabine 2000 mg/m2/day; however, when the dosage was increased to 2500 mg/m2/day (the maximum dosage approved by the Food and Drug Administration) she experienced abdominal pain and cramping. These symptoms were followed by nausea and vomiting, palmar-plantar erythrodysesthesia (hand-foot syndrome), and mucositis, resulting in admission to the hospital. Laboratory tests for liver function showed elevated levels of alkaline phosphatase and lactate dehydrogenase. The patient's lipase and amylase levels were also elevated, but an abdominal ultrasound was normal. After bowel rest and intravenous hydration, the patient's liver function tests and lipase and amylase levels returned to normal. Many chemotherapeutic agents have been documented to cause pancreatitis; however, we found no previously described reports of capecitabine-induced pancreatitis. Clinicians should be aware of this potential adverse effect, particularly in patients with preexisting risk factors for pancreatitis who are prescribed capecitabine.     

血尿淀粉酶检验在胰腺炎诊断中的应用价值分析

目的 分析胰腺炎患者采用血尿淀粉酶检验诊断的应用价值.方法 选择104例胰腺炎患者作为观察组,根据病情分型分为观察A组(轻症,73例)和观察B组(重症,31例);另选100例同期行常规健康检查者作为对照组.所有研究对象均接受血尿淀粉酶、血清炎症因子水平检测.比较对照组和观察组血尿淀粉酶及血清炎症因子水平,比较观察A组和...     

柳氮磺胺吡啶致急性胰腺炎

28岁男性患者,因再发溃疡性结肠炎,口服柳氮磺胺吡啶1g,4次/d,1周后出现上腹部持续性绞痛,恶心、呕吐,血清淀粉酶601U/L,尿淀粉酶1703U/L,诊断为急性胰腺炎入院。立即停用柳氮磺胺吡啶,经对症保守治疗后痊愈出院。随访2年7个月未再复发。     

Anti-inflammatory actions of perfluorooctanoic acid and peroxisome proliferator-activated receptors (PPAR) alpha and gamma in experimental acute pancreatitis

Perfluorooctanoic acid (PFOA) and agonists of peroxisome proliferator-activated receptors (PPAR) alpha and gamma were investigated for potential anti-inflammatory effects in cerulein-induced acute pancreatitis in rats. PFOA significantly reduced both leukocyte accumulation and prostanoid synthesis. The PPAR-alpha agonist clofibrate had no effect on leukocyte activation but significantly inhibited prostanoid synthesis whereas the PPAR-gamma agonist rosiglitazone significantly reduced leukocyte activation but did not affect synthesis of prostaglandins in the pancreas. Neither PFOA, nor clofibrate or rosiglitazone had an effect on the formation of the inflammatory edema or elevated levels of lipase activity in the blood serum. In summary, PFOA attenuates the accumulation of activated leukocytes and reduces the synthesis of prostanoids in the pancreas during cerulein-induced acute pancreatitis. An activation of PPAR-alpha causes inhibition of prostanoid synthesis while activation of PPAR-gamma inhibits leukocyte activation.     

西格列汀致急性胰腺炎

1例58岁女性2型糖尿病患者应用盐酸二甲双胍（0．5g,2次／d口服）及胰岛素（三餐前分别皮下注射胰岛素8、8、10U,睡前皮下注射甘精胰岛素8u）治疗,因效果不佳加用西格列汀（100mg,1次／d口服）。3周后,患者出现恶心、呕吐伴腹痛。实验室检查：血清淀粉酶499U／L,尿淀粉酶933U／L。腹部超声检查示腹腔积液。诊断为急性胰腺炎。停用西格列汀、盐酸二甲双胍,继续应用胰岛素,并给予抑酸、抑酶、补液等治疗。6d后,患者病情好转,血清淀粉酶76U／L,尿淀粉酶288U／L。     

尿毒症患者血清淀粉酶升高的临床意义分析

目的探讨尿毒症患者血清淀粉酶升高的临床意义。方法选择2010年1月至2012年1月在本院内科住院的尿毒症患者80例进行临床意义分析。结果 80例尿毒症患者的血清淀粉酶水平明显高于健康对照组,差异有统计学意义(P<0.05);80例尿毒症患者明确诊断合并急性胰腺炎12例,经禁食、抑制胰液和胰酶分泌等治疗7d后其血清淀粉酶水平较入院时降低,差异有统计学意义(P<0.05)。结论尿毒症患者多伴有血清淀粉酶水平升高,不能轻易诊断合并急性胰腺炎。     

三氧化二砷、黄磷、四氯化碳的急性肝脏毒作用的研究

大鼠每日分别经口染毒三氧化二砷（45mg/kg)、黄磷（3mg/kg)、四氯化碳（990mg/kg)，连续4日后，均出现肝脏病理改变，黄磷及四氯化碳组大鼠的血清GPT和GOT活性明显升高，但三氧化二砷组则无显著变化，三个染毒组大鼠的血清和肝微粒体过氧化脂质含量、血清IgM和补体C3含量均较对照组显著升高。     

Protective effects of N-acetylcysteine against carbon tetrachloride- and trichloroethylene-induced poisoning in rats

This research investigates the protective effect of N-acetylcysteine (NAC) against carbon tetrachloride (CCl₄)- and trichloroethylene (TCE)-induced hepatotoxicity in rats. A single dose of 1.25 ml/kg of 20% CCl₄ in corn oil, administered orally, or 20% TCE, administered intraperitoneally, produced significantly elevated levels of serum glutamic pyruvic transaminase (SGPT) and serum glutamic oxaloacetic transaminase (SGOT) activities. Histopathological examinations showed massive centrilobular necrosis and fat accumulation in CCl₄-treated animals. In the curative test, especially in animals treated with higher dosages of NAC, there was significant reduction in SGPT and SGOT levels. Although there was no sign of abnormality in the livers of rats treated with TCE, NAC demonstrated its action against TCE-induced elevation of transaminases in the enzyme assays. Compared to the curative tests, the overall performance of NAC against toxin-induced toxicity in the preventive tests was poor. Even at the highest dosage applied, the effect was not as prominent as that achieved in the curative test. It is therefore concluded that NAC is effective for lowering chemical-induced elevated levels of SGPT and SGOT in the curative mode.