Gabexate mesilate (FOY) protects against ceruletide-induced acute pancreatitis in the rat

Acute pancreatitis (AP) is believed to result from intraparenchymal activation of trypsin and other digestive enzymes within the pancreas followed by autodigestion of the gland. Gabexate mesilate (FOY), a synthetic guanidino acid ester exhibiting potent and versatile inhibitory actions on a number of proteinases (e.g., trypsin, kallikrein, C1-r, C1 esterase, plasmin, thrombin, phospholipase A2), was examined for its ability to protect the rat pancreas against development of AP induced by pharmacological doses of ceruletide (CRT). Rats were i.v. infused for 6 h with either CRT (5 micrograms/kg/h) or CRT + FOY (50 mg/kg/h). In FOY-treated rats the serum amylase and trypsinogen concentrations were reduced by 60 and 80%, respectively, compared to rats infused with CRT alone. Histologically, the extent of acinar cell vacuolization in the pancreas was significantly reduced and interstitial edema, although not assessed by quantitative morphometric techniques, appeared to be qualitatively lessened in the FOY-treated rats. The ability of FOY to inhibit significantly AP produced by supramaximal doses of CRT, coupled with its inhibitory properties on components of the coagulation and complement cascades, stress the importance of continued research on this compound as a potential therapeutic agent for treatment of AP and its systemic sequelae.     

Protection by gabexate mesilate (FOY) of the exocrine pancreas in rats with acute pancreatitis induced by a supramaximal dose of caerulein

Earlier studies have reported that interstitial oedematous pancreatitis characterized by hyperamylasaemia can be seen during the early stage of stimulation of supramaximal dose of caerulein. The present study investigated the changes in both cellular and lysosomal fragility and the protective effects of a synthetic protease inhibitor gabexate mesilate (FOY) on this non-invasive model of experimental pancreatitis. The infusion of FOY (50 mg/kg/h) prevented the caerulein-induced increase in serum amylase and pancreatic oedema formation and reduced the elevated amylase content significantly. The administration of FOY with caerulein also reduced the increased lactic dehydrogenase (LDH) discharge significantly and inhibited the cathepsin B leakage from lysosomes in an in vitro incubation system. These results indicate that FOY plays its protective role at the subcellular level--that is, in lysosomes by inhibiting some proteases such as phospholipase A2. The importance of esterases in the pathogenesis of acute pancreatitis is demonstrated. This type of esterase inhibitor may be valuable clinically in the treatment of acute pancreatitis and these results also suggest the role of lysosomal fragility in the pathogenesis of progression of acute pancreatitis.     

Protective effects of gabexate mesilate on acute pancreatitis induced by tacrolimus (FK-506) in rats in which the pancreas was stimulated by caerulein

We investigated the acute effects of the immunosuppressive agent, tacrolimus (FK-506), on the exocrine pancreas, in rats with or without stimulation of the pancreas, in rats with or without stimulation of the pancreas, and evaluated the protective effects exerted by gabexate mesilate (FOY). While an intravenous injection of FK-506 did not change serum amylase levels during the 5-h observation period, this agent increased pancreatic amylase and protein content, and decreased the content of pancreatic DNA. Histologically, we observed intra-acinar vacuolization and individual cell necrosis. When the pancreas was stimulated by two intraperitoneal injections of caerulein (5 μg/kg) at 1-h intervals, however, which treatment did not induce any evident pancreatic change, FK-506 significantly increased serum amylase, pancreatic wet weight, and pancreatic amylase and protein, and decreased pancreatic DNA. Histologically, there were significant dose-related differences in the severity of intra-acinar vacuolization, interstitial edema, neutrophil infiltration, individual cell necrosis, and hemorrhage. Levels of intrapancreatic elastase were elevated and local pancreatic blood flow was reduced. Treatment with FOY improved the FK-506-induced acute pancreatitis, but did not increase the pancreatic blood flow. These findings indicate that FK-506 enhances abnormal pancreatic enzyme secretion and suggest that therapeutic doses of this agent can induce acute pancreatitis when the pancreas is stimulated. A protease inhibitor may protect the exocrine pancreas in patients who receive FK-506 after organ transplantation.     

Multicenter double-blind trial of gabexate mesylate (FOY) in unselected patients with acute pancreatitis.

A multicenter, randomized, double-blind trial was carried out to evaluate the efficacy of gabexate mesylate (FOY) in acute pancreatitis. One hundred unselected patients were randomly allocated into two groups: 51 were assigned to receive FOY (12 mg/kg/day as continuous intravenous infusion for a minimum of 4 days and a maximum of 12 days), and 49 were allocated to placebo. The groups were comparable in demographic, clinical and biochemical parameters, etiology of pancreatitis, and disease severity, which was generally mild. Gallstones were the main etiological factor. All patients received fluid and electrolyte replacement, analgesia and nasogastric suction for at least 48 h after admission. Experimental therapy was initiated no later than 12 h after the beginning of symptoms. The results showed no statistically significant differences between the two groups with respect to the evolution of clinical and biochemical parameters, analgesic requirements, development of complications, hospitalization time or mortality at completion of the trial. In conclusion, early treatment with FOY does not appear to have any demonstrable beneficial effects in acute pancreatitis.     

Esterase inhibitors prevent lysosomal enzyme redistribution in two noninvasive models of experimental pancreatitis

Earlier studies have indicated that lysosomal enzymes such as cathepsin B become redistributed within pancreatic acinar cells during the early stages of both diet- and secretagogue-induced acute pancreatitis. As a result, cathepsin B and digestive zymogens became colocalized within large cytoplasmic vacuoles. As cathepsin B can activate trypsinogen, this colocalization could result in intracellular digestive enzyme activation. The present study investigates the protective effects of gabexate mesilate (FOY) and camostate (FOY 305) on both of these noninvasive models of experimental pancreatitis. These esterase inhibitors prevented the hyperamylasemia, pancreatic edema, and acinar cell vacuolization that characterize secretagogue-induced pancreatitis and the hyperamylasemia and mortality that characterize diet-induced pancreatitis. In addition, FOY and FOY 305 were found to significantly decrease the subcellular redistribution of cathepsin B that occurs in both models. These findings indicate that enzyme activity sensitive to inhibition by FOY and FOY 305 may be critical to the redistribution phenomenon that characterizes both of these models of pancreatitis.     

P amylase is always greater than S in spot urine of normal subjects. Diagnostic implications.

Single random samples of urine were collected from 50 control subjects; 27 patients with chronic pancreatitis; 19 with acute pancreatitis; 6 with acute on chronic pancreatitis; five in the recovery phase of acute attack; four patients with pseudocysts. Salivary (S) and pancreatic (P) amylase values were measured by cellulose acetate electrophoresis. The P amylase values always exceeded those of S amylase in the control specimens. In acute pancreatitis, both the lower and upper levels of total and P amylase were considerably higher than in the controls, and these high values tended to return to normal during the recovery phase of acute pancreatitis. The S amylase values were often very low or undetectable during the acute phase. Values for P amylase exceeded control values in patients with pseudocysts even in the presence of chronic pancreatitis. In chronic calcific pancreatitis, S amylase was higher than P amylase. We conclude that P amylase is always greater than S amylase in normal urine specimens, and a change in this pattern may be helpful in diagnosing various forms of pancreatitis.     

Serum amylase, pancreatic stents, and pancreatitis after sphincter of Oddi manometry

BACKGROUND: Serum amylase levels 2 hours after ERCP predict postprocedure pancreatitis. The value of serum amylase measurements after sphincter of Oddi manometry (SOM) and the effect of pancreatic-duct stent placement on serum amylase are unknown. METHODS: Records were reviewed for 88 SOM patients who had serum amylase measured 2 hours after the procedure. Post-SOM pancreatitis was defined as pain with a >3-fold elevation of serum amylase on the morning after SOM. "Possible pancreatitis" was defined as pain with a <3-fold elevation of serum amylase on the morning after SOM. RESULTS: Post-SOM pancreatitis and possible pancreatitis each occurred in 13% of the study cohort. Post-SOM pancreatitis was associated with the absence of a pancreatic stent and occurred in 0% of patients without a stent who had normal 2-hour serum amylase vs. 67% with elevated 2-hour serum amylase (p < 0.01). Among patients who received a stent, pancreatitis occurred in 6%, regardless of whether the 2-hour serum amylase was elevated. Possible pancreatitis occurred mainly in patients who received stents, and it also was associated with elevation of the 2-hour serum amylase. CONCLUSIONS: Elevation of the serum amylase level 2 hours after SOM predicts post-SOM pancreatitis but only in patients who do not receive a pancreatic stent. Among patients who received a stent, elevated 2-hour serum amylase levels predict subsequent findings that may be caused by attenuated pancreatitis.     

The Lipase to Amylase Ratio in Acute Pancreatitis

Objectives : The ratio of serum lipase to serum amylase has been proposed to distinguish acute episodes of alcoholic from nonalcoholic pancreatitis. We evaluated the efficacy of this test in a community hospital setting. Methods : Charts of all patients discharged with a diagnosis of acute pancreatitis over 19 months were retrospectively reviewed. Patients were excluded if their cre-atinine was greater than 3.0 mg/dl, if the amylase and lipase were not measured within 72 h of the onset of symptoms, or if the cause of pancreatitis was not known by the time of discharge. Results : Of the 56 patients, 31 had alcoholic pancreatitis. The lipase to amylase ratio did not differ significantly between patients with alcoholic and nonalcoholic pancreatitis. Median amylase and lipase were significantly higher in nonalcoholic pancreatitis; however, the wide ranges of both meant that neither amylase nor lipase accurately determined the cause of pancreatitis. Conclusion : The lipase to amylase ratio does not appear to be sufficiently sensitive or specific to distinguish alcoholic from nonalcoholic acute pancreatitis.     

Serum amylase determination in the emergency department evaluation of abdominal pain.

We hypothesized that selective ordering of serum amylase in the emergency department (ED) is justified because (a) most patients with elevated amylase can be prospectively identified by characteristic clinical findings, and (b) the diagnosis of pancreatitis is usually predominantly based on clinical findings, since amylase is known to be neither sensitive nor specific for pancreatitis. The study population included 133 consecutive patients with a chief complaint of abdominal pain who had amylase drawn over a 2-week period at a university hospital ED. Patients with known major trauma were excluded. Emergency department and hospital charts were reviewed for selected clinical variables. The first part of our hypothesis was evaluated by comparing clinical characteristics of cases (elevated amylase) and controls; the second part was tested by comparing clinical findings and amylase in cases (patients diagnosed as having pancreatitis) and controls. We found that 17 patients with and 116 without elevated amylase were similar with regard to all clinical variables, and that no combination of findings could be used to predict elevated amylase. Amylase level was not predictive of an ultimate diagnosis of pancreatitis, which was, however, strongly related to classical clinical findings. Pancreatitis risk factors, epigastric pain and tenderness, radiation of pain to the back, and nausea and vomiting were each statistically more common in patients diagnosed as having pancreatitis (regardless of amylase) than in patients in whom pancreatitis was excluded despite elevated amylase; all patients diagnosed with pancreatitis had at least two of these. Thus, selective ordering of amylase on the basis of clinical characteristics fails to identify a large proportion of patients with elevated amylase.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serum amylase measured four hours after endoscopic sphincterotomy is a reliable predictor of postprocedure pancreatitis

OBJECTIVE: Acute pancreatitis is a common complication after endoscopic sphincterotomy (ES) and endoscopic retrograde cholangiopancreatography (ERCP). The aim of this study was to detect the time when the peak of serum amylase was predictive for pancreatitis or severe hyperamylasemia, to plan a prolonged follow-up in the hospital and for outpatients. METHODS: In a prospective series of 409 consecutive patients undergoing ES, serum amylase activity was measured immediately before the procedure and 2, 4, 8, and 24 h thereafter; the data obtained at 2, 4, and 8 h were compared with those at 24 h and with the outcome. Sensitivity for long-lasting severe hyperamylasemia (more than five times the upper normal limit) and pancreatitis were also defined for all sampling times. RESULTS: At 24 h after ES, amylase was still more than five times the upper normal limit in 26 patients, 19 of whom had mild/moderate acute pancreatitis. There was a significant difference (p < 0.01 at all sampling times) between the 26 patients with 24-h severe hyperamylasemia and those with lower levels. The sensitivity of amylase measurement in detecting pancreatitis or long-lasting severe hyperamylasemia was highest at 8 h. However, the 4-h assessment appears to be a reliable predictor in practice, as more than two-thirds of cases of pancreatitis (all but one with computed tomography-confirmed pancreatitis) occurred among patients whose 4-h amylasemia was higher than five times the upper normal limit. CONCLUSIONS: Serum amylase assessment 4 h after ES minimizes the likelihood of underestimating the risk of postprocedure pancreatitis. It is therefore a reliable, cost-effective follow-up, particularly in outpatients.     

Studies on Duodenal Cyclic AMP Content in Pancreatic Disease after Administration of Pancreozymin and Secretin

Cyclic AMP (cAMP) output in the duodenal contents of 11 normal subjects, 18 patients with chronic pancreatitis, six convalescing from acute pancreatitis and five with pancreatic carcinoma was measured after a single dose of pancreozymin and secretin. The technic was indirect, utilizing recovery of duodenal contents by the Dreiling tube rather than direct measurements of fluid that was not contaminated by bile. In all patients groups, cAMP output reached a peak after this stimulation with a concomitant increase of bicarbonate and amylase outputs. A significantly decreased cAMP output was observed in all pancreatic disease groups compared to the normal group. Patients with chronic pancreatitis showed a slightly decreased cAMP output, considerably decreased bicarbonate output and normal amylase output. In acute pancreatitis cAMP output was reduced with normal bicarbonate and amylase outputs. In pancreatic carcinoma cAMP decreased significantly, bicarbonate output was moderately reduced and amylase output was normal. cAMP output in all groups studied did not correlate with either bicarbonate output or amylase output.     

Serum amylase and lipase concentrations and lipase/amylase ratio in assessment of etiology and severity of acute pancreatitis

We studied the behavior of serum amylase and lipase in 66 consecutive patients with acute pancreatitis in order to assess the ability of these tests and of the serum lipase-amylase ratio to establish the etiology and predict the severity of acute pancreatitis. Forty-two patients had biliary acute pancreatitis, 14 had alcoholic acute pancreatitis, and the remaining 10 nonbiliary, nonalcoholic (NBNA) acute pancreatitis. Serum amylase and lipase were abnormally high in all patients. The elevations of both serum amylase and lipase were significantly lower in patients with alcoholic pancreatitis than in those with biliary pancreatitis, although a considerable overlap was observed between the two groups. No statistically significant differences were found between NBNA patients and those with either biliary or alcoholic forms of the disease. The serum lipase-amylase ratios in patients with alcoholic pancreatitis ranged from 0.2 to 5.6, in those with biliary pancreatitis from 0.1 to 7.9, and in those with NBNA pancreatitis from 0.1 to 4.4. These differences were not statistically significant. No differences in serum enzyme levels were observed among patients without apparent imaging signs of acute pancreatitis (N=20), those with signs of Pancreatic edema (N=36), and those with necrotizing pancreatitis (N=10). The results indicate that serum amylase and lipase concentrations are not able to establish either the etiology or to predict the severity of acute pancreatitis as assessed by imaging techniques. Furthermore, the serum lipase-amylase ratio is not useful in distinguishing acute episodes of alcoholic from nonalcoholic acute pancreatitis.     

血清淀粉酶和脂肪酶浓度及其比值对急性胰腺炎诊断价值的研究

目的探讨血清淀粉酶、脂肪酶浓度及脂肪酶／淀粉酶浓度比值在急性胰腺炎的病因分类和指导疾病的分级诊断中的作用。方法收集急性胰腺炎患者128例,按照病因分为胆源性、酒精性、其他病因三组,按照病情严重程度结合CT检查结果分为轻、中、重三组,比较各组间血清淀粉酶、脂肪酶浓度,脂肪酶／淀粉酶浓度比值的差异。结果酒精性急性胰腺炎患者的血清淀粉酶水平低于胆源性和其他病因患者（P=0．005、0．026）,胆源性和其他病因组间淀粉酶浓度差异无统计学意义。各病因分组之间,脂肪酶浓度和脂肪酶／淀粉酶浓度比值的差异均无统计学意义。按照疾病严重程度分组研究中,淀粉酶、脂肪酶浓度以及脂肪酶／淀粉酶浓度比值在各组间的差异无统计学意义。结论血清淀粉酶浓度在鉴别酒精性和非酒精性急性胰腺炎方面有指示作用,而脂肪酶浓度及脂肪酶／淀粉酶浓度比值不足以用来鉴别急性胰腺炎的病因,也不能单独作为指示疾病严重程度的指标。     

Pancreatic enzymes in chronic renal failure

Serum was obtained from 55 patients, including 43 with stable chronic renal failure (CRF) (28 receiving chronic hemodialysis [CHD] and 15 receiving chronic ambulatory peritoneal dialysis [CAPD]), nine with peritonitis receiving CAPD, and three with pancreatitis receiving CAPD. Total serum amylase activity, lipase activity, isoamylase fractionation, and lipase concentration were used to measure pancreatic enzymes. Amylase activity was increased in 35 of 43 patients with CRF but was greater than threefold elevated in only three. Pancreatic isoamylase activity was greater than 80% in only one patient with CRF but was greater than 80% in all three patients with pancreatitis receiving CAPD. Lipase activity was increased in 26 patients and lipase concentration was elevated in 27. Peritoneal fluid from three patients with pancreatitis receiving CAPD contained high levels of amylase. Serum amylase and lipase are frequently elevated in patients with CRF in the absence of clinical pancreatitis. However, serum amylase activity greater than threefold elevated or the presence of pancreatic enzymes in the peritoneal fluid may suggest coexistent pancreatitis.     

Electrophoretic identification of an isoenzyme of amylase which increases in serum in liver diseases.

Isoenzymes of amylase were studied in serum from 72 persons by means of polyacrylamide gel electrophoresis and a direct saccharogenic assay for amylase activity. In 37 normal individuals, there were two major peaks of amylase actvity with mobilities similar to pancreatic and salivary amylases. In 11 patiets with acute pancreatitis, the area of activity corresponding with pancreatic amylases increased disproportionately. Electrophoretic patterns of amylase activity in normal and pancreatitis urine were almost identical to the respective serum patterns from the same persons. In contrast, a prominent slower-moving peak of amylase activity occurred in the serum of 8 of 12 patients who had hyperamylasemia associated with various liver diseases. Traces of this third peak were identifiable in one-third of normal serum specimens, but no increases in its activity were observed in any specimen from 11 patients with pancreatitis or from 12 other patients with hyperamylasemia unassociated with liver disease. The slower-moving peak was absent from the urine of patients whose serum contained it. The origin of the slower-moving serum amylase appearing in patients with liver disease is not established by these studies. It is possible either that a hepatic amylase is liberated from damaged liver cells or that the metabolism of an amylase not originating in the liver is altered as a result of liver dysfunction.     

Diagnosis of pancreatitis masked by hyperlipemia.

It is often difficult to confirm a diagnosis of acute pancreatitis in the presence of hyperlipemic serum because the serum amylase and lipase and the urinary amylase are frequently normal. We were able to substantiate the diagnosis of pancreatitis in seven patients with hypertriglyceridemia (greater than 1200 mg/100 ml) by the use of the simple amylase/creatinine clearance ratio and by the serial dilution of hyperlipemic serum. The amylase/creatinine clearance ration in the hyperlipemic pancreatitis patients (10.0%) was significantly (P GREATER THAN 0.001) higher than in normal patients (3.1%) and essentially the same as in nonlipemic pancreatitis patients (9.2%). The calculated serum amylase activity after serial dilution of the serum showed up to a tenfold increase in hyperlipemic pancreatitis, with no significant increase in normal controls, hyperlipemic controls, and nonlipemic pancreatitis.     

Pain at 24 hours associated with amylase levels greater than 5 times the upper normal limit as the most reliable indicator of post-ERCP pancreatitis

BACKGROUND: The frequency of post-ERCP/sphincterotomy pancreatitis is between 1.3% and 7.6% in prospective studies. This range likely reflects differences in definitions of pancreatitis and methods of data collection. METHODS: To identify clinical findings and enzymatic values consistent for clinical pancreatitis at 24 hours, the post-ERCP/sphincterotomy course of 1185 procedures was prospectively recorded. Patients were evaluated for pancreatic-type pain, white blood cell count, and serum amylase before and 24 hours after the procedure; pain and amylase levels were also recorded 6 to 8 hours after the procedure. CT was performed in all patients with pain associated with amylase levels greater than 3 times normal. All patients were evaluated clinically at 48 hours. RESULTS: Pancreatic-type pain never occurred in cases with amylase levels lower than 3 times normal; it was significantly (p < 0.001) associated with amylase levels greater than 5 times normal, either 6 to 8 hours or 24 hours after the procedure. Leukocytosis and CT findings consistent with pancreatitis were observed only in patients (41.7% and 29.5%, respectively) with 24-hour amylase levels greater than 5 times normal. None of the 18 patients with pain at 24 hours and serum amylase lower than 5 times normal had symptoms that persisted at 48 hours. Twenty-five (41.7%) of the 60 patients with pain at 24 hours and amylase higher than 5 times normal had 48-hour pain at 48 hours and hyperamylasemia. CONCLUSIONS: Features consistent with clinical pancreatitis were present only among patients with pancreatic-type pain at 24 hours and amylase levels higher than 5 times normal. Additional follow-up is required for these patients.     

Lipase/amylase ratio in biliary acute pancreatitis and alcoholic acute/acutized chronic pancreatitis

BACKGROUND: Alcoholic or biliary acute pancreatitis may need different therapeutic approaches. AIM: Assessing the validity of lipase/amylase ratio in differentiating biliary from alcoholic acute pancreatitis/acutized chronic pancreatitis. METHODS: Nine male patients (mean age and standard deviation: 39.8 +/- 7.0 years) with alcoholic acute pancreatitis/acutized chronic pancreatitis (group I) and 29 patients, 8 male and 21 female (mean age: 43.6 +/-19.9 years), with biliary acute pancreatitis (group II) were evaluated. Serum lipase and amylase levels were measured in patients with symptoms for no more than 48 hours. The lipase/amylase ratio was calculated based on serum lipase and amylase levels and expressed as multiples of their respective superior reference values. RESULTS: Mean levels of serum lipase (4,814 +/- 3,670 U/L) and amylase (1,282 +/- 777 U/L) in patients of group I were comparable to group II (2,697 +/- 2,391 and 1,878 +/- 1,319 U/L, respectively), but the mean lipase/amylase ratio was significantly higher in group I (4.4 +/- 3.6) than in group II (2.2 +/- 2.2). Lipase/amylase ratio >3 occurred at significantly higher proportions in patients of group I (66.7%) than of group II (24.1%), differentiating the two groups with sensitivity of 67% and specificity of 76%. CONCLUSIONS: 1) Amylase and lipase serum levels did not differ in the two groups evaluated; 2) the lipase/amylase ratio >3 was more often seen in alcoholic acute pancreatitis/acutized chronic pancreatitis than biliary acute pancreatitis, and it may be useful in differentiating these two causes of pancreatitis.     

Lipase/amylase ratio. A new index that distinguishes acute episodes of alcoholic from nonalcoholic acute pancreatitis.

Because of observations that patients with acute episodes of alcoholic pancreatitis had high serum lipase levels whereas patients with gall stone pancreatitis had high serum amylase levels, a prospective study was undertaken to determine whether the ratio of serum lipase to serum amylase, a newly computed ratio, would discriminate between acute episodes of alcoholic and nonalcoholic pancreatitis. In phase one, 30 consecutive patients with acute pancreatitis were entered into the study and divided into groups A and B. Patients with renal failure were excluded from the study. Group A consisted of 20 patients in whom the etiology of pancreatitis was alcohol. Group B consisted of 10 patients whose pancreatitis was nonalcoholic in etiology (predominantly gallstones). Serum lipase values in group A ranged 492 to 25,706 U/L (median, 3433 U/L) and in group B from 711 to 31,153 U/L (median, 1260 U/L). These differences were not significant statistically. Serum amylase values in group A ranged from 104 to 2985 U/L (median, 331 U/L) and in group B from 423 to 13,000 (median, 1187 U/L). Although these figures were statistically different (P less than 0.005), there was a considerable degree of overlap in the values between the two groups. The lipase/amylase ratio calculated from the blood sample obtained at presentation appeared to be a promising discriminatory index. The lipase/amylase ratio was calculated by using the amylase and lipase levels expressed as multiples of the upper limit of normal in each case. The lipase/amylase ratios in the alcoholic group ranged from 2.2 to 14.8, whereas the lipase/amylase ratio in nonalcoholic pancreatitis ranged from 0.31 to 1.93. These differences were statistically significant (P less than 0.005). A lipase/amylase ratio of greater than 2 was indicative of an alcoholic etiology, and a ratio of less than 2 suggested that the pancreatitis was nonalcoholic in nature. In phase two, this lipase/amylase ratio of 2 was applied prospectively to an unselected population of 21 consecutive patients with acute pancreatitis. Thirteen patients had a lipase/amylase ratio of greater than 2; in 11 of them, the etiology of the pancreatitis was alcohol. Eight patients had a lipase/amylase ratio of less than 2; of them, only 1 patient had an alcoholic etiology for the pancreatitis. These differences were statistically significant (P less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)     

血清淀粉酶监测对ERCP术后胰腺炎的预测

目的 探讨为预测ERCP术后急性胰腺炎或持续重度高淀粉酶血症发生而测定血清淀粉酶的最佳时间。方法 对198例行ERCP术的患者分别测定术前即刻和术后2h、4h、8h、24h的血清淀粉酶值，将2h、4h、8h的血清淀粉酶值分别与24h的血清淀粉酶值及最终临床结果比较。结果 198例患者中15例在ERCP术后24h的血清淀粉酶水平仍高于正常值上限的5倍（〉575IU／L），与其他淀粉酶水平较低的患者比较，在所有时间点上淀粉酶值都有显著性差异。虽然8h点的血清淀粉酶水平判断术后胰腺炎的敏感性最高，但考虑实用价值可将4h点作为一可靠预测指标。结论 ERCP术后4h血清淀粉酶水平是有利于随访、具有经济效益、预测术后胰腺炎或重度高淀粉酶血症发生的指标。