Serum Pancreatic Enzyme Levels Research Articles

Unexplained Elevated Serum Pancreatic Enzymes: A Reason to Suspect Celiac Disease

The frequency of elevated serum pancreatic enzymes in patients with celiac disease (CD) is unknown. The aim of this study was to evaluate the serum levels of pancreatic enzymes in CD patients. Serum pancreatic isoamylase and lipase levels were assayed in 90 adult and 112 pediatric consecutive CD patients at diagnosis and after 12 months of gluten-free diet (GFD). Serum elastase and trypsin levels were assayed in a subgroup of adult CD patients. Pancreatic ultrasonography was also performed. Twenty-six adult (29%) and 29 pediatric (26%) CD patients exhibited elevated values of serum pancreatic amylase and/or lipase; trypsin was elevated in 69% and elastase in 19%. The frequency of elevated serum pancreatic enzymes observed was identical in the patients with "typical" and "atypical" CD symptoms and in the asymptomatic patients. Most of the elevated values were lower than 2-fold the threshold limits. Elevated pancreatic enzymes were not associated with alcohol consumption, drug use, presence of abdominal pain, or diabetes mellitus. Abdominal ultrasound scan showed no abnormal findings in the pancreatic region in any of the CD patients. After 12 months of GFD, pancreatic amylase was elevated in 3 cases and lipase in 2 cases; these patients had not strictly adhered to the GFD. We demonstrated a frequency of about 25% of elevated pancreatic enzymes values in CD patients, including subjects without gastrointestinal manifestations and apparently asymptomatic subjects. The finding of elevated serum amylase or lipase level, in the absence of signs of pancreatic disease, would appear to suggest a need to screen for celiac disease.

Effects of short‐term propofol administration on pancreatic enzymes and triglyceride levels in children

This prospective, clinical trial evaluated the effects of short-term propofol administration on triglyceride levels and serum pancreatic enzymes in children undergoing sedation for magnetic resonance imaging. Laboratory parameters of 40 children, mean age (SD; range) 67 (66; 4-178) months undergoing short-term sedation were assessed before and 4 h after having received propofol. Mean (SD) propofol loading dose was 2.2 (1.1) mg.kg(-1) followed by continuous propofol infusion of 6.9 (0.9) mg.kg(-1).h(-1). Serum lipase levels (p = 0.035) and serum triglyceride levels (p = 0.003) were raised significantly after propofol administration but remained within normal limits. No significant changes in serum pancreatic-amylase levels were seen (p = 0.127). In two (5%) children, pancreatic enzymes and in four (10%) children triglyceride levels were raised above normal limits; however, no child showed clinical symptoms of pancreatitis. We conclude that even short-term propofol administration with standard doses of propofol may have a significant effect on serum triglyceride and pancreatic enzyme levels in children.

Ulinastatin for pancreatitis after endoscopic retrograde cholangiopancreatography: A randomized, controlled trial

Pancreatitis remains the major complication of endoscopic retrograde cholangiopancreatography (ERCP), and hyperenzymemia after ERCP is common. Because ulinastatin, a protease inhibitor, has proved effective in the treatment of acute pancreatitis, the aim of this study was to assess the efficacy of ulinastatin for the prevention of post-ERCP pancreatitis and hyperenzymemia. In a multicenter, randomized, double-blind, placebo-controlled trial, patients undergoing a first ERCP were randomized to receive ulinastatin (150,000 U) or placebo by intravenous infusion for 10 minutes starting immediately before ERCP. All patients were hospitalized at least 24 hours after ERCP for evaluation of clinical symptoms. Serum pancreatic enzyme levels were measured before and at 4 and 18 hours after ERCP. The primary end point was the incidence of post-ERCP pancreatitis and the secondary objective was the occurrence of hyperenzymemia. A total of 406 patients were enrolled (204 in the ulinastatin group and 202 in the placebo group). There were no differences between the 2 groups regarding baseline characteristics, details of fluoroscopic findings, or endoscopic procedure. The incidence of hyperenzymemia was significantly lower in the ulinastatin group than in the placebo group (amylase, P = .011; lipase, P = .008). Six patients in the ulinastatin group and 15 patients in the placebo group developed pancreatitis (2.9% vs. 7.4%, P = .041). There was no case of severe pancreatitis in either group. Patients who received ulinastatin did not present any side effects related to the medication. Prophylactic short-term administration of ulinastatin decreases the incidence of pancreatitis and hyperenzymemia after ERCP.

Pancreatic involvement in chronic viral hepatitis

To elucidate the frequency and characteristics of pancreatic disorders in the course of chronic viral hepatitis. We prospectively assessed the serum pancreatic enzyme levels and imaging findings in patients with chronic viral hepatitis and healthy control subjects. Serum amylase (t-Amy), salivary amylase (s-Amy), pancreatic amylase (p-Amy) and serum lipase levels were higher in hepatitis patients in comparison to control subjects. However, in asymptomatic viral carriers, only the serum t-Amy levels were higher than those of the controls. The levels of each enzyme rose with the progression of liver disease in patients with hepatitis B or C; whereas the levels of each enzyme within the same clinical stage of the disease did not differ between patients diagnosed with either hepatitis B or hepatitis C virus. Imaging findings demonstrated chronic pancreatitis in only 1 out of 202 patients (0.5%). Our data suggest that serum levels of pancreatic enzymes increase with the progression of liver disease in patients diagnosed with viral hepatitis. Pancreatic disease, asymptomatic in most cases, may represent an extrahepatic manifestation of chronic viral hepatitis.

Evaluation of the long-term pancreatic effects of constitutive nitric oxide synthase inhibition in dogs.

Constitutive and inducible isoforms of nitric oxide synthase (NOS) catalyze the synthesis of nitric oxide (NO) from L-arginine in various tissues and in different pathophysiologic states. Short-term treatment with NOS inhibitors has been associated with pancreatic enzyme elevations and pancreatic acinar cell degeneration; however, long-term pancreatic effects of NOS inhibition are not known. The purpose of this study was to evaluate the subchronic pancreatic effects of L-nitro-arginine (LNA), a compound that preferentially inhibits constitutive NOS isoforms. LNA was administered orally at doses of 10 and 30 mg/kg per day to 6 female dogs/group for 4 weeks. To differentiate whether the pancreatic effects of LNA may be related to its arginine structure, an additional group was given L-arginine (L-Arg) at plasma concentrations similar to the high dose of LNA (30 mg/kg per day). Pancreatic effects were monitored by changes in serum levels of pancreatic enzymes at regular intervals and by microscopic examinations at the end of the study. Both LNA and L-Arg were systematically available throughout the 4-week study period. LNA produced dose-related elevations (1.3-10-fold above concurrent control) in serum levels of pancreatic enzymes (amylase, lipase and trypsin-like immunoreactivity) during the 4-week treatment period with peak elevations occurring during the first week. Histologic assessments of the pancreas conducted at the end of the 4-week dosing period were unremarkable. Additionally, LNA treatment resulted in reduction in heart rate (40%), gastric distension and gastric mucosal erosion and ulceration. No pancreatic, cardiac, or gastric effects were seen with L-Arg, indicating that above effects were likely due to NOS inhibition. Results of this study confirmed previous observations of acute pancreatic alterations following the inhibition of constitutive NOS isoforms. However, these pancreatic alterations appear to be only transient effects as elevations in serum enzymes declined over time and no structural acinar cell damage was seen after continuous treatment with LNA for 4 weeks, suggesting an adaptation to NOS inhibition over time.

Should enteral feeding be the standard of care for acute pancreatitis?: Abou-Assi S, Craig K, O'Keefe SJD, Hypocaloric jejunal feeding is better than total parenteral nutrition in acute pancreatitis: results of a randomized comparative study. Am J Gastroenterol 2002;97:2255–62

This study was performed prospectively to define outcomes including length of hospital stay, duration of feeding, complications, hospital costs, and indications for nutritional support in patients admitted with acute pancreatitis (AP). Patients who failed to improve after 48 h of conservative treatment or who could not tolerate an oral diet were randomized to receive either nasojejunal (NJ) or total parenteral (TPN) feeding. The majority of cases were related to alcohol consumption or gallstones. The goal feeding rates were intended to provide 1.5 g protein/kg/day and 25–30 Kcal/kg/day. The two nutritionally supported groups were compared on an intention to treat basis. In all, 75% of patients admitted for AP improved after conventional therapy within 48 h and did not require nutritional support. Of the patients, 27 patients were randomized to TPN and 26 to NJ feeding. Three patients in the NJ group were switched to TPN (two needed surgery and one could not tolerate the NJ feeds), and two in the TPN group were converted to NJ feeding because of sepsis. The average length of hospital stay was shorter in the NJ group versus the TPN group (14 vs 18 days) but the difference was not significant. The introduction of oral feeding was tolerated better in the NJ group, with 80% advancing to an oral diet without difficulty in comparison to 63% in the TPN group. The average length of nutritional support was significantly shorter in the enteral nutrition (EN) patients who were fed by NJ tube than in patients on TPN (6.7 vs 10.8 days, p < 0.001). However, the EN group received fewer calories (49% vs 85%) and protein (42% vs 85%) in comparison to the TPN group ( p < 0.005). The disease severity as well as the serum pancreatic enzyme levels on admission and thereafter were comparable between the groups. Nutrition associated complications were significantly more common in the TPN group. These included hyperglycemia, septic complications, and catheter-related infections requiring prolonged therapy. The incidence of severe complication and death was similar in the two groups. A post hoc analysis of patients with severe pancreatitis showed similar results, with significantly more rapid resolution of the disease process in the NJ group. The average cost per hospital stay was considerably lower for patients who improved sufficiently to forgo nutritional support ($4,597) in comparison to patients who required nutritional support. Patients who received enteral feeding had a lower total average hospitalization cost of $26,464 versus $34,530 for those who required parenteral nutrition, based on intention to treat analysis. The significantly lower average nutritional costs in the enteral group of $394 per patient in comparison to $2,756 per patient in the parenteral group ( p = 0.0004) could be explained by the combination of the lower daily costs of enteral feeding ($23.3/day vs $222/day), and the shorter duration of feeding (6.7 vs 10.8 days). Consequently, the proportion of hospital costs resulting from enteral feeding was significantly lower than for parenteral feeding (1.8% vs 8.4%, p < 0.0001). The authors concluded that NJ feeding initiated 48 h postadmission for patients with AP was safer than TPN, and does not exacerbate the disease, is well tolerated and less costly than TPN.

Pancreatic Duct Stent Insertion for Functional Smoldering Pancreatitis

Background: Some patients with smoldering pancreatitis in the absence of necrosis, pseudocyst, and ductal disruption experience unremitting abdominal pain caused by persistent pancreatic inflammation. Experience with the use of pancreatic duct stents in this patient population was reviewed. Patients and Methods: Data for 11 patients with smoldering pancreatitis who underwent ERCP with pancreatic duct stent placement were reviewed retrospectively. All patients had severe, daily pain that worsened with ingestion of food, had required narcotic analgesics for control of pain, had lost weight, and had persistently elevated serum levels of pancreatic enzymes as well as pancreatic inflammatory changes on CT (without necrosis or pseudocyst). Six patients were being treated with parenteral nutrition. Observations: The mean duration of symptoms from the onset of pancreatitis until pancreatic duct stent insertion was 74 days (range 14-151 days). Stents were placed for a mean of 7 weeks (range 2-19 weeks). Pancreatic stent placement provided permanent pain relief in 10 (91%) patients within a mean of 9 days (range 3-20 days); one patient had persistent symptoms requiring celiac plexus blockade after 5 months. Parenteral nutrition and treatment with narcotic agents were discontinued for 10 patients within a mean of 15 days (range 7-39 days) after pancreatic duct insertion. Conclusions: Smoldering pancreatitis may result from functional obstruction, possibly caused by edema or spasm, of the papillary orifice. Insertion of a stent into the pancreatic duct alleviates pain, enables early resumption of oral intake of food, and facilitates pancreatic duct drainage. It also may help to prevent complications arising from persistent pancreatic inflammation.

Clinical Evaluation of Oral Administration of a Cholecystokinin-A Receptor Antagonist (Loxiglumide) to Patients with Acute, Painful Attacks of Chronic Pancreatitis: A Multicenter Dose–Response Study in Japan

Cholecystokinin (CCK)-receptor antagonists have been found to markedly reduce the severity of pancreatitis and improve survival in experimental animal models of acute pancreatitis. CCK appears to play an important role in the development and progression of acute pancreatitis, and the recent development of CCK antagonists has provided a new approach to the treatment of acute pancreatitis in humans. The therapeutic efficacy of a CCK-A receptor antagonist, loxiglumide, in patients with painful acute attacks of chronic pancreatitis was evaluated. A multicenter dose-response controlled trial was conducted at 110 institutions in Japan from June 1993 to December 1994. Chronic pancreatitis was diagnosed for all patients on the basis of the Japanese criteria for chronic pancreatitis. Two-hundred seven patients were randomized to oral treatment with loxiglumide (300, 600, and 1,200 mg/d) or placebo for 4 weeks. The efficacy of treatment was evaluated on the basis of clinical symptoms, physical signs, and serum pancreatic enzyme levels. The groups were comparable with respect to age, sex, etiology, complications, and previous treatment. The improvement rate of the abdominal and/or back pain was 46% in the loxiglumide 300-mg group, 59% in the 600-mg group, and 52% in the 1,200-mg group, and it was 36% in the placebo group (600 mg versus placebo: p < 0.05). The physical signs evaluated--abdominal tenderness and resistance--improved in all three loxiglumide groups, and the serum pancreatic amylase and trypsin levels decreased significantly in the 600-mg group (p < 0.05). The overall clinical improvement rate was 46% in the 300-mg loxiglumide group, 58% in the 600-mg group, and 52% in the 1,200-mg group, and it was 34% in the placebo group. These results indicate that oral administration of loxiglumide may be useful in the treatment of patients with acute, painful attacks of chronic pancreatitis, and 600 mg/d is recommended as a beneficial dosage.

Treatment of panniculitis in chronic pancreatitis by interventional endoscopy following extracorporeal lithotripsy

Clinical panniculitis, formerly known as WeberChristian disease, is a rare complication that occurs in up to 3% of pancreatic disorders such as acute or chronic pancreatitis, pancreatic adenocarcinoma,1-3 and rarely pancreatic-portal vein fistula.4,5 The clinicopathologic manifestation of pancreatogenic panniculitis is red, inflamed, and painful subcutaneous nodules mostly localized to the lower extremities. A history of excessive alcohol consumption and highly elevated serum levels of pancreatic enzymes is often present. Panniculitis can predate the underlying pancreatic disorder and may even be the only clinical symptom, stressing the importance of panniculitis as a marker for pancreatic disorders.3 The differential diagnosis comprises other types of panniculitis such as vasculitis or erythema nodosum. Definitive diagnosis is by histopathologic examination of a biopsy specimen, which exhibits a pathognomonic pattern of subcutaneous tissue with predominant necrotic adipose cells and fat lobuli surrounded by lipophages, polynuclear cells, and neutrophils. The presence of so-called ghost cells with absent nuclei that are composed of amorphous granular debris is pathognomonic. The presence of precipitates of calcium in these necrobiotic lesions confirms the hypothesis that adipose necrosis is caused by the local action of lipolytic or other tissue destructive enzymes released by the pancreas.3,4 The treatment of panniculitis is difficult and only the treatment of the primary pancreatic disorder and consequent correction of hyperlipasemia seem to lead to resolution of subcutaneous fat necrosis.6

Changes in serum amylase, lipase and leukocyte elastase during diabetic ketoacidosis and poorly controlled diabetes.

Diabetic ketoacidosis (DKA) is frequently associated with pancreatic enzyme abnormalities. In order to determine the main factors that lead to this increase, serum total amylase (TA), pancreatic amylase (PA), lipase (L) and leukocyte elastase (LE), an early predictor of acute pancreatitis, were measured in four groups of patients on admission. Group 1 consisted of 52 patients with DKA (age: 41.9 +/- 19.2 years; blood glucose (Glc): 27.4 +/- 11.5 mmol/L; pH: 7.20 +/- 0.16; plasma bicarbonate: 10.5 +/- 6.2 mmol/L; blood urea nitrogen (BUN): 0.60 +/- 0.44 g/L; HbA(1C): 12.5% +/- 2.8%). Group 2 consisted of 90 patients with poorly controlled non-ketotic diabetes (age: 53.4 +/- 16.0; Glc: 14.3 +/- 0.6; HCO(3)(-): 26.6 +/- 3.2; BUN: 0.38 +/- 0.20; HbA(1C): 11.3 +/- 2.1). Group 3 consisted of 22 patients with well-controlled diabetes (age: 53.7 +/- 12.8; Glc: 10. 1 +/- 5.2; HCO(3)(-): 27.4 +/- 3.8; BUN: 0.36 +/- 0.19; HbA(1C): 6.8 +/- 0.8). Group 4 (controls) comprised 27 non-diabetic patients (age: 46.0 +/- 15.0; Glc: 4.9 +/- 0.5; HCO(3)(-): 28.4 +/- 2.5; BUN: 0.30 +/- 0.16; HbA(1C): 5.2 +/- 0.7) (means +/- SD). Increased enzyme activities were more frequent in group 1 (TA: 30.7; PA: 27.0; L: 36.5; LE: 73%) than in groups 2 (TA: 8.9; PA: 7.1; L: 8.9; LE: 45. 5%), 3 (TA: 13.6; PA: 9.0; L: 18.1; LE: 31.8%) and 4 (TA: 7.0; PA: 3. 0; L: 0.0; LE: 29.6%). Mean serum enzyme activities were significantly different in the 4 groups (ANOVA, P < 0.01) and were higher in group 1 than in groups 2, 3 and 4 (Student's t-test; group 1 vs 2 or 3 or 4: P < 0.001). In groups 1 + 2 + 3 + 4 (all patients), the four enzymes correlated with one another and also with Glc, BUN and HCO(3)(-) (P < 0.001). In group 1, TA correlated negatively with HCO(3)(-) (P < 0.001) and pH (P < 0.05); PA and L correlated positively with Glc and BUN (P < 0.01) and negatively with HCO(3)(-) (respectively, p < 0.01 and 0.05). PA correlated positively with pH (P < 0.01); LE correlated with Glc (P < 0.05) and BUN (P < 0.01). In conclusion, this study suggests that the serum levels of pancreatic enzymes increase with the degree of diabetic disequilibrium, and mainly correlate with metabolic factors such as hyperglycaemia, dehydration and acidosis. Increased pancreatic enzyme activities in patients with DKA, even in combination with abdominal pain, should not be diagnosed as acute pancreatitis; this could be important, particularly for younger clinicians.

A CASE OF PANCREATIC HEMANGIOMA

A 46-year-old woman came to our hospital because of a feeling of abdominal fullness. An echograrn revealed a rough, mixed pattern tumor 3.5 cm in diameter in the pancreatic body. Abdominal CT showed a heterogeneously enhanced low-density tumor. Dynamic CT showed that the tumor was enhanced poorly in the early phase. A doppler echogram revealed the absence of any blood flow signal in the tumor. MRI visualized the tumor as a low-intensity mass on T 1-weighted images, and a high intensity mass on T 2-weighted images. ERP showed a normal main pancreatic duct, and the tumor filled with contrast medium. Serum levels of pancreatic enzymes (amylase, lipase, etc.), tumor markers (CEA, CA 19-9, etc.), and pancreatic hormones (insulin, glucagon, etc.) were normal. At laparotomy, the tumor was located in the pancreatic body, and was welldefined, smooth-surfaced, covered with a greyish white capsule, oval in shape, and elastic-soft on palpation. Distal pancreatectomy with splenectomy was performed. Histopathologically, the diagnosis was cavernous hemangioma arising in the pancreas.

Increased serum trypsin and elastase-1 levels in patients undergoing L-asparaginase therapy.

Although there is abundant literature on the association of L-asparaginase and acute pancreatitis in patients undergoing chemotherapy, few studies have investigated the usefulness of pancreatic enzyme measurement in the early diagnosis of L-asparaginase-induced acute pancreatitis. We measured levels of serum pancreatic enzymes before, during, and after L-asparaginase therapy in nine children with acute lymphocytic leukaemia or non-Hodgkin lymphoma. Serum levels of amylase, pancreatic isoamylase, and lipase did not change between the 1st and 30th day of L-asparaginase administration. However, the serum trypsin and elastase- levels, 10 and 20 days after beginning L-asparaginase therapy, were significantly higher than those prior to therapy. L-asparaginase may induce subclinical pancreatitis and the estimation of serum trypsin and elastase-1 may be useful in the early diagnosis of L-asparaginase-induced acute pancreatitis.

Serum Pancreatic Enzymes in Human Immunodeficiency Virus-Infected Children: A Collaborative Study of the Italian Society of Pediatric Gastroenterology and Hepatology

Background: Numerous studies have shown pancreatic disease in adult human immunodeficiency virus (HIV)-infected patients, but there are very few reports on pediatric patients. Our aim was to determine the prevalence of increased serum pancreatic enzyme levels and their relationship to clinical manifestations of acute pancreatitis in HIV-infected children. Methods: Forty-seven consecutive, symptomatic HIV-infected children (24 male; median age, 7.3 years; range, 1-17 years) and 45 sex- and age-matched controls without gastroenterologic disease were enrolled. In all subjects serum total amylase, pancreatic amylase, and lipase were assayed with commercial kits. The following were recorded: disease progression (CDC class), nutritional status (weight Z-score), CD4 lymphocyte count, drug treatment during the previous 12 months, presence of opportunistic infections, clinical evidence of acute pancreatitis (increased serum pancreatic enzymes associated with vomiting, abdominal distention, and intolerance when eating). Results: Ten of 47 HIV patients had increased serum total amylase values; however fewer patients had increased specific pancreatic enzymes: 6 of 47 for pancreatic amylase (range, 1.8- to 19.8-fold normal limit) and 7 of 47 for lipase (range, 1.4- to 4-fold normal limit). Values were normal in all controls. Two HIV patients with increased total amylase had clinically evident parotid inflammation. None of the patients with increased serum pancreatic amylase and/or lipase had clinical symptoms of acute pancreatitis. Regression analysis showed no correlation between increased serum pancreatic enzyme levels and disease progression (CDC class), immunologic status (CD4 count), nutritional status, drug administration, or opportunistic infections. Conclusions: Fifteen per cent of HIV-infected children had biochemical evidence of pancreatic involvement; however, this condition was unrelated to clinical signs of pancreatitis. Neither drug administration nor opportunistic infections seem to determine the increased serum pancreatic enzyme levels.

Plasma cholecystokinin levels in acute pancreatitis.

Recent studies have shown that cholecystokinin (CCK) is involved in the induction and development of acute pancreatitis in experimental animals. In the present study we determined basal plasma CCK concentrations by a specific and sensitive radioimmunoassay using antiserum OAL656 in 17 patients with acute pancreatitis due to gallstone in the common bile duct (n = 7), alcoholic (n = 4), post endoscopic retrograde pancreatography (n = 1), and unknown causes (n = 4), and 37 patients with cholelithiasis (n = 18) and choledocholithiasis (n = 19). Plasma CCK concentrations in patients with gallstone pancreatitis on hospital day 1 (mean +/- SEM, 6.78 +/- 1.39 pM) were significantly higher than those in patients with other causes (1.33 +/- 0.16 pM) or in 20 healthy control subjects (1.55 +/- 0.11 pM). There was no relationship between plasma CCK and serum pancreatic enzyme levels, the severity of acute pancreatitis, or serum bilirubin concentrations. Plasma CCK levels in patients with acute symptomatic cholelithiasis (n = 7; 4.35 +/- 0.90 pM) and choledocholithiasis (n = 8; 4.52 +/- 1.17 pM) were significantly higher than those in patients without symptoms (cholelithiasis, n = 11, 1.40 +/- 0.17 pM; choledocholithiasis, n = 11, 1.88 +/- 0.49 pM) but tended to be lower than those in patients with gallstone pancreatitis. These present observations suggest that the increase in plasma CCK levels in gallstone pancreatitis appears not to be the cause but to be the result of gallstone pancreatitis probably due to a transient disturbance of bile flow into the duodenum by stones or edema of the bile duct. Our present results provide some evidence for the usefulness of CCK receptor antagonists for the treatment of biliary colics and acute pancreatitis.

Papillary roof incision using the Erlangen-type pre-cut papillotome to achieve selective bile duct cannulation

Background: Prior studies evaluating pre-cutting the major papilla to access the bile duct when standard cannulation fails have usually used the needle-knife papillotome. We conducted a prospective study to evaluate the efficacy and safety of an Erlangen-type pre-cut papillotome for pre-cutting. Patients and Methods: Three hundred twenty-seven patients (114 men, mean age 67 years) who underwent first-time sphincterotomy at our institution were included. Pre-cutting was performed if free and wire-guided cannulation of the bile duct failed according to an algorithm. Results: Pre-cutting was performed in 123 patients (38%) and selective cannulation was successful in all. Post-ERCP serum pancreatic enzyme levels were more frequently elevated in the pre-cut group (50%) than the non-pre-cut group (27%, p < 0.001); however, there was no difference in the incidence of post-ERCP pancreatitis (pre-cut = 2.7%, 95% CI: 0.66% to 7.6%; non-pre-cut = 1.6%, 95% CI: 0.3% to 4.7%). The incidence of bleeding was similar (pre-cut, 2.4%, non-pre-cut, 3.9%; p > 0.05). Conclusion: Pre-cutting the major papilla for biliary access using the Erlangen-type pre-cut papillotome is an effective and reasonably safe procedure when performed by endoscopists with extensive experience in pancreatobiliary endoscopy. (Gastrointest Endosc 1996;44:689-95.)

Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC

We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.

PANCREATIC CYTOPROTECTIVE EFFECTS OF PROSTAGLANDIN E1 IN PANCREATECTOMIZED PATIENTS

We studied the changes in serum levels of pancreatic enzymes during perioperative period of patients undergoing pancreatic surgery to examine the cytoprotective effect of prostaglandin E1 (PGE1) with improvement of pancreatic micro-circulation. Subjects were 16 patients who underwent pancreatectomy or gastrectomy with extended removal of lymph nodes surrounding the pancreas. They were randomly divided into a group treated with PGE1 comprising of 8 patients and control group comprising of another 8 patients. Primary diseases involved 9 advanced gastric cancers, 3 bile-duct or pancreatic cancers, and 4 pancreatic cystadenomas. PGE1 was continuously given at a dose of 0.01μg/kg/min from the start of surgery until 24 hours after the surgery. Gabexate mesilate was given to each group at a dose of 400mg/day for 5 days. The incidence of abnomally high levels of serum pancreatic amylase on the seventh day after the surgery was 88% in control and 13% in PGE1 group, with a significant difference (p<0.05). Postoperative levels of pancreatic amylase and trypsin were significantly lower in the PGE1 gruop than control group (p<0.05). These results suggest that perioperative administration of PGE1 may provide effective pancreatic cytoprotection and consequent prevention against acute pancreatitis following surgery which has a high motality rate.

Chronic Pancreatitis as a Complication of Ulcerative Colitis —Report of 2 Cases—

Abstract: We report on two patients with chronic pancreatitis associated with ulcerative colitis. Both patients had ulcerative colitis involving the entire colon and rectum. The diagnosis of chronic pancreatitis was based on the typical findings of endoscopic retrograde cholangiopancreatography (ERCP) and episodes of hyperamylasemia. The changes in the levels of serum pancreatic enzymes are considered to have paralleled the activity of the colitis. None of the classical etiologies for pancreatitis was found in either case. The time sequence and exclusion of known causes of pancreatitis suggest an association between these two conditions.These two cases, together with other reported cases, provide some evidence for the hypothesis that chronic pancreatitis may be one of the extraintestinal complications of ulcerative colitis. The symptoms of ulcerative cblitis, such as diarrhea and abdominal pain, may mimic the symptoms of chronic pancreatitis. Pancreatitis and ulcerative colitis are probably mutually exacerbating factors. Therefore, the recognition of this phenomenon contributes substantially to the management of ulcerative colitis. (Dig Endosc 1994; 6 : 59–65)

Disseminated adenoviral infection presenting as acute pancreatitis

Adenoviruses are gradually being recognized as a significant source of morbidity and mortality in the immunocompromised patient population. We report a bone marrow transplant patient who developed severe abdominal pain accompanied by marked elevations in serum pancreatic and hepatic enzyme levels. She died shortly thereafter. Autopsy revealed hemorrhagic pancreatitis and fulminant hepatic necrosis. Both the pancreas and liver contained intranuclear inclusions consistent with adenovirus; electron microscopy confirmed that there were, indeed, adenoviral particles. This report of adenoviral pancreatitis emphasizes the diversity of manifestations seen with adenoviral infection.

Variations in time of serum pancreatic enzyme levels in chronic pancreatitis and clinical course of the disease

Thirty-four patients with chronic calcified pancreatitis were evaluated clinically and biochemically (at a time when painful relapses were not present) every 9 mo for 3 yr; 25 of them were also studied at 4 and 9 yr. Serum elastase-1, trypsin, lipase, and amylase in the same sera were measured at each visit; levels on entry and variations during the study were compared with the clinical and functional data of the patients. On entry, low levels of elastase-1 were found in 11.7% of the patients, high levels in 41.1%; in contrast, high levels of trypsin and lipase were found in only a small number of patients (5.8 and 11.7%, respectively), whereas low levels were present in a substantial number (47.8 and 32.3% for trypsin and lipase, respectively). Over time, we found a significant (p = 0.000002) reduction in elastase-1 levels. Such reduction was not found for trypsin, lipase, or amylase. The reduction of serum elastase-1 was significantly (p less than 0.003) more frequent in patients presenting a reduction in painful relapses than in patients with a stable or increased attach rate; this association was weaker (p less than 0.05) for lipase and trypsin, and absent for amylase. No correlation was found between circulating enzymes and either alcohol consumption or age of patients. In patients with severe exocrine impairment, low levels of elastase were found in only 20% of the cases, whereas trypsin and lipase were reduced in 73.3 and 53.3% of the cases, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)