Pancreatic Enzyme Content Research Articles

Analytical validation of radioimmunoassays for the quantification of select pancreatic enzymes in jejunal fluid and fecal extracts from dogs

Pancreatic enzymes, such as trypsin and lipase, are essential for the digestion of dietary components in the small intestine. Measurement of both enzymes in jejunal fluid and fecal specimens from dogs has not been reported and will be a prelude for further investigations. Therefore, the aim of the study was to validate radioimmunoassays (RIAs) for the measurement of canine trypsin-like immunoreactivity (cTLI) and pancreatic lipase immunoreactivity (cPLI) in jejunal fluid and fecal specimens from dogs. Jejunal fluid and fecal specimens were collected from five healthy Beagles. A commercial 125I-RIA was used for measuring cTLI concentrations and an in-house 125I-RIA was modified for the quantification of cPLI in jejunal fluid and fecal specimens. Both RIAs were analytically validated for canine jejunal fluid and fecal specimens by determining dilutional parallelism, spiking recovery, and intra- and inter-assay variability. For both cTLI and cPLI in jejunal fluid, observed-to-expected ratios for dilutional parallelism and spiking recovery ranged from ⩾77.0% to ⩽115.3% and ⩾79.0% to ⩽120.0%, respectively, and from ⩾87.2% to ⩽118.5% and ⩾74.6% to ⩽116.1%, respectively, for fecal specimens. Intra- and inter-assay coefficients of variation (%CV) for both cTLI and cPLI in jejunal fluid were ⩽7.6% and ⩽10.0%, respectively, and were ⩽10.8% and ⩽9.0%, respectively, for fecal specimens. Both RIAs were demonstrated to be linear, accurate, precise, and reproducible for use with jejunal fluid and fecal specimens from dogs. These results are important for the investigation of pancreatic enzyme concentrations in the gastrointestinal lumen in response to changes in dietary components.

The Aberrant Aberration

Question: A 59-year-old man was referred for evaluation of a mass found during laparoscopic cholecystectomy performed 11 days prior. The patient initially sought medical evaluation for a palpable mass in his right upper quadrant in addition to a 25-lb weight loss. Ultrasonography revealed a dilated gallbladder with wall thickening and a 2.0 × 1.8 × 1.4-cm mass on the superolateral aspect. At the time of laparoscopic cholecystectomy, a mass adherent to the radial hepatic margin was identified and seemed to invade the perimuscular connective tissue. Pathology was interpreted as invasive, moderately differentiated adenocarcinoma. The patient was referred to our institution. Preoperative testing revealed a CA19–9 level of 277 U/mL (normal, <55 U/mL). He subsequently underwent locoregional lymphadenectomy and partial right hepatectomy (segments IVb and V) for complete oncologic resection. On postoperative day 5, increasing bilious output from his Jackson-Pratt (JP) drain was noted, raising suspicion for bile leak. Endoscopic retrograde cholangiopancreatography (ERCP) demonstrated a bile leak from the cystic duct remnant (Figure A) and other notable findings (Figure B). The cystic duct remnant leak was initially treated with endoscopic sphincterotomy and placement of two 10-F, 9-cm plastic stents into the extrahepatic bile duct. Over the subsequent days, increasing output from the JP drain was noted. The high-volume drainage was noted to have an amylase concentration >17,000 U/L. The previously bilious effluent now appeared colorless and repeat ERCP was performed. What is the diagnosis? See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI. In addition to the bile leak, there was radiographic evidence of pancreaticobiliary maljunction (PBM) with the pancreatic duct arising from a low-inserting cystic duct remnant (Figure C). Standard endoscopic management of the cystic duct leak using endoscopic sphincterotomy and biliary diversion through stenting (Figure B) was unsuccessful. At repeat ERCP, the anomalous pancreatic duct could not be accessed for diversion of flow through the duodenum; thus, a 7-F, 5-cm pancreatic stent with additional side-holes was placed into the cystic duct remnant. Two 10-F, 9-cm plastic stents were replaced in the extrahepatic bile duct for diversion and to prevent migration of the cystic duct stent. The drain output decreased to <20 mL and the patient was discharged. Repeat ERCP 1 month later revealed complete resolution of the leak. PBM has a prevalence of 0.03% and occurs frequently in patients with choledochal cysts.1Yamao K. Mizutani S. Nakazawa S. et al.Prospective study of the detection of anomalous connections of pancreatobiliary ducts during routine medical examinations.Hepatogastroenterology. 1996; 43: 1238-1245PubMed Google Scholar PBM is defined as a union of the pancreatic and biliary ducts outside the duodenal wall leading to a long common channel (often ≥15 mm). The junction is beyond the influence of the sphincter of Oddi, resulting in reciprocal reflux of biliary and pancreatic juices. Persistent reflux of proteolytic pancreatic enzymes and phospholipase A2 is postulated to injure the biliary epithelium and induce metaplasia or promote carcinogenesis.2Shimada K. Yanagisawa J. Nakayama F. Increased lysophosphatidylcholine and pancreatic enzyme content in bile of patients with anomalous pancreaticobiliary ductal junction.Hepatology. 1991; 13: 438-444Crossref PubMed Scopus (122) Google Scholar In addition to evidence of PBM the pancreas duct was directly arising from a low inserting cystic duct. This variant of PBM has not been previously described, but certainly resulted in direct reflux of pancreatic juices into the cystic duct and gallbladder, likely contributing to gallbladder cancer. The association of PBM and gallbladder cancer was established in the 1980s, and most reports cite an incidence of 10%–15% of gallbladder cancer arising in this setting.

Analysis of Concentration of Pancreatic Enzymes in the Amniotic Fluid in Fetal Duodenal Atresia and Jejunal Atresia

Analysis of Concentration of Pancreatic Enzymes in the Amniotic Fluid in Fetal Duodenal Atresia and Jejunal Atresia

Increased variability and abnormalities in pancreatic enzyme concentrations in otherwise asymptomatic subjects with type 2 diabetes

BackgroundRecent studies have demonstrated an increased incidence of pancreatitis in patients with type 2 diabetes compared with obese nondiabetic individuals. Serum lipase and pancreatic amylase concentrations are used in conjunction with clinical findings to diagnose pancreatitis.MethodsIn two large clinical trials of overweight/obese nondiabetic and type 2 diabetic subjects, lipase and pancreatic amylase were measured at screening and 2–5 weeks later at baseline (prior to treatment with study medication).ResultsLipase and pancreatic amylase concentrations were above the upper limit of normal (ULN) in 13% and 6% of type 2 diabetic subjects, respectively, and were approximately three-fold (3 ×) higher than the proportion of nondiabetic subjects with levels above ULN. Elevations exceeding ULN were seen in many subjects asymptomatic for pancreatitis; however, elevations >2 × ULN and >3 × ULN were uncommon, and elevations >3 × ULN were often associated with a history of dyslipidemia, hyperlipidemia, and gastrointestinal disorders. Additionally, enzyme concentrations varied within this 2–5-week screening period, including shifts between elevated and normal levels.ConclusionResults from this post hoc analysis suggest that, although pancreatic enzymes can be a useful marker for pancreatitis within the proper clinical context, diagnosis of pancreatitis may be confounded in populations known to have asymptomatic elevations associated with disease, such as type 2 diabetes. Further effort is needed to clarify the etiology and epidemiology of pancreatic enzyme elevations in type 2 diabetes.

The Effects of Morphine–Neostigmine and Secretin Provocation on Pancreaticobiliary Morphology in Healthy Subjects: A Randomized, Double‐blind Crossover Study Using Serial MRCP

Secretin-stimulated magnetic resonance cholangiopancreatography (MRCP) is used for the diagnosis of sphincter of Oddi dysfunction (SOD), but it does not correlate well with sphincter of Oddi manometry. Serial MRCP following morphine-neostigmine provocation may be of value in the assessment of SOD, but the effects of these pharmacological agents on pancreaticobiliary morphology in healthy subjects have not been studied. The aim of the present study was to use serial MRCP to characterize the effects of morphine-neostigmine and secretin provocation on serum pancreatic enzyme responses and pancreaticobiliary ductal morphology in healthy subjects. Following a baseline scan and serum lipase and amylase assays, 10 healthy subjects were randomized in a double-blind manner to receive morphine (10 mg intramuscularly [IM]), neostigmine (1 mg IM) and saline (intravenously [IV]); OR saline (IM), saline (IM) and secretin (1 U/kg IV). A MRCP study was performed at 5, 30, 60, 90, 120, 150, and 180 min thereafter, with blood samples taken every 60 min for 4 h. Pancreatic duct (PD) diameter, visible PD length, common bile duct (CBD) diameter, and gallbladder volume were recorded. Crossover studies were performed 10 days later. Serum pancreatic enzyme concentrations were significantly greater (amylase, P = 0.003; lipase, P = 0.04) after morphine-neostigmine than after secretin. Following morphine-neostigmine and secretin provocation, the mean (SEM) percentage increase in PD diameter was 28.7 (7.2) versus 12.9 (3.3); P < 0.0001, and visible PD length was 49.4 (11.5) versus 28.1 (8.2); P < 0.0001, respectively. The effects of morphine-neostigmine were more pronounced than those of secretin in healthy subjects. The diagnostic utility of morphine-neostigmine stimulated serial MRCP for SOD merits further evaluation.

Upregulation of bradykinin receptors is implicated in the pain associated with caerulein‐induced acute pancreatitis

Although the way for pain management associated with acute pancreatitis has been searched for, there are not enough medications available for it. The aim of the present study was to investigate the role of bradykinin (BK) in pain related to acute pancreatitis. After repeated injections of caerulein (50 μg/kg and 6 times), mice showed edema in the pancreas, and blood concentrations of pancreatic enzymes (amylase and lipase) were clearly elevated. A histopathological study demonstrated that caerulein caused tissue damage characterized by edema, acinar cell necrosis, interstitial hemorrhage, and inflammatory cell infiltrates. Furthermore, the mRNA levels of interleukin-1β and monocyte chemotactic protein (MCP)-1 were significantly increased in the pancreas of caerulein-treated mice. The sensitivity of abdominal organs as measured by abdominal balloon distension was enhanced in caerulein-injected mice, suggesting that caerulein caused pancreatic hyperalgesia. Moreover, repeated treatment with caerulein resulted in cutaneous tactile allodynia of the upper abdominal region as demonstrated by the use of von Frey filaments, indicating that caerulein-treated mice exhibited referred pain. Under this condition, the mRNA levels of bradykinin B1 receptor (BKB1R) and bradykinin B2 receptor (BKB2R) were significantly increased in the dorsal root ganglion (DRG). Finally, we found that des-Arg⁹-(Leu⁸)-bradykinin (BKB1R antagonist) and HOE-140 (BKB2R antagonist) attenuated the acute pancreatitis pain-like state in caerulein-treated mice. These findings suggest that the upregulation of BK receptors in the DRG may, at least in part, contribute to the development of the acute pancreatitis pain-like state in mice.

Practical Guidelines for Acute Pancreatitis

Introduction: The following is a summary of the official guidelines of the Italian Association for the Study of the Pancreas regarding the medical, endoscopic and surgical management of acute pancreatitis. Statements: Clinical features together with elevation of the plasma concentrations of pancreatic enzymes are the cornerstones of diagnosis (recommendation A). Contrast-enhanced computed tomography (CT) provides good evidence for the presence of pancreatitis (recommendation C) and it should be carried out 48–72 h after the onset of symptoms in patients with predicted severe pancreatitis. Severity assessment is essential for the selection of the proper initial treatment in the management of acute pancreatitis (recommendation A) and should be done using the APACHE II score, serum C-reactive protein and CT assessment (recommendation C). The etiology of acute pancreatitis should be able to be determined in at least 80% of cases (recommendation B). An adequate volume of intravenous fluid should be administered promptly to correct the volume deficit and maintain basal fluid requirements (recommendation A); analgesia is crucial for the correct treatment of the disease (recommendation A). Enteral feeding is indicated in severe necrotizing pancreatitis and it is better than total parenteral nutrition (recommendation A). The use of prophylactic broad-spectrum antibiotics reduces infection rates in CT-proven necrotizing pancreatitis (recommendation A). Infected pancreatic necrosis in patients with clinical signs and symptoms of sepsis is an indication for intervention, including surgery and radiological drainage (recommendation B). Conclusions: The participants agreed to revise the guidelines every 3 years in order to re-evaluate each question on the management of acute pancreatitis patients according to the most recent literature.

Pancreaticobiliary Reflux in Patients with and without Cholelithiasis: Is It a Normal Phenomenon?

Pancreaticobiliary reflux is a pathologic phenomenon occurring in patients with gallstones. However, the occurrence of pancreaticobiliary reflux has not been studied in patients without gallstones. The objective of the present study was to measure the bile levels of amylase and lipase in patients without gallstones submitted to cholecystectomy as part of another surgical procedure, and to compare these values with the bile levels of amylase and lipase of patients submitted to cholecystectomy for gallstone disease. A prospective observational and comparative study was designed. A sample of 136 consecutive patients was included. Amylase and lipase levels were measured in bile. At our institution, normal plasma concentrations of amylase are 28-100IU/l and lipase 13-60IU/l. Normal values for pancreatic enzyme concentrations in bile have not been established. Therefore, bile amylase and lipase concentrations exceeding normal plasma concentrations were deemed to be elevated. Of the patients in the present study, 103 (76%) had gallstones and 33 (24%) had healthy gallbladders without gallstones. According to normal plasma levels for amylase and lipase, these enzymes in bile were elevated in 83.5% patients with gallstones, compared to elevated levels of amylase in 6% patients and lipase in 3% patients without gallstones (P<0.0001). Pancreaticobiliary reflux is a common phenomenon in patients with gallstones and an uncommon phenomenon in patients with healthy gallbladders without gallstone disease.

Unilateral pleural effusion—but where from?

In December, 2007, a 63-year-old woman presented with a week’s history of shortness of breath, 4 months of ankle swelling, and weight gain. She had no chest pain, palpitations, cough, or fever. She had been diagnosed with non-A, non-B hepatitis in 1980. There was a large right-sided pleural eff usion on chest radiograph, shown to be loculated by CT. Thoracentesis yielded 1·5 L of clear, yellow transudate. CT of the abdomen showed a shrunken liver consistent with cirrhosis without ascites. No abnormalities were found in full blood count, renal function, liver function, concentrations of thyroid hormones, pancreatic enzymes, and brain natriuretic peptide, electrocardiogram, tuberculin test, pelvic ultrasonography, echocardiogram, or urine analysis. Hepatitis B and C, Wilson’s disease, haemochromatosis, α-1 antitrypsin defi ciency, and autoimmune hepatitis were excluded. A liver biopsy sample showed regenerative nodule formation consistent with cirrhosis of unknown cause. Doppler ultrasonography of the portal vein was normal, whereas oesophagogastroduodenoscopy showed mosaic patterning of the stomach consistent with portal hypertensive gastropathy. Repeat thoracentesis on day 4 drained 1·5 L of fl uid. Treatment with fl uid restriction, low salt diet, furosemide, and spironolactone was started, but fl uid reaccumulated within 3 days. On day 8, talc pleurodesis was done and she was discharged. 2 weeks later she was readmitted with recurrent pleural eff usion. Hepatic hydrothorax was considered a possible diagnosis. Hepatic vein catheterisation (fi gure) revealed a hepatic vein pressure gradient (HVPG) of 21 mm Hg (normal value: 1-5 mm Hg). Transjugular intrahepatic portosystemic shunt (TIPS) was undertaken, after which the HVPG was 4 mm Hg and no reaccumulation of pleural fl uid occurred. 4 days later, the patient became encephalopathic with a rise in concentrations of bilirubin (68 μmol/L) and aminotransferases (aspartate amino transferase 750 U/L, alanine aminotransferase 291 U/L). Intracranial processes were ruled out as a potential cause of altered mental status. Lactulose treatment was initiated and a reduction in TIPS size was considered but she developed aspiration pneumonia necessitating intubation and died within 4 days. The family declined autopsy. Hepatic hydrothorax is a signifi cant pleural eff usion in a cirrhotic patient in the absence of a primary cardiopulmonary cause; it is a complication of portal hypertension, with a prevalence of 5–12%. Although usually right-sided, it can be left-sided or bilateral. The cause is thought to be leakage of ascitic fl uid via a diaphragmatic defect. Diagnosis of hepatic hydrothorax without ascites and obvious signs of portal hypertension is challenging. Doppler ultrasonography of the portal vein can show portal hypertension, but HVPG is the gold standard. Scintigraphic demonstration of a diaphragmatic defect by use of radiolabelled human serum albumin is helpful, and in retrospect might have been useful in our patient. Treatment of hepatic hydrothorax is challenging, with liver transplant the ultimate goal. Diuretics, fl uid restriction, and repetitive thoracenteses are used to prevent pulmonary complications. Diaphragmatic repair, pleurodesis, and TIPS are reserved for refractory cases. Rapid migration of fl uid from peritoneum to the pleural space means pleurodesis is often unsuccessful. 30-day mortality with TIPS ranges from 19% to 68%; complications include hepatic encephalopathy, stent occlusion, infection, bleeding, acute renal failure, and acute respiratory distress syndrome. Rapid onset of encephalopathy after TIPS can be due to infection or to insuffi cient arterial liver perfusion as a result of arterial-stent fi stula, arterial-biliary fi stula, or stent-related stenosis of the artery causing liver infarction. In patients with unilateral pleural eff usion, after exclusion of cardiac and pulmonary causes, a hepatic cause should be considered. Defects should be demonstrated by scintigraphy if the diagnosis is in doubt before extensive work-up. TIPS is an eff ective treatment, but serious side-eff ects can occur even in patients with well-compensated liver disease.

Abnormalities in Pancreatic Enzyme Levels in Otherwise Asymptomatic Subjects with Type 2 Diabetes

Purpose: The literature has been mostly silent on the epidemiology of pancreatitis in type 2 diabetes (T2D). Recent data demonstrated a 2-3-fold increased risk of acute pancreatitis in T2D compared to a nondiabetic cohort. Clarifying the risk of pancreatitis is relevant to drug development and the understanding of risk with both old and new diabetes therapies. Methods: We report data from clinical trials demonstrating variability of pancreatic (p) enzyme concentrations in 2 cohorts of subjects: one with T2D subjects (BMI 25-45 kg/m2) and one with overweight/obese but healthy subjects (BMI 27-45 kg/m2) participating in 2 large, randomized, controlled clinical trials. In both trials, pre-treatment samples for serum lipase and p-amylase were collected from all study participants at screening, from enrolled subjects 2-4 weeks later and measured again after 12-24 weeks of study participation. Both trials used the same central laboratory. Results: A higher incidence of abnormal p-enzyme levels was observed in the T2D study population where 12-14% of subjects had abnormal lipase and 5-7% had abnormal p-amylase levels above the upper limit of normal (ULN) at baseline. This abnormal incidence was 2-3 times higher compared to the non-diabetic study population. The incidence of abnormal lipase levels >3 times the upper limit of normal (ULN) was 1.4% at baseline and was unchanged during active treatment with both conventional and experimental diabetes agents. Elevations in individual subjects were mostly transient and not associated with abdominal pain. No pattern of symptoms or adverse events differentiated T2D subjects with elevations versus those without. Abdominal computed tomography of a subset of subjects with lipase >2-3XULN revealed no evidence of pancreatic inflammation. Conclusion: These findings, including enzyme elevations exceeding 2 and 3 times ULN in asymptomatic subjects with T2D, may confound the evaluation of pancreatitis and warrant further effort to clarify the epidemiology of both p-enzyme elevations and the risk of pancreatitis in this population. Disclosure: Dr Simon Bruce-Employee and stockholder of Amylin Pharmaceuticals Dr Jaret Malloy-Employee and stockholder of Amylin Pharmaceuticals Dr Colleen Burns-Employee and stockholder of Amylin Pharmaceuticals Dr Lisa Porter-Employee and stockholder of Amylin Pharmaceuticals. This research was supported by an industry grant from Amylin Pharmaceuticals.TableTable

Pancreatic enzyme elevation in chronic myeloid leukemia patients treated with nilotinib after imatinib failure

An increase in the serum concentration of pancreatic enzymes (amylase and lipase) was reported in a proportion of imatinib-resistant and/or intolerant Philadelphia-positive chronic myeloid leukemia patients treated with nilotinib. Acute pancreatitis was very rare, and the relevance of these laboratory alterations remains unknown. We report on 8 chronic myeloid leukemia patients who developed serum lipase/amylase elevation during treatment with nilotinib. After a median follow-up of 26 months, none of these patients developed an acute pancreatitis or clinical signs of pancreatic disease. Pancreatic hyperenzymemia never led to permanent drug discontinuation and required nilotinib temporary interruption in one case only. The median cumulative duration of dose interruptions and response to treatment were comparable in patients with or without pancreatic enzyme elevation. The mechanisms of action of nilotinib on pancreatic enzymes deserves to be investigated: however, in our experience, the relevance of pancreatic hyperenzymemia was clinically very limited.

Pancreatic response in healthy dogs fed diets of various fat compositions

To indirectly assess the pancreatic response in healthy dogs that were fed diets of different fat compositions with or without supplemental pancreatic enzymes and medium-chain triglycerides (MCTs). 10 healthy adult dogs. Dogs were fed 4 diets once in random order at 1-week intervals; food was withheld from the dogs for > or = 12 hours prior to the feeding of each diet. Diets A and B contained 16% and 5% crude fat, respectively; diet C was composed of diet A with pancreatic enzymes; and diet D was composed of diet B with pancreatic enzymes and MCTs. Serum canine trypsin-like immunoreactivity (cTLI) and canine pancreatic lipase immunoreactivity (cPLI) concentrations were measured before (0 hours) and at 1 to 2 and 6 hours after feeding. Serum gastrin concentration was measured at 0 hours and at 5 to 10 minutes and 1 to 2 hours after feeding. A gastrin assay validation study was performed to confirm accuracy of test results in dogs. Data were analyzed by use of a repeated-measures general ANOVA. Serum cTLI, cPLI, or gastrin concentrations in the dogs did not differ among the different diets fed, among dogs, or over time. When multiple comparisons were analyzed, diet D caused the least amount of measurable pancreatic response, although this difference was not significant. Results did not indicate a significant effect of dietary fat content or addition of supplemental MCT oil or pancreatic enzymes in diets on serum cTLI, cPLI, or gastrin concentrations in healthy dogs.

EFFECTS OF ORAL AND PARENTERAL FEEDING ON PANCREATIC ENZYME CONTENTS

Journal Article Effects of Oral and Parenteral Feeding on Pancreatic Enzyme Contents Get access Nutrition Reviews, Volume 33, Issue 6, June 1975, Pages 187–188, https://doi.org/10.1111/j.1753-4887.1975.tb05100.x Published: 01 June 1975

Serum TNF-Alpha Levels in Acute and Chronic Pancreatitis

Aim: Acute and chronic pancreatitis are inflammations of pancreatic tissue which have systemic effects and clinical presentations such as bacteremia and septic shock. Inflammatory markers have growing importance in diagnosis and identification of the severity of the pancreatitis. We aimed to determine TNF-alpha levels in acute and chronic pancreatitis and evaluate the relation between TNF-alpha levels and the pancreatic enzyme concentrations in two forms of the disease. Methods: 13 patients with acute pancreatitis, 36 patients with chronic pancreatitis and 14 healthy controls were included to our study. TNF-alpha determinations were performed with ELISA method. Results: TNF-alpha concentrations were 13.30±4.42 (7.04-21.35) pg/ml and 9.88±4.68 (3.99-27.73) pg/ml 10.09±1.01 (8.69-14.96) pg/ml in patients with acute and chronic pancreatitis and healthy controls respectively. TNF-alpha concentrations were significantly higher in patients with acute pancreatitis than the patients with chronic pancreatitis. But there was no significant difference between healthy controls and patients with either acute or chronic pancreatitis for TNF-alpha levels. There was no significant correlation between TNF-alpha concentrations and pancreatic enzyme levels. Conclusion: We concluded that in acute pancreatitis TNF-alpha levels were higher than the chronic form of the disease. But its concentrations did not correlate with the severity of the disease. By investigation of the other inflammatory markers and acute phase reactants with TNF-alpha, this process will be more clarified.

Elevated serum amylase and lipase in pediatric diabetic ketoacidosis*

Pancreatic enzyme concentrations are frequently elevated in children with diabetic ketoacidosis (DKA). We sought to determine the clinical and biochemical characteristics associated with patients with these elevations. Our hypothesis was that pancreatic enzyme elevations would be associated with biochemical markers of hypoperfusion. Prospective cohort study. Three university-affiliated children's hospitals. We collected data on consecutive children <18 yrs of age hospitalized with the diagnosis of DKA. Serum electrolyte and lactate concentrations and venous pH and Pco2 were measured every 3 hrs from hours 0 to 12 and then every 6 hrs until hour 24. Serum calcium, phosphate, and magnesium concentrations were measured every 6 hrs from hours 0 to 24. Serum amylase, lipase, and triglyceride concentrations were measured at hour 0 and then 12, 24, and 48 hrs after the initiation of therapy. We performed multivariable analyses to test for associations between clinical variables and pancreatic enzyme elevation in 67 children with DKA. Lipase was elevated in 21 (31%) and amylase in 16 (24%) of the children. Pancreatic enzyme values peaked 12-24 hrs after admission. There was no significant correlation between pancreatic enzyme elevation and abdominal pain. In multivariable analyses, an elevated blood urea nitrogen (BUN) concentration was associated with elevated serum amylase (odds ratio 1.04 per unit increase; 95% confidence interval, 1.01-1.09; p = .02), and elevated BUN concentrations and hypophosphatemia were associated with elevated serum lipase (odds ratio 1.04 per unit increase; 95% confidence interval, 1.00-1.08; p = .04; and odds ratio 0.35 per unit increase; 95% confidence interval, 0.15-0.81; p = .01, respectively). Elevation of pancreatic enzymes is common in children with DKA, but clinical pancreatitis is rare. Pancreatic enzyme levels reach a peak 12-24 hrs after initiation of treatment for DKA. Pancreatic enzyme elevation is associated with increased BUN concentrations at presentation but is not associated with abdominal pain.

Spontane Milzruptur bei chronischer Pankreatitis

A 50-year-old woman complained of upper abdominal pain for several weeks, getting worse and radiating towards the left shoulder in the 24 hours preceding her hospital admission. Plain X-ray film of the abdomen revealed plaque-like calcifications projecting onto the tail of the pancreas. Ultrasound imaging demonstrated splenic rupture with free intra-abdominal fluid. During an emergency laparotomy the spleen was removed. At first the postoperative course was uneventful. But epigastric pain recurred a few days after discharge. Serum amylase and lipase concentrations were elevated (280 U/l and 553 U/l, respectively). Endoscopic retrograde cholangiopancreatography revealed chronic pancreatitis with a 3 cm pseudocyst in the tail of the pancreas. A papillotomy was performed, after which the symptoms rapidly regressed and the pancreatic enzyme concentrations fell. This was thus a case of spontaneous splenic rupture associated with previously undiagnosed chronic pancreatitis with inflammatory papillary stenosis and pseudocyst in the pancreatic tail.

A Case of Fulminant Type 1 Diabetes with Pulmonary Hypertension

Some patients with idiopathic type 1 diabetes have a fulminant disorder characterized by the absence of insulitis and of diabetes-related antibodies, a remarkably abrupt onset and high serum pancreatic enzyme concentrations. This is referred to as fulminant type 1 diabetes. Cardiopulmonary disorders are rarely observed around the onset of fulminant type 1 diabetes. A 51-ye ar-old woman suffering from nausea and vomiting was transferred to our hospital. Laboratory findings r evealed high blood glucose level and the evidence of diabetic ketoacidosis, but the serum HbA1c was normal nevertheless. The low level of plasma C-peptide indicated the loss of endogenous insulin secretion. T he patient satisfied the criteria for the diagnosis of fulminant type 1 diabetes. Electrocardiogram (ECG) revealed nonspecific ST-T-wave abnormalities. Transthoracic echocardiogram demonstrated that she had severe pulmonary hypertension and minimal pericardial effusion. In a week, pulmonary hypertension improved to mild degree without specific treatment. Acute myocarditis was suspected based upon flulike symptoms, nonspecific ST-T-wave abnormalities, minimal pericardial effusion and asymptomatic pulmonary hypertension. We considered it worthwhile reporting this case because fulminant type 1 diabete s with acute myocarditis has never been published yet. (J Kor Diabetes Assoc 31:444~450, 2007)

Morphological studies of graft pancreatitis following pancreas transplantation.

Morphological findings in the initial stages of graft pancreatitis were studied systematically in sequential biopsies of 16 human pancreatic allografts. In 14 patients clinical and morphological signs of graft pancreatitis developed in the early postoperative period. In all cases disturbances in the integrity of structures within acinar cells occurred during ischaemia. In ten cases activation of autophagocytosis occurred following reperfusion, with acceleration of cellular metabolism. After reperfusion a marked leucocyte reaction occurred with a later single acinar cell necrosis in six cases. At the same time, high serum pancreatic enzyme concentrations were observed in all patients following transplantation. Exocrine secretion from the allografts via the pancreatic duct was reduced, correlating with the severity of graft pancreatitis. Studies in this clinical situation might complement analyses of the cascade of morphological and pathophysiological reactions during the early stages of other types of acute pancreatitis.

Induced Growth and Maturation of the Gastrointestinal Tract After Phaseolus vulgaris Lectin Exposure in Suckling Rats

In mammals, the postnatal development of the gastrointestinal tract is characterized by vast structural and functional changes. Using a suckling rat model, we investigated whether red kidney bean lectin, phytohemagglutinin (PHA), a potent gut mitogen in adult rats, can accelerate the growth and maturation of the gastrointestinal tract. At either 10 or 14 days of age, suckling rats were daily gavage fed with PHA (0.05 mg/g body weight) or saline for 3 days. At 1 or 3 days after this treatment, gastrointestinal organ growth, intestinal morphology, disaccharidase pattern, macromolecular absorption capacity, and pancreatic enzyme contents were studied. After PHA exposure, increased small intestinal growth and number of crypt cells were observed, whereas the proportion of enterocytes with supranuclear vacuoles in the distal intestine was decreased. The macromolecular absorption of the markers bovine immunoglobulin (Ig)G and bovine serum albumin and plasma levels of maternal IgG decreased, and intestinal disaccharidases switched toward an adult-like pattern. The pancreas weight and pancreatic protein and trypsin contents increased. These changes were partly reversible when the PHA treatment began at 10 days of age, but they persisted when the treatment began at 14 days of age. PHA induced enhanced growth and precocious functional maturation of the gastrointestinal tract in suckling rats. The effects persisted if the PHA treatment started at 14 days of age, but not before, suggesting an age dependent mechanism. These findings may lead to a better understanding of gastrointestinal maturation and constitute a basis for the treatment of mammals having an immature gut.

Procena stepena maturacije zida pseudociste pankreasa u odnosu na izbor operativne procedure

The aim of this study is to present our experience in the diagnosis and treatment of pancreatic pseudocysts. A pancreatic pseudocyst is an incapsulated collection of pancreatic juice, enclosed by nonepithelial elements, containing a high concentration of pancreatic enzymes, bicarbonates and necrotic detritus. It is a common complication of acute pancreatitis and trauma of the pancreas. In the period between 1996 and 2001, 53 surgical procedures were performed for pancreatic pseudocyst at the Institute for Digestive Diseases (First Surgical University Hospital), 35 male patients (67%) and 17 female patients (33%) underwent surgery. In 39 (75%) patients the method of choice was cystojejunostomy by Roux. In 4 cases distal pancreatectomy for pseudocysts localized within the pancreatic tail was performed, complete pseudocyst excision only was performed in one case and complete pseudocyst excision combined with cystojejunostomy was also performed in one case. Cystogastrostomy and drainage in one case and partial cystectomy and drainage also in one case. Surgical internal drainage is the method of choice for the treatment of pancreatic pseudocysts, involving low morbidity and mortality rates.