Serum Pancreatic Enzymes Research Articles

Diagnosing acute pancreatitis in children: What is the diagnostic yield and concordance for serum pancreatic enzymes and imaging within 96 h of presentation?

Background/objectivesThere are limitations and challenges with the diagnosis of acute pancreatitis (AP) in children. We evaluated the diagnostic yield and concordance for serum pancreatic enzymes and imaging in children with AP. MethodsA retrospective review of laboratory and radiographic results within 96 h of AP presentation (January 2000–July 2011) was performed at two paediatric hospitals. Observed agreement and kappa statistics (κ) were determined between outcomes of bloods (lipase and/or amylase) and imaging (ultrasound (US) and/or computed tomography (CT)). ResultsA total of 103/131 (79%) AP cases had both bloods and imaging performed (within 96 h). Overall, lipase, amylase, US and CT were consistent with an AP diagnosis in 93% (93/100), 54% (43/80), 27% (21/77) and 67% (28/42) of cases respectively. The diagnostic yield for combinations of blood(s) and imaging(s) tests was higher than any single test and blood tests alone. The observed agreement between bloods ‘lipase or amylase’ and imaging ‘US or CT,’ was 40%. The κ was −0.083 suggesting no agreement. In 55% of cases, enzymes were positive whilst imaging was negative and the converse was evident in 5% of cases. There was no agreement between the various diagnostic tests, except between amylase and US, which had fair agreement. ConclusionElevations in serum lipase contributed to the diagnosis more often than other tests. Combinations of blood(s) and imaging(s) tests have an increased diagnostic yield. Serum enzyme elevation and imaging changes poorly correlated. At least 5% of cases of AP may be missed if imaging is not performed.

Mo1344 Diagnosing Acute Pancreatitis in Children: What Is the Diagnostic Yield and Concordance for Serum Pancreatic Enzymes and Imaging?

Mo1344 Diagnosing Acute Pancreatitis in Children: What Is the Diagnostic Yield and Concordance for Serum Pancreatic Enzymes and Imaging?

Utility of serum pancreatic enzyme levels in diagnosing blunt trauma to the pancreas: A prospective study with systematic review

IntroductionReliability of serum pancreatic enzyme levels in predicting pancreatic injuries has been a parameter of interest and the present recommendations on its utility are based primarily on anecdotal observations. The aim of this study was to evaluate the utility of serum pancreatic enzyme assessment in predicting blunt pancreatic injury with imaging and surgical correlation and compare our results with a systematic review of literature till date. MethodsA prospective cohort study conducted over 4 years in a tertiary care referral centre with 164 consecutive patients who presented to the emergency department with a history of blunt abdominal trauma and had serum pancreatic enzyme assessment, USG and subsequent diagnostic CECT were analyzed. The CT findings and AAST grade of pancreatic injury, various intra-abdominal injuries and time elapsed since injury and other associated factors were correlated with serum pancreatic enzyme levels. For systematic review of literature MEDLINE database was searched between 1940 and 2012, also the related citations and bibliographies of relevant articles were analyzed and 40 articles were included for review. We compared our results with the systematic critique of literature till date to formulate recommendations. Results33(21%) patients had pancreatic injury documented on CT and were graded according to AAST. Statistically significant elevated serum amylase levels were observed in patients with pancreatic and bowel injuries. However, elevated serum lipase was observed specifically in patients with pancreatic injury with or without bowel injury. Combined serum amylase and lipase showed 100% specificity, 85% sensitivity in predicting pancreatic injury. Elevated (n=28, 85%) vs. normal (n=5, 15%) serum amylase and lipase levels showed sole statistically significant association with time elapse since injury to admission, with a cutoff of 3h. ConclusionsBased on our results and the systematic review of the literature till date we conclude, persistently elevated or rising combined estimation of serum amylase and lipase levels are reliable indicators of pancreatic injury and is time dependent, nondiagnostic within 6h or less after trauma. In resource constrained countries where CT is not available everywhere it may support a clinical suspicion of pancreatic injury and can be reliable and cost-effective as a screening tool.

A comprehensive predictive scoring method for difficult laparoscopic cholecystectomy

CONTEXT:Laparoscopic cholecystectomy (LC) is the gold standard cholecystectomy. LC is the most common difficult laparoscopic surgery performed by surgeons today. The factors leading to difficult laparoscopic cholecystectomy can be predicted.AIMS:To develop a scoring method that predicts difficult laparoscopic cholecystectomy.SETTINGS AND DESIGN:Bidirectional prospective study in a medical college setup.MATERIALS AND METHODS:Following approval from the institutional ethical committee, cases from the three associated hospitals in a medical college setup, were collected using a detailed proforma stating the parameters of difficulty in laparoscopic cholecystectomy. Study period was between May 10 and June 12. Preoperative, sonographic and intraoperative criteria were considered.STATISTICAL ANALYSIS USED:Chi Square test and Receiver Operater Curve (ROC) analysis.RESULTS:Total 323 patients were included. On analysis, elderly patients, males, recurrent cholecystitis, obese patients, previous surgery, patients who needed preoperative Endoscopic retrograde cholangiopancreatography (ERCP), abnormal serum hepatic and pancreatic enzyme profiles, distended or contracted gall bladder, intra-peritoneal adhesions, structural anomalies or distortions and the presence of a cirrhotic liver on ultrasonography (USG) were identified as predictors of difficult LC. A scoring system tested against the same sample proved to be effective. A ROC analysis was done with area under receiver operator curve of 0.956. A score above 9 was considered difficult with sensitivity of 85% and specificity of 97.8%.CONCLUSIONS:This study demonstrates that a scoring system predicting the difficulty in LC is feasible. There is scope for further refinement to make the same less cumbersome and easier to handle. Further studies are warranted in this direction.

Acute pancreatitis in children and adolescents.

In this Topic Highlight, the causes, diagnosis, and treatment of acute pancreatitis in children are discussed. Acute pancreatitis should be considered during the differential diagnosis of abdominal pain in children and requires prompt treatment because it may become life-threatening. The etiology, clinical manifestations, and course of acute pancreatitis in children are often different than in adults. Therefore, the specific features of acute pancreatitis in children must be considered. The etiology of acute pancreatitis in children is often drugs, infections, trauma, or anatomic abnormalities. Diagnosis is based on clinical symptoms (such as abdominal pain and vomiting), serum pancreatic enzyme levels, and imaging studies. Several scoring systems have been proposed for the assessment of severity, which is useful for selecting treatments and predicting prognosis. The basic pathogenesis of acute pancreatitis does not greatly differ between adults and children, and the treatments for adults and children are similar. In large part, our understanding of the pathology, optimal treatment, assessment of severity, and outcome of acute pancreatitis in children is taken from the adult literature. However, we often find that the common management of adult pancreatitis is difficult to apply to children. With advances in diagnostic techniques and treatment methods, severe acute pancreatitis in children is becoming better understood and more controllable.

High-Dose Intravenous Immunoglobulin (IVIG) Adjuvant Therapy for Cell-Mediated Pancreas Transplant Rejection

High-Dose Intravenous Immunoglobulin (IVIG) Adjuvant Therapy for Cell-Mediated Pancreas Transplant Rejection

EUS And s-MRCP Findings In Asymptomatic Subjects with Chronic Pancreatic Hyperenzymemia

Context A long-standing increase of serum pancreatic enzymes in asymptomatic subjects is considered a benign idiopathic condition called “non-pathological chronic pancreatic hyper­enzymemia” (CPH). However, recent studies showed secretin-MRCP (s-MRCP) has brought to light abnormal pancreatic findings in a significant proportion of these subjects. Objective To evaluate pancreatic morphological abnormalities using s-MRCP and EUS in CPH patients. Methods Consecutive patients affected by CPH were investigated with s-MRCP and EUS. EUS findings were compared with consecutive age- and sex-matched controls who underwent EUS investigation for unrelated to pancreaticobiliary disease (CTR). Results Fifty-five CPH subjects and 55 CTR patients were enrolled. Abnormal s-MRCP pancreatic findings were present in 23 CPH cases (41.8%): 10 chronic pancreatitis, according to Cambridge classification; 5 pancreas divisum; 3 pancreatic cyst; 5 Vater’s papilla dysfunction. Pathological EUS pancreatic findings were present in 28 CPH cases (50.9%): 7 pancreatic cystic lesion, 5 pancreas divisum, 1 papillitis, 1 NET, 14 chronic pancreatitis (CP) defined by presence of “consistent with CP” or “suggestive of CP” findings using Rosemont criteria. All cases of CP who undergone s-MRCP had pathological EUS findings suggestive for CP too. Normal EUS findings were more significantly frequent in control patients (n=45) than CPH patient (n=27) (P<0.05). The two groups have same frequencies in detection of cystic lesions, pancreas divisum, papillitis, NET, but chronic pancreatitis was more common in CPH (25.5% vs . 7.3%; P<0.05). Conclusions About half of the patients with asymptomatic chronic pancreatic hyper­enzymemia had some pancreatic abnormalities using s-MRCP and EUS. Both these procedures should characterize the diagnostic work-up of these subjects before the hyperenzymemia can be defined with certainly as non-pathological or benign.

A low-grade increase of serum pancreatic exocrine enzyme levels by dipeptidyl peptidase-4 inhibitor in patients with type 2 diabetes

A potential adverse effect of dipeptidyl peptidase-4 inhibitors (DPP-4i) on the pancreas remains controversial. We evaluated the DPP-4i effects on pancreatic amylase and lipase activity in patients with type 2 diabetes. These enzymes were slightly but significantly increased, suggesting DPP-4i cause a low-grade inflammatory change in the exocrine pancreas.

Nilotinib-Associated Acute Pancreatitis

To report a case of acute pancreatitis in a patient receiving nilotinib for chronic myelogenous leukemia (CML). A 69-year-old man recently diagnosed with chronic phase CML received nilotinib 300 mg twice daily and was admitted with acute pancreatitis that appeared the day after the first dose. The patient had normal levels of triglycerides and denied alcohol use. Serum pancreatic enzymes were within normal limits the day before nilotinib initiation. Abdominal computed tomography demonstrated a normal liver, bile duct without stones, and findings that were consistent with focal pancreatitis. The patient's history was significant for concomitant use of enalapril and simvastatin; both have been associated with pancreatitis, but the patient had been taking these medications for at least 5 years without adverse effects. Nilotinib was immediately discontinued. Abdominal pain resolved and serum pancreatic enzymes levels returned to normal 2 weeks later. One of the adverse effects of some tyrosine kinase inhibitors is increased levels of serum pancreatic enzymes. Accordingly, nilotinib labeling includes "high lipase levels in serum" as an adverse event. There are few case reports of acute pancreatitis associated with nilotinib in the literature and some are incomplete. We present a well-documented case of nilotinib-associated acute pancreatitis. Consistent with Badalov's new classification system for drug-induced acute pancreatitis and with the Naranjo probability scale, this case represents a possible adverse reaction of pancreatitis associated with nilotinib therapy. As rechallenge is unethical, treatment with nilotinib has not been resumed. This case demonstrates a possible association between acute pancreatitis and nilotinib use. Although a rare phenomenon, clinicians should be alert for signs and symptoms of pancreatitis, as treatment with nilotinib for CML is becoming more common.

Asymptomatic and Persistent Elevation of Pancreatic Enzymes in an Ulcerative Colitis Patient

Azathioprine has been extensively used in the management of inflammatory bowel diseases. It might cause pancreatic damage in the form of either asymptomatic elevation in serum amylase/lipase or overt acute pancreatitis. Here we report the case of a 61-year-old patient with ulcerative colitis who had been treated with azathioprine for three years, achieving clinical remission. During treatment he presented an asymptomatic elevation of serum pancreatic enzymes, without any signs of pancreatitis at imaging. This evidence brought us to reassess the drug dosage, without achieving a normalization of biochemical analysis. Autoimmune pancreatitis was excluded. One year after the suspension of azathioprine, we still face persistent high levels of amylase/lipase. Normalization of enzymatic values in patients who develop intolerance to azathioprine, in the form of either asymptomatic elevation in serum amylase/lipase or overt acute pancreatitis, is usually achieved in about two months after stopping drug intake. Asymptomatic elevation in serum pancreatic enzymes in the absence of pancreatic disease is reported in the literature and defined as “Gullo's syndrome,” but nobody of the subjects studied had been treated in the past with pancreatotoxic drugs. Might this case be defined as “benign pancreatic hyperenzymemia”?

Pancreatic duct drainage using EUS-guided rendezvous technique for stenotic pancreaticojejunostomy

The patient was a 30-year-old female who had undergone excision of the extrahepatic bile duct and Roux-en-Y hepaticojejunostomy for congenital biliary dilatation at the age of 7. Thereafter, she suffered from recurrent acute pancreatitis due to pancreaticobiliary maljunction and received subtotal stomach-preserving pancreaticoduodenectomy. She developed a pancreatic fistula and an intra-abdominal abscess after the operation. These complications were improved by percutaneous abscess drainage and antibiotic therapy. However, upper abdominal discomfort and the elevation of serum pancreatic enzymes persisted due to stenosis from the pancreaticojejunostomy. Because we could not accomplish dilation of the stenosis by endoscopic retrograde cholangiopancreatography, we tried an endoscopic ultrasonography (EUS) guided rendezvous technique for pancreatic duct drainage. After transgastric puncture of the pancreatic duct using an EUS-fine needle aspiration needle, the guidewire was inserted into the pancreatic duct and finally reached to the jejunum through the stenotic anastomosis. We changed the echoendoscope to an oblique-viewing endoscope, then grasped the guidewire and withdrew it through the scope. The stenosis of the pancreaticojejunostomy was dilated up to 4 mm, and a pancreatic stent was put in place. Though the pancreatic stent was removed after three months, the patient remained symptom-free. Pancreatic duct drainage using an EUS-guided rendezvous technique was useful for the treatment of a stenotic pancreaticojejunostomy after pancreaticoduodenectomy.

Effect of short‐term propofol administration on pancreatic enzymes and lipid biochemistry in children between 1 month and 36 months

Use of propofol in pediatric age group has been marred by reports of its adverse effects like hypertriglyceridemia and acute pancreatitis, although a causal relation has not yet been established. This prospective, clinical trial was carried out to evaluate the effects of short-term propofol administration on serum lipid profile and serum pancreatic enzymes in children of ASA physical status I and II aged between 1month and 36months. Anesthesia was induced with Propofol (1%) in the dose of 3mg·kg(-1) intravenously and was maintained by propofol infusion (0.5%) at the rate of 12mg·kg(-1·) h(-1) for the first 20min and at 8mg·kg(-1·) h(-1) thereafter. The mean dose of propofol administered was 12.02±2.75mg·kg(-1) (fat load of 120.2±27.5mg·kg(-1) ). Lipid profile, serum amylase, and lipase were measured before induction of anesthesia, at 90min, 4h, and finally 24h after induction. Serum lipase levels (P<0.05), serum triglyceride levels (P<0.05), and serum very low-density lipoproteins VLDL levels (P<0.05) were raised significantly after propofol administration from baseline although remained within normal limits. Serum cholesterol levels and serum low-density lipoproteins LDL levels showed a statistically significant fall over 24h. No significant changes in serum pancreatic amylase levels were seen (P>0.05). None of the patients developed any clinical features of pancreatitis in the postoperative period. We conclude that despite a small, transient increase in serum triglycerides and pancreatic enzymes, short-term propofol administration in recommended dosages in children of ASA status I and II aged between 1month and 36months does not produce any clinically significant effect on serum lipids and pancreatic enzymes.

The results of the Tokyo Trial of Prevention of Post-ERCP Pancreatitis with Risperidone (Tokyo P3R): a multicenter, randomized, phase II, non-placebo-controlled trial

A previous study suggested that ulinastatin effectively prevented post-ERCP pancreatitis (PEP) and hyperenzymemia (PEH) in patients at average risk. In experimental models, risperidone, a selective serotonin 2A antagonist, ameliorated acute pancreatitis. We assessed the effect of risperidone combined with ulinastatin for the prevention of PEP in high-risk patients. In a multicenter, randomized, controlled, phase II trial, patients undergoing therapeutic ERCP were randomly assigned to receive ulinastatin (150000U) with or without risperidone (1mg). A risperidone tablet was taken orally 30-60min before ERCP and ulinastatin was administered intravenously for 10min immediately prior to ERCP. The primary end point was the incidence of PEP; secondary end points were PEH severity and enzyme levels (amylase, pancreatic amylase, lipase). A total of 226 patients (113 per group) were included in the study. Six patients in the risperidone+ulinastatin group and ten patients in the ulinastatin group developed pancreatitis (5.3 vs. 8.8%, p=0.438). The incidence of moderate/severe PEP was lower in the risperidone+ulinastatin group (1.8%) than in the ulinastatin group (4.4%), but this difference was not significant. Although the incidence of PEH did not differ significantly, post-ERCP levels of all pancreatic enzymes were significantly lower in the risperidone+ulinastatin group. Prophylactic oral risperidone administration in combination with ulinastatin did not reduce the incidence and severity of PEP in high-risk patients as compared with ulinastatin alone. However, risperidone showed an additive effect with ulinastatin, reducing serum pancreatic enzyme levels.

Lipemic Arthropathy Simulating Septic Arthritis in a Patient with Severe Necrotizing Pancreatitis: A Case Report

Background: Necrotizing pancreatitis is a severe inflammatory systemic disease with effects beyond the pancreas. Steatonecrosis from the pancreatic lipase released secondary to pancreatic inflammation has been reported in the literature. Pancreatic arthritic syndrome with pancreatitis, arthritis, subcutaneous nodules and presence of fat necrosis has been described. It has been associated with poorer prognosis. We report a case of lipemic arthropathy simulating septic arthritis in a patient with severe necrotizing pancreatitis. Case: A 53-year-old Caucasian gentleman with past medical history of Crohn's disease, post-renal transplant secondary to end stage renal disease, hepatitis C, hypertension and hyperlipidemia presented to our institution with severe abdominal pain, nausea, vomiting and hypotension. Biochemical abnormalities are consistent with acute pancreatitis and acute renal failure. The episode of pancreatitis was presumed to be secondary to pentasa. The patient required aggressive supportive therapy in the intensive care setting. The patient gradually improved throughout the subsequent days with improved renal function and hemodynamic stability. Ten days after initial presentation, he reported left-sided knee pain. He was initially treated symptomatically; however, he developed a moderate size effusion and worsening pain. Rheumatology was consulted and joint aspiration was performed. The fluid was chlyous in nature and analysis revealed the presence of fat globules and a WBC count of 14,000 with 85% segs. No crystals were noted. On microscopy, few polys were noted. Gram stain and culture remained negative. Patient was initiated on prednisone taper with noted improvement and was discharged to rehabilitation center. Conclusion: Pancreatitis is a diffuse inflammatory disease and can precipitate fat necrosis with varying manifestations. Various case reports describing such scenarios with fat necrosis involving different organ systems have been published in the literature. The arthritis observed in patients with pancreatic disease and raised serum pancreatic enzymes may be associated with intraarticular fat necrosis and creamy synovial fluid. Fluid lipid analysis show raised levels of triglycerides and free fatty acids. Unlike septic arthritis, it is treated with steroid taper.Figure: [830]

Fulminant Type 1 diabetes in a pregnant woman as an initial manifestation of the insulin autoimmune syndrome

Fulminant Type 1 diabetes is a subtype of Type 1 diabetes characterized by (1) abrupt onset of diabetes, (2) very short duration of hyperglycaemia with mildly elevated HbA(1c) (< 69 mmol/mol, 8.5%), (3) rapid progression to diabetic ketoacidosis, (4) very low C-peptide level, and (5) often associated with elevated serum pancreatic enzymes, and absence of diabetes-related autoantibodies. We encountered a case of fulminant Type 1 diabetes that developed with an initial manifestation of the insulin autoimmune syndrome and rapidly progressed to diabetic ketoacidosis during pregnancy. A 31-year-old Korean woman presented with recurrent sudden onset of sweating and change of consciousness during sleep at 19 weeks gestation. During a 72-h fasting test, hypoglycaemia (1.72 mmol/l) occurred at 4 h after the start of the test. At that time, there was a high insulin level (370.2 μU/ml), a paradoxically low C-peptide level (0.01 nmol/l) and a positive insulin autoantibody test. An oral glucose tolerance test revealed postprandial hyperglycaemia. She was initially diagnosed as the insulin autoimmune syndrome. On the day 5 of admission, she developed diabetic ketoacidosis. Her HbA(1c) was 62 mmol/mol (7.8%). The rapid progression of diabetic ketoacidosis altered the diagnosis to fulminant Type 1 diabetes. This case differed from typical fulminant Type 1 diabetes because it presented with hypoglycaemia, and positive insulin and anti-phospholipid antibody tests. Her HLA typing was HLA-DQA1*0302, 0501, HLA-DRB1*0301 (DR3), 0901(DR9). Her glucose level was subsequently very well controlled with multiple insulin injections and she successfully delivered a healthy baby.

Low serum pancreatic enzyme levels predict mortality and are associated with malnutrition–inflammation–atherosclerosis syndrome in patients with chronic kidney disease

Serum levels of amylase and lipase are frequently increased in patients with chronic kidney disease (CKD). Relatively low serum pancreatic enzyme levels in CKD may represent a state of pancreatic insufficiency and may contribute to protein-energy wasting (PEW). We aimed to investigate the relationships of serum pancreatic enzyme levels with PEW, inflammation, and mortality in CKD patients. Two hundred and thirty CKD patients (male/female: 144/86; mean age, 59 ± 16 years) were enrolled. Serum total α-amylase and lipase activities were measured by enzymatic colorimetric assays. Mean follow-up time was 18 ± 10 months. Forty-seven patients (20 %) died during this period. Serum amylase levels were increased in 95 patients (41 %) and serum lipase levels were increased in 71 patients (30 %) out of the 230 patients. Diabetic patients had significantly lower serum amylase levels than non-diabetic ones (86 ± 46 vs. 111 ± 60 IU/L, p < 0.0001). Patients with ischemic heart disease also had significantly lower serum amylase (82 ± 37 vs. 108 ± 60 IU/L, p < 0.0001) and lipase levels (39 ± 36 vs. 57 ± 57 IU/L, p = 0.007). Serum amylase and lipase levels were directly correlated with serum creatinine (r = 0.173, p = 0.009 and r = 0.374, p < 0.0001) and albumin (r = 0.410, p < 0.0001 and 0.287, p < 0.0001), and inversely correlated with CRP (r = -0.223, p = 0.001 and r = -0.147, p = 0.027). The Kaplan-Meier analysis revealed survival advantages for both high-amylase and high-lipase groups in end-stage renal disease (ESRD) (CKD stage 5) patients (log rank, p < 0.001 and p = 0.02, respectively). In the Cox regression analysis, serum amylase was found to be an independent predictor for mortality. Serum amylase activity was found to be an independent predictor of mortality in ESRD patients. Relatively low serum pancreatic enzyme levels in CKD may be regarded as a novel component of the malnutrition-inflammation-atherosclerosis syndrome.

L-Asparaginase-Induced Pancreatic Injury is Associated with an Imbalance in Plasma Amino Acid Levels

BackgroundThe use of L-asparaginase (ASNase) to modify amino acid metabolism is one of the most effective chemotherapeutic means of inducing remission in acute lymphoblastic leukemia (ALL). However, severe pancreatitis sometimes occurs in patients receiving ASNase, because of an unknown mechanism.ObjectiveThe purpose of the present study was to evaluate the relationship between ASNase-induced pancreatic injury and plasma amino acid levels in patients undergoing ASNase therapy.MethodsA total of 29 children aged 1–13.25 years (median age 4 years; male:female ratio 19:10) with ALL, who received induction therapy according to the Tokyo Children’s Cancer Study Group L04–16 protocol, were studied. Levels of plasma amino acids and serum rapid turnover proteins (RTPs), pancreatic enzymes, and pancreatic protease inhibitors were measured before and 1, 2, 3, 4, 5, and 7 weeks after the first administration of ASNase.ResultsPlasma asparagine levels were significantly lower after the first injection of ASNase (p<0.01) and had almost recovered 2 weeks after the last ASNase injection. At 4 weeks after the first ASNase injection, serum aspartic acid, trypsin, and pancreatic secretory trypsin inhibitor (PSTI) levels remained significantly higher than those before the first ASNase injection (p<0.01), and serum levels of prealbumin and transferrin remained significantly lower than those before the first ASNase injection (p<0.01). Plasma amino acid and serum RTP levels gradually normalized after the last ASNase injection.ConclusionsLevels of serum trypsin and PSTI were elevated during the 2 weeks after administration of ASNase, which suggested the presence of subclinical pancreatitis. This period is similar to the time period in the present study when the levels of plasma amino acids changed, thus suggesting that ASNase-induced pancreatic injury could be caused by the imbalance of plasma amino acid levels.

L-Asparaginase-Induced Pancreatic Injury is Associated with an Imbalance in Plasma Amino Acid Levels

BackgroundThe use of L-asparaginase (ASNase) to modify amino acid metabolism is one of the most effective chemotherapeutic means of inducing remission in acute lymphoblastic leukemia (ALL). However, severe pancreatitis sometimes occurs in patients receiving ASNase, because of an unknown mechanism.ObjectiveThe purpose of the present study was to evaluate the relationship between ASNase-induced pancreatic injury and plasma amino acid levels in patients undergoing ASNase therapy.MethodsA total of 29 children aged 1–13.25 years (median age 4 years; male:female ratio 19:10) with ALL, who received induction therapy according to the Tokyo Children’s Cancer Study Group L04–16 protocol, were studied. Levels of plasma amino acids and serum rapid turnover proteins (RTPs), pancreatic enzymes, and pancreatic protease inhibitors were measured before and 1, 2, 3, 4, 5, and 7 weeks after the first administration of ASNase.ResultsPlasma asparagine levels were significantly lower after the first injection of ASNase (p<0.01) and had almost recovered 2 weeks after the last ASNase injection. At 4 weeks after the first ASNase injection, serum aspartic acid, trypsin, and pancreatic secretory trypsin inhibitor (PSTI) levels remained significantly higher than those before the first ASNase injection (p<0.01), and serum levels of prealbumin and transferrin remained significantly lower than those before the first ASNase injection (p<0.01). Plasma amino acid and serum RTP levels gradually normalized after the last ASNase injection.ConclusionsLevels of serum trypsin and PSTI were elevated during the 2 weeks after administration of ASNase, which suggested the presence of subclinical pancreatitis. This period is similar to the time period in the present study when the levels of plasma amino acids changed, thus suggesting that ASNase-induced pancreatic injury could be caused by the imbalance of plasma amino acid levels.

Prospective Evaluation of Subjects With Chronic Asymptomatic Pancreatic Hyperenzymemia

Chronic asymptomatic pancreatic hyperenzymemia (CAPH) has been described since 1996 as a benign disease. Recent studies described pathological findings at magnetic resonance cholangiopancreatography with secretin stimulation (s-MRCP) in more than half of the CAPH subjects. The aim of this study was to investigate the frequency and clinical relevance of s-MRCP findings in patients with CAPH. Subjects prospectively enrolled from January 2005 to December 2010 underwent s-MRCP and biochemical tests routinely performed. Data relative to 160 subjects (94 males, 66 females, age 49.6±13.6 years) were analyzed. In all, 51 (32%) subjects had hyperamylasemia, 9 (6%) hyperlipasemia, and 100 (62%) an increase in both enzyme levels. The time between the first increased dosage of serum pancreatic enzymes and our observation was 3.3±3.9 years (range: 1-15). Familial pancreatic hyperenzymemia was observed in 26 out of 133 subjects (19.5%). Anatomic abnormalities of the pancreatic duct system at s-MRCP were found in 24 out of 160 subjects (15%). Pathological MRCP findings were present in 44 subjects (27.5%) before and in 80 subjects (50%) after secretin administration (P<0.0001). Five subjects (3.1%) underwent surgery, 3 for pancreatic endocrine tumor, 1 for pancreatic adenocarcinoma, and 1 for intraductal papillary-mucinous neoplasia (IPMN) involving the main pancreatic duct, and 18 patients (11.3%) needed a follow-up (17 for IPMN and 1 for endocrine tumor). Alterations of the pancreatic duct system at s-MRCP in subjects with CAPH can be observed in 50% of the subjects and are clinically relevant in 14.4% of cases.

Pancreaticoportal Fistula and Disseminated Fat Necrosis After Revision of a Transjugular Intrahepatic Portosystemic Shunt

A 59-year old man with alcohol related cirrhosis and portal hypertension was referred for transjugular intrahepatic portosystemic shunt (TIPS) to treat his refractory ascites. Ten years later, two sequential TIPS revisions were performed for shunt stenosis and recurrent ascites. After these revisions, he returned with increased serum pancreatic enzyme levels and disseminated superficial fat necrosis; an iatrogenic pancreaticoportal vein fistula caused by disruption of the pancreatic duct was suspected. The bare area of the TIPS was subsequently lined with a covered stent-graft, and serum enzyme levels returned to baseline. In the interval follow-up period, the patient has clinically improved.