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Pancreatic Enzymes (pancreatic + enzyme)

Distribution by Scientific Domains

Medical Sciences	100%

Terms modified by Pancreatic Enzymes

pancreatic enzyme secretion

pancreatic enzyme supplementation

Selected Abstracts

Pancreatic Enzymes and Microvascular Cell Activation in Multiorgan Failure

MICROCIRCULATION, Issue 1 2001
GEERT W. SCHMID-SCHÖNBEIN
ABSTRACT Cell activation in the microcirculation leads to an inflammatory cascade and is accompanied by many cardiovascular complications. There is a need to identify the trigger mechanisms that lead to the production of in vivo activating factors. We review here mechanisms for cell activation in the microcirculation and specifically the production of humoral cell activators in physiological shock. The elevated levels of activating factors in plasma could be traced to the action of pancreatic enzymes in the ischemic intestine. New interventions against the production of the activators are proposed. The evidence suggests that pancreatic enzymes in the ischemic intestine may attack several tissue components and generate cellular activators that are associated with multiorgan dysfunction in physiological shock. [source]

Systematic review: efficacy and safety of pancreatic enzyme supplements for exocrine pancreatic insufficiency

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2010
J. R. TAYLOR
Summary Background, Pancreatic enzyme supplements are standard therapy for fat malabsorption in patients with exocrine pancreatic insufficiency. The FDA determined that published data are insufficient to support the efficacy and safety of these agents. Aim, To determine if pancreatic enzyme supplements are: (i) superior to placebo for treating fat malabsorption and (ii) superior to other supplements based on randomized cross-over trials. Methods, A computer-assisted search of MEDLINE and EMBASE was performed to identify relevant studies. Data extraction on study design, improvement in coefficient of fat absorption, diarrhoea and adverse events using prespecified forms. Results, A total of 12 manuscripts met inclusion criteria. Most studies (10/12) compared pancreatic enzyme supplements that used different delivery systems, while using similar quantities of enzymes. These studies found no consistent difference in fat malabsorption or gastrointestinal symptoms between different active treatments. Two small placebo-controlled trials (n = 65 patients) demonstrate that pancreatic enzyme supplements are superior to placebo for fat absorption. Data are inadequate to determine if pancreatic enzyme supplements lead to weight gain or improvement in diarrhoea. Conclusions, Based on data from randomized cross-over trials, pancreatic enzyme supplements appear to improve fat malabsorption. No specific branded product or specific delivery system is superior for treatment of fat malabsorption in patients with exocrine pancreatic insufficiency. [source]

Systematic review: pancreatic enzyme treatment of malabsorption associated with chronic pancreatitis

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2009
A. K. WALJEE
Summary Background, Pancreatic enzyme supplementation is standard treatment for malabsorption caused by chronic pancreatitis. The FDA recently required all manufacturers to submit New Drug Applications to continue to market these agents because published data demonstrated variation in formulation, bioavailability and shelf-life while providing limited data about efficacy and safety. Aim, To review systematically the design and results of randomized, parallel-design trials of pancreatic enzyme supplements in chronic pancreatitis patients with steatorrhea. Methods, A computer-assisted search of MEDLINE and EMBASE was performed to identify relevant studies. Two authors performed duplicate data extraction on study design, improvement in coefficient of fat absorption (CFA), diarrhoea and adverse events using pre-specified forms. Agreement between investigators for data extraction was greater than 95%. Results, Of 619 articles found through literature searching, 20 potentially relevant articles were identified and four manuscripts met inclusion criteria. No studies performed head-to-head comparisons of different supplements. Enzyme supplementation is more likely to improve CFA compared with placebo, but fat malabsorption remained abnormal. Important differences in patient population, study endpoint, study design, pancreatic enzyme dosage and measurement of CFA were present across trials, which precluded comparison of different agents. Conclusions, Enzyme supplementation improves CFA compared to placebo, but may not abolish steatorrhoea. [source]

Inhibition of endogenous pancreatic enzyme secretion by oral pancreatic enzyme treatment

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2003
J. Walkowiak
Abstract Background ,The existence of a feedback mechanism for exocrine pancreatic secretion in humans is controversial. Exclusion of proteases from the duodenum stimulates exocrine pancreatic secretion. Conversely, addition of exogenous enzymes could reduce the enzyme secretion. Further investigation of the feedback mechanism should be performed under the most physiological conditions. In the present study we investigated exocrine pancreatic function by measuring fecal enzyme output in healthy volunteers consuming a normal diet, before and during a time course of exogenous pancreatic enzyme supplementation. Material and methods ,Twenty-five healthy subjects (HS) were given two different doses (30 and 60 FIP proteases kg,1 d,1) divided by the number of meals. In all subjects, fecal elastase-1 (E1) concentrations and chymotrypsin (ChT) activities were measured without and with enzyme supplements after 7 days of treatment. In eight subjects, E1 concentrations and ChT activities were measured daily for 10 consecutive days. The subjects were given a dose regimen of 100 FIP proteases kg,1 d,1 (divided by the number of meals) for the first 7 days. Results ,Oral pancreatic treatment dose-dependently inhibited endogenous pancreatic secretion measured with the use of E1 concentrations. In both regimen groups, the differences were statistically significant. The exogenous enzymes, which interfere with colorimetric method for ChT, dose-dependently increased ChT output. However, only the higher dose resulted in a statistically significant difference. In the subgroup of eight HS, time-dependent changes of fecal enzyme output occurred with a decrease of E1 concentrations and an increase of ChT activity from the second up to eighth or ninth day of the experiment. Conclusion ,Exogenous applied pancreatic enzymes, dose- and time-dependently inhibited endogenous pancreatic secretion. The obtained results strongly support the existence of a protease mediated feedback mechanism in humans. [source]

Monitoring 6-thioguanine nucleotide concentrations in Japanese children and adolescents with inflammatory bowel disease

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2010
Yoshikazu Ohtsuka
Abstract Background and Aim:, 6-Mercaptopurine (6-MP) and azathioprine (AZA) are widely used as maintenance therapy in children with inflammatory bowel disease (IBD). However, proper 6-thioguanine nucleotide (6-TGN) concentrations in Japanese children with IBD have not been reported. Methods:, This retrospective review examines 32 ulcerative colitis (UC) patients and 19 Crohn's disease (CD) patients (12.87 ± 3.56 years) who required 6-MP or AZA to maintain disease remission. All patients were treated with 6-MP or AZA for at least 3 weeks prior to this study in addition to previous treatment. 6-MP dose, 6-TGN levels, assayed by high-performance liquid chromatography, as well as laboratory data were evaluated. Results:, Thirty-five children were successfully kept in remission with 6-MP and AZA therapy after weaning off corticosteroids. Overall, 123 measurements (59 active disease, 64 in remission) were analyzed. The mean 6-TGN concentration of the entire study population was 499.61 ± 249.35 pmol/8 × 108 red blood cell. The mean 6-MP dose in patients with active disease (0.910 ± 0.326 mg/kg per day) was significantly higher than for patients in remission (0.749 ± 0.225) (P = 0.0016). A significant inverse correlation was found between white blood cell counts and 6-TGN concentrations (r = 0.275, P < 0.002). Two patients experienced leukopenia with alopecia, and four transiently experienced increased serum levels of pancreatic enzymes, although no thiopurine S-methyl transferase mutations were confirmed. Conclusion:, The doses of 6-MP or AZA needed to maintain remission in Japanese children with IBD are lower than those reported in Western countries. However, 6-TGN concentrations in this population are higher than previously reported. [source]

Reconstruction of the pancreatic duct after pancreaticoduodenectomy: A modification of the Whipple procedure

JOURNAL OF SURGICAL ONCOLOGY, Issue 1 2001
Stylianos Katsaragakis MD
Abstract Background and Objectives: Pancreaticoduodenectomy is still associated with high morbidity and mortality even though there has been significant progress in the field of pancreatic surgery and postoperative follow-up. The pancreatoenteric anastomosis, regardless of the technique used, is a major cause for both morbidity and mortality after Whipple procedure. To overcome all problems resulting from anastomotic leakage, we used external drainage of the pancreatic duct. Methods: In 24 patients who underwent pancreaticoduodenectomy in our Department from 1986 to 1995, a modification to the standard Whipple procedure was performed. Instead of pancreaticoenteric anastomosis, external drainage of the pancreatic duct remnant was performed. The pancreatic duct was intubated with a silastic tube, the external end of which was sutured to the skin. All patients received substitution therapy with pancreatic enzymes. Results: Mortality in our group of patients was 4%. No complications due to the external drainage of the pancreatic duct were reported, while no patient developed diabetes mellitus after surgery. Conclusions: External drainage of the pancreatic duct remnant can be used alternatively to pancreatoenteric anastomosis after pancreatoduodenectomy. The technique is safe and simple to perform and appears to reduce overall operative time. It may be an option for patients with significant comorbidity and/or intraoperative hemodynamic instability which mandates expeditious completion of the operation. J. Surg. Oncol. 2001; 77:26,29. © 2001 Wiley-Liss, Inc. [source]

Review article: pain and chronic pancreatitis

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 7 2009
J. G. LIEB II
Summary Background, Pain in chronic pancreatitis chronic pancreatitis is a frustrating and challenging symptom for both the patient and clinician. It is the most frequent and most significant symptom. Many patients fail the currently available conservative options and require opiates or endoscopic/surgical therapy. Aim, To highlight the pathophysiology and management of chronic pancreatitis pain, with an emphasis on recent developments and future directions. Methods, Expert review, utilizing in addition a comprehensive search of PubMed utilizing the search terms chronic pancreatitis and pain, treatment or management and a manual search of recent conference abstracts for articles describing pain and chronic pancreatitis. Results, Pancreatic pain is heterogenous in its manifestations and pathophysiology. First-line medical options include abstinence from alcohol and tobacco, pancreatic enzymes, adjunctive agents, antioxidants, and non-opiate or low potency opiate analgesics. Failure of these options is not unusual. More potent opiates, neurolysis and endoscopic and surgical options can be considered in selected patients, but this requires appropriate expertise. New and better options are needed. Future options could include new types of pancreatic enzymes, novel antinociceptive agents nerve growth factors, mast cell-directed therapy, treatments to limit fibrinogenesis and therapies directed at the central component of pain. Conclusions, Chronic pancreatitis pain remains difficult to treat. An approach utilizing conservative medical therapies is appropriate, with more invasive therapies reserved for failure of this conservative approach. Treatment options will continue to improve with new and novel therapies on the horizon. [source]

Pancreatic Enzymes and Microvascular Cell Activation in Multiorgan Failure

The Pancreas as a Source of Cardiovascular Cell Activating Factors

MICROCIRCULATION, Issue 3 2000
ERIK B. KISTLER
ABSTRACT Objective: Physiological shock leads to elevated levels of plasma factors that activate circulating leukocytes and endothelial cells, thereby compromising microvascular functions. The nature and source of these plasma-derived activators are unknown. To examine the possible origin of these factors, we homogenized rat internal organs and measured their activity on cardiovascular cells in vivo and in vitro. Methods: Fresh tissue samples from small intestine, spleen, heart, liver, kidney, adrenals, and pancreas were homogenized. Their ability to induce leukocyte pseudopod formation and nitroblue tetrazolium (NBT) reduction was tested and their impact in vivo on blood pressure, survival, and microvascular cell injury was examined. Results: A dramatic increase (p < 0.001) in leukocyte activation compared to controls was observed with pancreas homogenate but not with homogenates from the other organs. Leukocyte activation was induced by homogenates of other tissues only after prior incubation with substimulatory concentrations of pancreatic homogenate. Pancreatic serine proteases, trypsin and chymotrypsin, which did not stimulate leukocytes, also generated activity from other tissues. Leukocyte pseudopod formation could be significantly inhibited by adding the serine protease inhibitor 6-amidino-2-naphthyl p -guanidinobenzoate dimethanesulfonate (ANGD) during tissue homogenization (p < 0.001). Injection of pancreatic homogenate into rats led to increased plasma hydrogen peroxide levels and an instantaneous drop in mean arterial pressure that was often lethal. These responses were prevented by prior infusion of ANGD (p < 0.001). Intravital microscopy of the rat mesentery confirmed that superfusion of filtered pancreatic homogenate leads to significant increases in cell death (p < 0.05), as detected by propidium iodide, and hydrogen peroxide formation (p < 0.05), as determined by dichlorofluorescein diacetate (DCFH) fluorescence. Conclusion: These results suggest that pancreatic enzymes attack tissue and generate cellular activators that are associated with organ dysfunction in shock. [source]

Neonatal diabetes mellitus because of pancreatic agenesis with dysmorphic features and recurrent bacterial infections

PEDIATRIC DIABETES, Issue 3pt1 2008
Doris Taha
Abstract:, Pancreatic agenesis is a rare cause of neonatal diabetes mellitus (NDM). It can be associated with malformations of the heart, the biliary tract, and the cerebellum. We report an infant with NDM because of pancreatic agenesis, intra-uterine growth retardation, dysmorphic features, and recurrent bacterial infections. He was born to healthy consanguineous parents. With adequate replacement of insulin and pancreatic enzymes, his blood glucose levels were controlled and his weight slowly increased. However, he continued to develop recurrent serious bacterial infections and died at the age of 11 months with sepsis and respiratory failure. Analysis of the PTF1A and PDX1 genes, which have been associated with congenital agenesis of the pancreas, did not reveal any mutation. Genetic abnormalities of chromosome 6 associated with transient neonatal diabetes as well as mutations in the KCNJ11 and ABCC8 genes encoding the pancreatic potassium channel were also excluded as a cause of the NDM in this patient. The association of permanent neonatal diabetes because of pancreatic agenesis, dysmorphism, and non-specific immunodeficiency is previously undescribed and may represent a new possibly autosomal recessive syndrome. [source]

Acute pancreatic damage associated with convulsive status epilepticus: A report of three cases

PSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 6 2001
Katsuhiko Ogawa
Abstract Three cases involving a previously unreported association of acute pancreatic damage following convulsive status epilepticus (SE) are presented. A review of literature failed to reveal a similar association between SE and acute pancreatic damage. As possible pathophysiological mechanisms of this so far unknown sequel of SE, increased intraduodenal pressure during SE leading to the reflux of the duodenal contents into the pancreatic duct, along with altered metabolism of oxygen-derived free radicals during a prolonged seizure with hypoxia and ischemia resulting in acinar cell injury are suggested. We believe that SE should be considered as an additional risk factor of acute pancreatitis and that pancreatic enzymes should be monitored in patients who have prolonged seizures. [source]

Effect of fat digestion on superior mesenteric artery blood flow in humans

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 1 2007
T. Symersky
Summary Background and aim:, Intraluminal nutrients stimulate superior mesenteric artery (SMA) blood flow. Of the macronutrients, especially fat affects the magnitude of the SMA blood flow response to a meal. Little is known however on the influence of fat hydrolysis on SMA flow. Methods:, We compared in eight healthy volunteers the SMA flow response (Doppler ultrasonography) to continuous intraduodenal fat perfusion (LCT, 240 kCal h,1) during conditions with normal hydrolysis (placebo, control), increased hydrolysis (pancreatic enzyme supplementation; 50 kU lipase) and impaired hydrolysis (orlistat 240 mg). Results:, Intraduodenal LCT significantly (P<0·01) increased SMA flow in all experiments over basal. The SMA flow response to fat during pancreatic enzyme supplementation (1·49 ± 0·1 l min,1) was significantly (P<0·05) higher compared with placebo (1·11 ± 0·16 l min,1). Lipase inhibition with orlistat did not significantly affect fat stimulated SMA flow compared with placebo: 0·89 ± 0·08 l min,1 versus 1·11 ± 0·16 l min,1. Conclusions:, Administration of pancreatic enzymes significantly increases fat stimulated SMA flow. Fat digest products in the intestinal lumen contribute to the regulation of SMA blood flow. [source]

The effect of equicaloric medium-chain and long-chain triglycerides on pancreas enzyme secretion

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 5 2002
T. Symersky
Summary It has been shown previously that medium chain triglycerides (MCT) do not affect gallbladder emptying and cholecystokinin (CCK) release. The effect of MCT on exocrine pancreas secretion in humans is unknown. We have compared the effect of enteral administration of MCT versus long chain triglycerides (LCT) on exocrine pancreatic secretion. Eight healthy subjects (three female, five male; mean age 22 ± 1·9 years) participated in two experiments, performed in random order. Duodenal contents, obtained by aspiration, were used to calculated the output of pancreatic enzymes and bilirubin. An equicaloric amount of either MCT or LCT (2 kcal min,1) oil was continuously administered in the proximal jejunum for 2 h. Gallbladder volume was measured by ultrasonography and blood samples were drawn for determination of CCK. The experiments consisted of 1 h basal secretion, 2 h of continuous oil administration and 1 h poststimulation. During the LCT feeding the pancreatic enzyme secretion, bilirubin output, gallbladder emptying and CCK release increased significantly (P<0·05) over basal levels. MCT had no effect on pancreatic enzyme secretion nor gallbladder emptying or CCK release. We conclude that enteral administration of MCT in the proximal jejunum does not stimulate exocrine pancreatic secretion nor gallbladder contraction or CCK release, in contrast to an equicaloric amount of LCT. [source]

A pitfall in screening with decoy cells after simultaneous pancreas kidney transplantation

CLINICAL TRANSPLANTATION, Issue 6 2008
L.R. Lard
Abstract:, In this report, we describe a bladder-drained simultaneous pancreas-kidney transplant (SPKT) recipient with a polyoma virus-associated nephropathy (PVAN) in whom the urine cytology failed to detect decoy cells despite repeated attempts. Several tests were performed to confirm our hypothesis that pancreatic enzymes can degrade decoy cells and granulocytes. This case illustrates an important pitfall in the urinary screening for PVAN with cytology and for urinary tract infections with urine sediment in bladder-drained SPKT recipients. [source]