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Pancreatic Insufficiency (pancreatic + insufficiency)
Kinds of Pancreatic Insufficiency Selected AbstractsBreed Associations for Canine Exocrine Pancreatic InsufficiencyJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2007Daniel J. Batchelor Background:Knowledge of breed associations is valuable to clinicians and researchers investigating diseases with a genetic basis. Hypothesis:Among symptomatic dogs tested for exocrine pancreatic insufficiency (EPI) by canine trypsin-like immunoreactivity (cTLI) assay, EPI is common in certain breeds and rare in others. Some breeds may be overrepresented or underrepresented in the population of dogs with EPI. Pathogenesis of EPI may be different among breeds. Animals:Client-owned dogs with clinical signs, tested for EPI by radioimmunoassay of serum cTLI, were used. Methods:In this retrospective study, results of 13,069 cTLI assays were reviewed. Results:An association with EPI was found in Chows, Cavalier King Charles Spaniels (CKCS), Rough-Coated Collies (RCC), and German Shepherd Dogs (GSD) (all P < .001). Chows (median, 16 months) were younger at diagnosis than CKCS (median, 72 months, P < .001), but not significantly different from GSD (median, 36 months, P= .10) or RCC (median, 36 months, P= .16). GSD (P < .001) and RCC (P= .015) were younger at diagnosis than CKCS. Boxers (P < .001), Golden Retrievers (P < .001), Labrador Retrievers (P < .001), Rottweilers (P= .022), and Weimaraners (P= .002) were underrepresented in the population with EPI. Conclusions and Clinical Implications: An association with EPI in Chows has not previously been reported. In breeds with early-onset EPI, immune-mediated mechanisms are possible or the disease may be congenital. When EPI manifests later, as in CKCS, pathogenesis is likely different (eg, secondary to chronic pancreatitis). Underrepresentation of certain breeds among dogs with EPI has not previously been recognized and may imply the existence of breed-specific mechanisms that protect pancreatic tissue from injury. [source] The chemotaxis defect of Shwachman-Diamond Syndrome leukocytesCYTOSKELETON, Issue 3 2004Vesna Stepanovic Abstract Shwachman-Diamond Syndrome (SDS) is a rare autosomal recessive, multisystem disorder presenting in childhood with intermittent neutropenia and pancreatic insufficiency. It is characterized by recurrent infections independent of neutropenia, suggesting a functional neutrophil defect. While mutations at a single gene locus (SBDS) appear to be responsible for SDS in a majority of patients, the function of that gene and a specific defect in SDS neutrophil behavior have not been elucidated. Therefore, employing 2D and 3D computer-assisted motion analysis systems, we have analyzed the basic motile behavior and chemotactic responsiveness of individual polymorphonuclear leukocytes (PMNs) of 14 clinically diagnosed SDS patients. It is demonstrated that the basic motile behavior of SDS PMNs is normal in the absence of chemoattractant, that SDS PMNs respond normally to increasing and decreasing temporal gradients of the chemoattractant fMLP, and that SDS PMNs exhibit a normal chemokinetic response to a spatial gradient of fMLP. fMLP receptors were also distributed uniformly through the plasma membrane of SDS PMNs as in control PMNs. SDS PMNs, however, were incapable of orienting in and chemotaxing up a spatial gradient of fMLP. This unique defect in orientation was manifested by the PMNs of every SDS patient tested. The PMNs of an SDS patient who had received an allogenic hematopoietic stem cell transplant, as well as PMNs from a cystic fibrosis patient, oriented normally. These results suggest that the defect in SDS PMNs is in a specific pathway emanating from the fMLP receptor that is involved exclusively in regulating orientation in response to a spatial gradient of fMLP. This pathway must function in parallel with additional pathways, intact in SDS patients, that emanate from the fMLP receptor and regulate responses to temporal rather than spatial changes in receptor occupancy. Cell Motil. Cytoskeleton 57:158,174, 2004. © 2004 Wiley-Liss, Inc. [source] Exocrine pancreatic insufficiency and malnutrition after gastrointestinal surgeryHPB, Issue 2009Christos Dervenis No abstract is available for this article. [source] Pancreatic enzyme replacement therapy: exocrine pancreatic insufficiency after gastrointestinal surgeryHPB, Issue 2009J. Enrique Domínguez-Muñoz Abstract Exocrine pancreatic insufficiency (EPI) and resultant maldigestion occurs in up to 80% of patients following gastric, duodenal or pancreatic surgery. Accurate diagnosis is required to determine the appropriate intervention, but the conventional method of faecal fat quantification is time-consuming and not always readily available. The optimized 13C-mixed triglyceride (13C-MTG) breath test is an accurate alternative post-surgery. Pancreatic enzyme replacement therapy (PERT) is indicated post-surgery in patients with clinically evident steatorrhoea, weight loss or maldigestion-related symptoms. Given its favourable safety profile, PERT is also appropriate in asymptomatic patients with high faecal fat excretion as such patients are at high risk for nutritional deficits. However, published data evaluating PERT in this setting are limited. Uncoated powder preparations may be preferred in cases of low gastric acidity and partial or total gastric resection. In clinical studies, enteric-coated microspheres were associated with greater weight gain after surgery vs. uncoated preparations. This was confirmed in a recent study using the 13C-MTG breath test; fat absorption increased from <40% without therapy to almost 60% with enteric-coated minimicrospheres (40 000 lipase units/meal), with >60% of patients achieving normal breath test results (i.e. normal fat digestion) during PERT. A therapeutic algorithm for the treatment of EPI after surgery is also discussed. [source] Exocrine pancreatic insufficiency as an end stage of pancreatitis in four dogsJOURNAL OF SMALL ANIMAL PRACTICE, Issue 7 2003P. J. Watson Chronic pancreatitis is a common cause of exocrine pancreatic insufficiency (EPI) in humans and cats but is rarely recognised in dogs in which pancreatic acinar atrophy (PAA) is reportedly more common. This paper describes four dogs which developed EPI secondary to pancreatitis. Two of the dogs also had diabetes mellitus which developed before EPI. One diabetic dog had concurrent hyperadrenocorticism and was euthanased five months after presentation; the other diabetic dog died 48 months after diagnosis. The remaining dogs were alive 78 and 57 months after diagnosis. The number of affected dogs was comparable to the number of cases of presumed PAA seen over the same time period in the same institution. Chronic pancreatitis may be a more common cause of EPI in dogs than previously assumed and may be under-recognised because of difficulties in diagnosis. The relative importance of chronic pancreatitis as a cause of canine diabetes mellitus remains to be ascertained. [source] Systematic review: efficacy and safety of pancreatic enzyme supplements for exocrine pancreatic insufficiencyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2010J. 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] Breed Associations for Canine Exocrine Pancreatic InsufficiencyJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2007Daniel J. Batchelor Background:Knowledge of breed associations is valuable to clinicians and researchers investigating diseases with a genetic basis. Hypothesis:Among symptomatic dogs tested for exocrine pancreatic insufficiency (EPI) by canine trypsin-like immunoreactivity (cTLI) assay, EPI is common in certain breeds and rare in others. Some breeds may be overrepresented or underrepresented in the population of dogs with EPI. Pathogenesis of EPI may be different among breeds. Animals:Client-owned dogs with clinical signs, tested for EPI by radioimmunoassay of serum cTLI, were used. Methods:In this retrospective study, results of 13,069 cTLI assays were reviewed. Results:An association with EPI was found in Chows, Cavalier King Charles Spaniels (CKCS), Rough-Coated Collies (RCC), and German Shepherd Dogs (GSD) (all P < .001). Chows (median, 16 months) were younger at diagnosis than CKCS (median, 72 months, P < .001), but not significantly different from GSD (median, 36 months, P= .10) or RCC (median, 36 months, P= .16). GSD (P < .001) and RCC (P= .015) were younger at diagnosis than CKCS. Boxers (P < .001), Golden Retrievers (P < .001), Labrador Retrievers (P < .001), Rottweilers (P= .022), and Weimaraners (P= .002) were underrepresented in the population with EPI. Conclusions and Clinical Implications: An association with EPI in Chows has not previously been reported. In breeds with early-onset EPI, immune-mediated mechanisms are possible or the disease may be congenital. When EPI manifests later, as in CKCS, pathogenesis is likely different (eg, secondary to chronic pancreatitis). Underrepresentation of certain breeds among dogs with EPI has not previously been recognized and may imply the existence of breed-specific mechanisms that protect pancreatic tissue from injury. [source] In vitro comparative study of three pancreatic enzyme preparations: dissolution profiles, active enzyme release and acid stabilityALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2008A. ALOULOU Summary Background, Various pancreatic enzyme preparations are used for the treatment of pancreatic insufficiency but their bioequivalence is often unknown. Aim, To determine in vitro the pH-dependent release and acid resistance of enzymes from three commercially available pancreatin capsules, two containing enteric-coated (Creon 25000; Eurobiol 25000) and one uncoated (Eurobiol 12500) microspheres. Methods, Dissolution experiments were performed at pH values ranging from 4.0 to 5.8. Lipase, chymotrypsin and amylase activities were measured in the solution as a function of time. Results, Eurobiol 25000 started to release its enzymes significantly at pH 5.0 (t1/2 = 71 min), whereas the enzymes from Creon 25000 were only released at higher pH value (5.4; t1/2 = 49.2 min). Unlike chymotrypsin, lipase and amylase were highly sensitive to acidic conditions at the lowest pH values tested. Both enzymes were also found to be sensitive to proteolytic inactivation at the highest pH values tested. Overall, Eurobiol 25000 released higher amounts of active amylase and lipase than Creon 25000 at the pH values usually found in duodenal contents. The uncoated Eurobiol 12500 preparation was, however, the only one that could immediately release rather high levels of active chymotrypsin and lipase at low pH (4.5). Conclusion, These findings suggest that pH-sensitive enteric-coated pancreatin products containing similar amounts of enzymes might not be bioequivalent depending on the pH of duodenal contents. [source] 24 Electrogastrography EGG in pancreas diabetesNEUROGASTROENTEROLOGY & MOTILITY, Issue 6 2006E SCHAFER Background:, Timing and criteria of testing for gastric dysmotility in pancreatic diabetes is not well established. Aim:, To investigate the pattern of EGG and autonomic neuropathy (AN) in patients with pancreas diabetes mellitus to clarify the relationship between autonomic neuropathy, alcohol consumption, glucose homeostasis, diabetes duration, and EGG. Patients and methods:, Thirty patients with pancreas diabetes mellitus were enrolled into the study. Mean duration of diabetes mellitus was 11 (0,25) years, mean blood glucose levels: 8.13 ± 2.7 mmoll,1, HbA1c 8.3 ± 2.96%; 25/30 patients were treated with insulin, the others were on rigorous diet, all of them received high dose pancreatin substitution therapy. Ten matched controls without diabetes and pancreatic insufficiency were also examined. AN was evaluated by the cardiovascular reflex tests according to the Ewing's criteria (Diab. Care 8 (5): 491,497, 1985.), EGG was monitored for 30,30 min in both fasting and in postprandial states, using a Digitrapper EGG (Synectic Med., Stockholm). EGG rhythm disturbances (bradygastria: 0,2 cpm, tachygastria: 4,10 cpm) and meal evoked EGG signal amplitude (power) changes were determined. Results:, 9/30 pts had mild to moderate parasympathetic AN, 1/30 pts had sympathetic AN, 5/30 pts had both parasympathetic and sympathetic AN; 17/30 pts demonstrated myoelectric abnormalities: 5/30 pts had predominant bradygastria, 3/30 tachygastria, and in other 9/30 pts only an absence of increase in the postprandial signal amplitude was found. Overall, 7/30 pts with abnormal EGG did not demonstrated AN. Abnormal EGG showed no correlation with actual blood sugar values or HbA1c, but it was associated with diabetes duration more than 10 years. Conclusion:, Our results suggest that beside neuropathy other factors such as alcohol toxicity, sympathetic and parasympathetic imbalance or long-term inappropriate glucose metabolism may be involved in the gastric myoelectric abnormalities provoked by pancreas diabetes. [source] Acute Oxalate Nephropathy Causing Late Renal Transplant Dysfunction Due to Enteric HyperoxaluriaAMERICAN JOURNAL OF TRANSPLANTATION, Issue 8 2008A. C. Rankin Calcium oxalate (CaOx) deposition in the renal allograft is an under recognized and important cause of acute tubular injury and early allograft dysfunction. We present a case of late transplant dysfunction due to acute oxalate nephropathy. The patient presented with diarrhea and deteriorating graft function, and a diagnosis of enteric hyperoxaluria secondary to pancreatic insufficiency was made. This had occurred, as the patient had been noncompliant with his pancreatic enzyme replacement therapy. Treatment to reduce his circulating oxalate load was initiated, including twice-daily hemodialysis, low fat and oxalate diet and appropriate administration of pancreatic enzyme supplements. Graft function subsequently recovered. The possibility of fat malabsorption leading to enteric hyperoxaluria should be considered in renal graft recipients presenting with loose stools and graft dysfunction. [source] Liver disease as risk factor for cystic fibrosis-related diabetes developmentACTA PAEDIATRICA, Issue 5 2007L Minicucci Abstract Aim: To evaluate clinical and genetic factors, besides pancreatic insufficiency, associated with increased risk of cystic fibrosis-related diabetes. Methods: Case-control (1:1) study on 138 cystic fibrosis patients. Data were collected on gender, age at diagnosis, reason for cystic fibrosis diagnosis, family history of type 1 or 2 diabetes mellitus, pre-existing severe liver disease, and class of cystic fibrosis transmembrane regulation mutation. Moreover, information was obtained on lung involvement and degree of exocrine pancreatic insufficiency evaluated 1 year before the diagnosis of cystic fibrosis-related diabetes in patients and age-matched controls. Results: Compared to controls, patients with cystic fibrosis-related diabetes had a higher probability of having already been diagnosed with liver disease (16.7% versus 1.7%, OR = 11.6, 95% CI 1.43,93.0). Moreover, in the year before diabetes onset, cases had slightly worse pulmonary function compared to controls (FEV1= 58.4 ± 27% predicted versus 67.4 ± 21% predicted; p = 0.05). No significant effects related to the other factors considered were found. Conclusion: Severe liver disease was found to significantly increase the risk of developing cystic fibrosis-related diabetes. Patients with liver disease should be scheduled for earlier diabetes screening in order to identify and possibly treat glucose intolerance. [source] | ||||||||||