Effect of early enteral nutrition support for the management of acute severe pancreatitis: A protocol of systematic review.

BACKGROUND: This study aims to assess the effect of early enteral nutrition support (EENS) for the management of acute severe pancreatitis (ASP). METHODS: This study will search Cochrane Library, PUBMED, EMBASE, Cumulative Index to Nursing and Allied Health Literature, Allied and Complementary Medicine Database, CNKI, and WANGFANG from their inception to the present without language limitations. In addition, this study will also search clinical trial registry and reference lists of included trials. Eligible comparators will be standard care, medications, and any other interventions. Two authors will independently scan all citations, titles/abstracts, and full-text studies. The study methodological quality will be appraised using Cochrane risk of bias tool. If it is possible, we will pool out data and perform meta-analysis. Strength of evidence for each main outcome will be evaluated using the Grading of Recommendations Assessment, Development, and Evaluation. RESULTS: This study will summarize the most recent evidence to assess the effect of EENS for the management of ASP. CONCLUSION: The findings of this study will help to determine whether EENS is effective for patients with ASP. STUDY REGISTRATION: INPLASY202070009.

Omega-3 fatty acid exposure with a low-fat diet in patients with past hypertriglyceridemia-induced acute pancreatitis; an exploratory, randomized, open-label crossover study.

BACKGROUND: Omega-3 fatty acids (OM3-FAs) are recommended with a low-fat diet for severe hypertriglyceridemia (SHTG), to reduce triglycerides and acute pancreatitis (AP) risk. A low-fat diet may reduce pancreatic lipase secretion, which is required to absorb OM3-ethyl esters (OM3-EEs), but not OM3-carboxylic acids (OM3-CAs). METHODS: In this exploratory, randomized, open-label, crossover study, 15 patients with SHTG and previous AP were instructed to take OM3-CA (2 g or 4 g) and OM3-EE 4 g once daily for 4 weeks, while adhering to a low-fat diet. On day 28 of each treatment phase, a single dose was administered in the clinic with a liquid low-fat meal, to assess 24-h plasma exposure. Geometric least-squares mean ratios were used for between-treatment comparisons of baseline (day 0)-adjusted area under the plasma concentration versus time curves (AUC0-24) and maximum plasma concentrations (Cmax) for eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). RESULTS: Before initiating OM3-FA treatment, mean baseline fasting plasma EPA + DHA concentrations (nmol/mL) were 723 for OM3-CA 2 g, 465 for OM3-CA 4 g and 522 for OM3-EE 4 g. At week 4, mean pre-dose fasting plasma EPA + DHA concentrations increased by similar amounts (+ 735 - + 768 nmol/mL) for each treatment. During the 24-h exposure assessment (day 28), mean plasma EPA + DHA increased from pre-dose to the maximum achieved concentration by + 32.7%, + 45.8% and + 3.1% with single doses of OM3-CA 2 g, OM3-CA 4 g and OM3-EE 4 g, respectively. Baseline-adjusted AUC0-24 was 60% higher for OM3-CA 4 g than for OM3-EE 4 g and baseline-adjusted Cmax was 94% higher (both non-significant). CONCLUSIONS: Greater 24-h exposure of OM3-CA versus OM3-EE was observed for some parameters when administered with a low-fat meal at the clinic on day 28. However, increases in pre-dose fasting plasma EPA + DHA over the preceding 4-week dosing period were similar between treatments, leading overall to non-significant differences in baseline (day 0)-adjusted AUC0-24 and Cmax EPA + DHA values. It is not clear why the greater 24-h exposure of OM3-CA versus OM3-EE observed with a low-fat meal did not translate into significantly higher pre-dose fasting levels of DHA + EPA with longer-term use. TRIAL REGISTRATION: ClinicalTrials.gov, NCT02189252, Registered 23 June 2014.

Nutrition Interventions in Pediatric Pancreatitis: Guidelines We Can Trust.

OBJECTIVE: Despite the fact that pediatric pancreatitis is an uncommon disease, its prevalence has increased in recent years. Nevertheless, until 4 years ago, the lack of nutritional guidelines for pediatric pancreatitis was evident, with all recommendations being based on clinical practice guidelines (CPGs) for adults. The aim of the present study was to review and critically appraise guidelines for the medical nutrition therapy (MNT) of pediatric pancreatitis. METHODS: A comprehensive search was performed in electronic databases (PubMed, Scopus, National Institute for Health and Care Excellence), the International Guidelines Network, BMJ best practice, and the Scottish Intercollegiate Guidelines Network to identify CPGs on the MNT of pediatric pancreatitis. The validated AGREE II tool was used for guidelines appraisal by a team of 3 independent multidisciplinary reviewers. RESULTS: A total of 4 CPGs were retrieved with pediatric pancreatitis MNT information. Out of the 4 advising bodies in total, the joint society paper published by the ESPGHAN/NASPGHAN received the highest score in almost all domains, whereas the Belgian consensus obtained the lowest score in all domains but stakeholder involvement, and was not recommended by 2 out of 3 reviewers. CONCLUSIONS: Pediatric pancreatitis guidelines appear heterogenous in quality, rigour, and transparency. Our study points out existing gaps and biases in the CPGs, and delineates the need for improving the domains identified as being of low-quality.

Dietary pomegranate supplement alleviates murine pancreatitis by modulating Nrf2-p21 interaction and controlling apoptosis to survival switch.

Dietary supplementation of polyphenol-rich pomegranate extract (POMx) has been shown to have anti-oxidant and anti-inflammatory activities. Here, we evaluate the efficacy of POMx in mitigating pancreatitis in mice and provide a mechanistic outline of the process. Age-matched male Swiss albino mice were injected with Lipopolysaccharide (LPS) and given POMx supplement alone or in combination with LPS. After 4 weeks of treatment histological scoring for pancreatic edema and vacuolization was performed. Serum insulin levels were estimated and the glucose tolerance test (IPGTT) data revealed that POMx reduced inflammation induced hyperglycemia in mice. Analysis of TLR4, IκB expression, and NF-κB nuclear translocation, and concentrations of IL-6 and TNFα showed that POMx is able to modulate the molecular instigators of inflammatory responses. Annexin V assay indicated that POMx protects against inflammation-mediated apoptosis in the pancreas. Expression profile of SAPK/JNK pathway, p53, Bax, Bcl-2 and Caspase-3 validate an apoptotic to survival shift in POMx treatment group. Co-immunoprecipitation studies show that POMx stabilizes p21 and Nrf2 interaction and increases its nuclear translocation. The study also proves that the nuclear fraction of Nrf2 is able to bind to the Bcl-2 promoter and activate an anti-apoptotic program. The findings of our study underline an anti-inflammatory, anti-oxidative and anti-apoptotic role of POMx and provide a mechanistic idea of how POMx confers protection during pancreatitis.

Guidance for supplemental enteral nutrition across patient populations.

Enteral nutrition is preferred over parenteral nutrition as a result of the greater safety of enteral nutrition therapy and comparative convenience. A wide variety of enteral nutrition products have been developed, including disease-specific products to help manage the nutritional needs of patients with kidney failure, liver failure, lung disease, diabetes, and other conditions. An assessment of each patient's nutritional needs and digestive function should be conducted prior to initiation of enteral nutrition therapy. Other considerations in determining the appropriate route and method of enteral nutrition administration include the time and nursing involvement required for administration, potential complications of medication administration, and concerns related to pancreatic dysfunction in certain groups. Tailored guidelines and treatment considerations are reviewed in this manuscript the application of enteral nutrition in various patient populations.

[FATTY ACID COMPOSITION OF PHOSPHOLIPIDS AND ESTERIFIED CHOLESTEROL OF THE BLOOD PLASMA OF RABBIT UNDER ARGININE ACUTE PANCREATITIS].

The content and fatty acid composition of phospholipids and esterified cholesterol were studied in the blood plasma of rabbits under acute arginine pancreatitis and its correction using linseed oil. It is established that the transport and anti-inflammatory functions of blood plasma deteriorates under acute arginine pancreatitis due to a decrease of the content of polyunsaturated fatty acids in phospholipids. The amount of cholesterol esterified with saturated and monounsaturated fatty acids increases in the blood plasma of rabbits. The concentration of phospholipids and esterified cholesterol is normalized and their fatty acid composition is improved in the lipid composition of the blood plasma of rabbits with acute arginine pancreatitis fed with linseed oil.

Familial chylomicronemia syndrome and response to medium-chain triglyceride therapy in an infant with novel mutations in GPIHBP1.

BACKGROUND: Severe hypertriglyceridemia predisposes to attacks of acute pancreatitis, a serious condition complicated by multiorgan failure, pancreatic necrosis, and mortality rates up to 20% in adults and 6.5% in children. OVERVIEW: We describe an infant who suffered from an episode of acute pancreatitis from severe hypertriglyceridemia. Two major challenges complicate the case: identifying the etiology of severe hypertriglyceridemia and finding an efficacious treatment. A thorough history, physical examination, and laboratory workup failed to identify a clear etiology, prompting a genetic workup that identified compound heterozygous mutations in the glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1) gene. This patient's hypertriglyceridemia responded to an infant formula rich in medium chain triglycerides (MCTs), and she remained free of pancreatitis 6 months later. CONCLUSIONS: This case highlights the need to pursue a genetic evaluation in the absence of secondary causes of severe hypertriglyceridemia in infants. Patients with mutations in GPIHBP1 fail to respond to currently available lipid-lowering agents so dietary management-specifically, an extremely low-fat diet and supplementation with MCT-remains the cornerstone of therapy. Treatment in infants should focus on dietary measures rather than pharmacologic agents.

Factors associated with intolerance after refeeding in mild acute pancreatitis.

OBJECTIVES: This study aimed to describe the mode of refeeding, frequency of intolerance, and related factors in mild acute pancreatitis (AP). METHODS: We included all cases of mild AP between January 2007 and December 2009 in an observational, descriptive, and retrospective study. We analyzed demographic and etiological data, admission variables, treatment, refeeding mode, intolerance frequency, and treatment. Intolerance-related variables were determined using a Cox regression. RESULTS: Two-hundred thirty-two patients were included (median age, 74.3 years, bedside index for severity in AP score, 1). Oral diet was reintroduced at 3 days (range, 0-11 days) in 90.9% of cases with a liquid diet. Intolerance to refeeding appeared in 28 patients (12.1%) at a median time of 1 day (range, 0-14 days). Oral diet was reduced or suspended in 71.4%; analgesic and antiemetic drugs were required in 64% and 35.7% of patients, respectively. The variables independently associated with intolerance to refeeding were choledocholithiasis (hazard ratio [HR], 12.35; 95% confidence interval [CI], 2.98-51.19; P = 0.001), fasting time (HR, 1.33; 95% CI, 1.09-1.63; P = 0.005), refeeding with complete diet (HR, 4.93; 95% CI, 1.66-14.66; P = 0.04), length of symptoms before admission (HR, 1.004; 95% CI, 1.001-1.006; P = 0.012), and metamizole dose (HR, 1.11; 95% CI, 1.02-1.21; P = 0.014). CONCLUSIONS: Intolerance to refeeding is an infrequent event. We have identified several factors independently associated with intolerance.

Atualidades em terapia nutricional na pancreatite aguda / News in nutritional therapy in acute pancreatitis

Objetivo: investigar na literatura científica as atuais recomendações emterapia nutricional na pancreatite aguda.Método: revisão na literatura científica, com ênfase em diretrizes e artigosde revisões sistemáticas publicados nos anos de 2007 a 2012, em revistas indexadas em bases de dados virtuais. As palavras-chave utilizadas foram: pancreatite aguda, terapia nutricional, nutrição enteral, nutrição parenteral. Um total de três diretrizes e 14 artigos de revisões sistemáticas foram utilizados. Resultados: a dieta por via oral, recomendada para a pancreatite aguda leve, é baseada na tolerância digestiva sem grandes alterações. A terapia nutricional enteral, quando indicada, deve considerar o início precoce, infusão contínua, posicionamento da sonda enteral, tipo de fórmula, uso de fórmula hiperproteica, normoglicídica e normolipídica, uso de triglicerídeos de cadeia média e de ácidos graxos ômega-3. A indicação da via parenteral só deve ocorrer na impossibilidade do uso do trato digestivo para a oferta de nutrientes de forma total ou parcial, com a adoção de procedimentos envolvendo oferta de calorias (25-30kcal/kg/dia não protéicas) e proteínas (1,25 a 1,5g/kg/dia) que podem ser reduzidasconforme quadro clínico, de macronutrientes (glicose contribuindocom 50% a 70% do total de calorias e os lipídios correspondendo a 0,8 a 1,5g/kg/dia) e micronutrientes, além da suplementação com glutamina (dosagem superior a 0,3 g/kg/dia). Conclusão: enquanto a dieta via oral nos casos da pancreatite aguda leve não exige atenção criteriosa, o contrário ocorre em relação à nutricional artificial (enteral e parenteral) e esforços são necessários para o aperfeiçoamento dos procedimentos que devem ser respaldados pela literatura científica.

Objective: To investigate the scientific literature on the current recommendations nutritional therapy in acute pancreatitis. Method: Review the scientific literature, with an emphasis on guidelines and systematic reviews of articles published in the years 2007 to 2012 in journals indexed in virtual databases. The keywords used were: acute pancreatitis, nutritional therapy, enteral nutrition, parenteral nutrition. Atotal of 14 articles and three guidelines for systematic reviews were used.Results: The oral diet, is recommended for mild acute pancreatitis, digestivetolerance is based on without major changes. The enteral nutrition therapy, when indicated, should consider early, continuous infusion, placement of enteral feeding, formulae type, use of high protein formulae, and adequate in glucose and lipids, use of medium chain triglycerides and omega-3. The indication of the parenteral route shouldonly occur in the impossibility to use the digestive tract for the supply ofnutrients in whole or in part, with the adoption of procedures involvingsupply of calories (25-30kcal/kg/day non protein) and proteins (1,25 to1.5g/kg/day) can be reduced as clinical, nutrients (glucose contributing50% to 70% of total calories and lipids corresponding to 0.8 to 1.5g/kg/day) and micronutrients in addition to supplementation with glutamine(dosage greater than 0.3 g/kg/day).Conclusion: While the oral diet in cases of mild acute pancreatitis does not require careful attention, the opposite occurs in relation to artificial nutrition (enteral and parenteral) and efforts are needed to improve the procedures that must be supported by the scientific literature.

Drivers of oxidative stress in acute pancreatitis: the role of nutrition therapy.

Severe acute pancreatitis is a disease process distinguished by increasing oxidative stress and potential destruction of the pancreatic gland. An initial injury to the acinar cell initiates a sentinel event, which leads to a vicious cycle of inflammation and cell death by either apoptosis or necrosis. Whether the acute inflammation resolves or goes on to a pattern of chronicity may be related to genetic predisposition, failure to remove injurious agents, and innate systems for antioxidant defense. The degree to which nutrition therapy can modulate oxidative stress, maintain intestinal function, and preserve the structure of the acinar cell is truly amazing. Understanding the mechanisms involved in this complex disease process and the manner in which these mechanisms are influenced by dietary agents affords new and exciting therapeutic options for the future.

Acute pancreatitis in obesity: adipokines and dietary fish oil.

BACKGROUND: Acute pancreatitis is a substantial clinical problem accounting for 240,000 hospital admissions yearly in the United States. Obesity is epidemic and is clearly an independent risk factor for increased severity of acute pancreatitis (AP). Adipose tissue is an endocrine organ that secretes a variety of metabolically active substances termed adipokines. However, the role of adipokines in modulating acute pancreatitis severity remains incompletely understood. Dietary fish oil is rich in omega-3 free fatty acids and attenuates adipose tissue-induced inflammation. Therefore, we hypothesized that feeding obese mice diets rich in fish oil would alter the adipokine milieu and attenuate the severity of pancreatitis. METHODS: Lean (C57BL/6 J) and obese (LepDb) mice were fed either a soybean oil- or fish oil-rich diet for 4 weeks. AP was induced by six hourly intraperitoneal injections of cerulein (50 µg/kg). Serum adipokine levels were measured, and pancreatitis severity was assessed histologically and by measuring pancreatic concentrations of interleukin-1 beta (IL-1ß), interleukin-6 (IL-6), myleoperoxidase (MPO), and monocyte chemoattractant protein-1 (MCP-1). RESULTS: Obese mice developed more severe pancreatitis than lean mice. Fish oil significantly decreased serum leptin (lean and obese) and increased serum adiponectin (lean only). Fish oil did not alter the baseline pancreatic inflammatory milieu, nor did it change histologic or biochemical pancreatitis severity. CONCLUSION: These data demonstrate that a diet rich in fish oil altered the adipokine milieu in lean and congenitally obese mice; however, fish oil did not improve pancreatitis severity induced with cerulein hyperstimulation.

Hypertriglyceridemic acute pancreatitis during pregnancy: prevention with diet therapy and omega-3 fatty acids in the following pregnancy.

Acute pancreatitis complicating pregnancy is rare and has previously been associated with high mortality rates. We report a case of repeated hypertriglyceridemia during pregnancy. During the patient's first pregnancy, acute pancreatitis was elicited in the third trimester by pregnancy-induced hypertriglyceridemia. The patient was treated successfully with a conservative treatment course. The hypertriglyceridemia recurred during her second pregnancy. She carried the pregnancy to term without incident while maintaining a diet low in fat diet and high in omega-3 fatty acids. Early diagnosis and intensive treatment can help to preserve the lives of the patient and the fetus. Prophylactic diet therapy and omega-3 fatty acids may prevent recurrent hypertriglyceridemia during pregnancy.

What is the best way to feed patients with pancreatitis?

PURPOSE OF REVIEW: Patients with acute pancreatitis have traditionally been treated with 'bowel rest'. Recent data, however, suggest that this approach may be associated with increased morbidity and mortality. This paper reviews evolving concepts in the nutritional management of patients with acute pancreatitis. RECENT FINDINGS: Both experimental and clinical data strongly support the concept that enteral nutrition started within 24 h of admission to hospital reduces complications, length of hospital stay and mortality in patients with acute pancreatitis. Clinical trials suggest that both gastric and jejunal tube feeding is well tolerated in patients with severe pancreatitis. Although there is limited data for the optimal type of enteral feed, a semielemental formula with omega-3 fatty acids is recommended. On the basis of current evidence, immune modulating formulas with added arginine and probiotics are not recommended. SUMMARY: Nutritional support should be viewed as an active therapeutic intervention that improves the outcome of patients with acute pancreatitis. Enteral nutrition should begin within 24 h after admission and following the initial period of volume resuscitation and control of nausea and pain. Patients with mild acute pancreatitis should be started on a low-fat oral diet. In patients with severe acute pancreatitis, enteral nutrition may be provided by the gastric or jejunal route.

Repercusiones nutricionales y manejo de la pancreatitis crónica / Nutritional repercussions and management of chronic pancreatitis

El páncreas es un órgano retroperitoneal que segrega agua, bicarbonato y enzimas digestivos a través del conducto pancreático principal (CPP) al duodeno. La pancreatitis crónica (PC) está causada típicamente en el adulto por abuso crónico de alcohol, y, con menor frecuencia, hipertrigliceridemia, hiperparatiroidismo primario o fibrosis quística. La disfunción exocrina ocasiona malabsorción grasa y la consiguiente esteatorrea. El daño en la función endocrina es un hallazgo tardío que se presenta como hiperglucemia o diabetes mellitus franca. El cuidado de pacientes con PC conlleva, de forma primordial, el tratamiento del dolor. Un cambio significativo en su patrón o la aparición súbita y persistente de otros síntomas obligan a descartar otras entidades, incluyendo úlcera péptica, obstrucción biliar, pseudoquistes, cáncer de páncreas, estenosis de conductos pancreáticos o litiasis. Por tanto es importante asegurar el diagnóstico. El manejo del dolor debe realizarse de forma escalonada y prudente tratando de evitar la dependencia de opiáceos. Debe advertirse a los pacientes que interrumpan la ingesta de alcohol. El tratamiento de la mal absorcióngrasa comienza con pequeñas tomas de alimento y restricción grasa. El uso de suplementos de enzimas pancreáticos puede mejorar los síntomas y reducir la mala absorción en pacientes que no respondan al tratamiento dietético. Deben usarse dosis elevadas de enzimas con cada comida. Se recomienda tratamiento supresor dela acidez gástrica para evitar la inactivación de los enzimas. Puede ser necesaria la suplementación con triglicéridos de cadena media (MCT) y vitaminas liposolubles. El manejo de otras complicaciones (como pseudoquistes, obstrucción biliar o duodenal, ascitis pancreática, trombosis de la vena esplénica y pseusoaneurismas) con frecuencia requiere maniobras agresivas manteniendo al paciente bajo nutrición parenteral para minimizar la estimulación pancreática

The pancreas is a retroperitoneal organ that releaseswater, bicarbonate and digestive enzymes by the mainpancreatic duct (MPD) into the duodenum. Chronic pancreatitis (CP) is typically caused, in adults, by chronic alcohol abuse and, less frequently hypertriglyceridemia, primary hyperparathyroidism or chystic fibrosis. Exocrine dysfunction results in malabsorption of fat and subsequent steatorrhea. Damage to pancreatic endocrine function is a late finding in CP and results in hyperglycaemia or overt diabetes mellitus. Care of patients with CP principally involves management of pain. A significant change in the pain pattern or the sudden onset of persistent symptoms suggests the need to rule out other potentialetiologies, including peptic ulcer disease, biliaryobstruction, pseudocysts, pancreatic carcinoma, andpancreatic duct stricture or stones, then is important toestablish a secure diagnosis. Management of pain shouldthen proceed in a judicious stepwise approach avoidingopioids dependence. Patients should be advised to stopalcohol intake. Fat malabsorption and other complicationsmay also arise. Management of steatorrhea shouldbegin with small meals and restriction in fat intake. Pancreatic enzyme supplements can relieve symptoms andreduce malabsorption in patients who do not respond todietary restriction. Enzymes at high doses should be usedwith meals. Treatment with acid suppression to reduceinactivation of the enzymes from gastric acid are recommended. Supplementation with medium chain triglycerides and fat soluble vitamin replacement may be required. Management of other complications (such as pseudocysts, bile duct or duodenal obstruction, pancreatic ascites, splenic vein thrombosis and pseudoaneurysms)often requires aggressive approach with the patient kept on total parenteral nutrition to minimize pancreatic stimulation (AU)

Nutrición por sonda nasogástrica en la pancreatitis aguda grave / Nasogastric enteral nutrition in severe acute pancreatitis

Fundamento y objetivo: Valorar la tolerancia a la nutrición por sonda nasogástrica de los pacientes con pancreatitis aguda grave. Pacientes y método: Incluimos a 12 pacientes con pancreatitis aguda grave (3 o más criterios de Ranson; proteína C reactiva > 210 mg/dl) y evolución clínica desfavorable ingresados durante el año 2006. Una vez establecida la gravedad de la pancreatitis, se inició alimentación por sonda nasogástrica (10 F) con dieta polipeptídica pobre en grasas (Dietgrif®) mediante bomba de perfusión continua. Se valoraron la tolerancia a la dieta y las complicaciones. Resultados: La edad media (desviación estándar) de los pacientes (4 mujeres y 8 varones) era de 70 (11) años y la estancia media fue de 86 días (intervalo: 14-405 días). La etiología de la pancreatitis fue biliar en 8 casos, alcohólica en uno y desconocida en 3. Todos los pacientes desarrollaron complicaciones médicas y/o pancreáticas. Siete presentaban necrosis pancreática significativa en la tomografía computarizada. Tres ingresaron en la unidad de cuidados intensivos y 2 fallecieron. Ocho de los 12 pacientes (67%) toleraron perfectamente la dieta por sonda nasogástrica independientemente de sus complicaciones. En 3 hubo que interrumpir inicialmente la dieta por íleo paralítico y precisaron nutrición parenteral total de forma transitoria. Sólo en un caso fue imposible la nutrición enteral debido a estenosis duodenal. Conclusiones: La nutrición por sonda nasogástrica en los pacientes con pancreatitis aguda grave es bien tolerada y podría plantearse como una alternativa a las otras formas de nutrición

Background and objetive: To establish the nasogastric enteral nutrition tolerance in patients with severe acute pancreatitis. Patients and method: A total of 12 patients with severe acute pancreatitis ($ 3 Ranson criteria; C-reactive protein > 210 mg/dl) and adverse clinical course were included during 2006. When we verified the disease severity, nasogastric (10 F) enteral nutrition was initiated. We used a low fat semi-elemental feed (Dietgrif®) in a slow infusion rate. We evaluated the enteral nutrition tolerance and the adverse events. Results: The patient (4 women and 8 men) mean age (standard deviation) was 70 (11) years and the mean hospital stay was 86 days (range: 14-405 days). The etiology of pancreatitis was: gallstones 8, alcohol abuse one and unknown 3. All patients had medical and/or pancreatic complications. Seven had significant pancreatic necrosis detected in the abdominal computed tomography. Three patients were admitted in the critical care unit and 2 died. The nasogastric enteral nutrition was well tolerated in 8 out of 12 patients (67%) regardless of their medical or pancreatic complications. Only in 3 patients we had initially to discontinue the feeding because of ileus and total parenteral nutrition was provisionally necessary. Enteral nutrition was impossible in one patient because of duodenal stenosis. Conclusions: Nasogastric enteral nutrition is well tolerated in patients with severe acute pancreatitis and it is an alternative to others nutritional routes

Parenteral nutrition and urban legends.

PURPOSE OF REVIEW: To assess the recent literature regarding parenteral nutrition to identify publications that have purported to support various beliefs about the utility of parenteral nutrition, and then to critically evaluate the data presented in those (as well as prior) publications. RECENT FINDINGS: Artificial nutrition improves nutritional markers but not clinical outcomes, suggesting that malnutrition is not causatively associated with a poor outcome. There are no convincing data that parenteral nutrition is beneficial in severely malnourished surgical patients. Glutamine supplementation of parenteral nutrition solutions may reduce the infectious complication rate, but it is unknown if glutamine-supplemented parenteral nutrition is better than no parenteral nutrition. Most, but not all, systematic reviews have demonstrated that enteral nutrition produces fewer problems than parenteral nutrition; no data suggest that either modality is better than doing no artificial nutrition. Randomized trials have not uniformly been able to demonstrate that parenteral nutrition is efficacious in acute pancreatitis. There is some, but not convincing, data that a regimen of glutamine, growth hormone, and a specialized diet will reduce the need for parenteral nutrition in patients with short bowel syndrome. SUMMARY: It is important for clinicians to be able to critically evaluate the medical literature.

Comparison of early enteral nutrition in severe acute pancreatitis with prebiotic fiber supplementation versus standard enteral solution: a prospective randomized double-blind study.

AIM: To compare the beneficial effects of early enteral nutrition (EN) with prebiotic fiber supplementation in patients with severe acute pancreatitis (AP). METHODS: Thirty consecutive patients with severe AP, who required stoppage of oral feeding for 48 h, were randomly assigned to nasojejunal EN with or without prebiotics. APACHE II score, Balthazar's CT score and CRP were assessed daily during the study period. RESULTS: The median duration of hospital stay was shorter in the study group [10 +/- 4 (8-14) d vs 15 +/- 6 (7-26) d] (P < 0.05). The median value of days in intensive care unit was also similar in both groups [6 +/- 2 (5-8) d vs 6 +/- 2 (5-7) d]. The median duration of EN was 8 +/- 4 (6-12) d vs 10 +/- 4 (6-13) d in the study and control groups, respectively (P > 0.05). Deaths occurred in 6 patients (20%), 2 in the study group and 4 in the control group. The mean duration of APACHE II normalization (APACHE II score < 8) was shorter in the study group than in the control group (4 +/- 2 d vs 6.5 +/- 3 d, P < 0.05). The mean duration of CRP normalization was also shorter in the study group than in the control group (7 +/- 2 d vs 10 +/- 3 d, P < 0.05). CONCLUSION: Nasojejunal EN with prebiotic fiber supplementation in severe AP improves hospital stay, duration nutrition therapy, acute phase response and overall complications compared to standard EN therapy.

A double-blind, randomised, controlled trial to study the effects of an enteral feed supplemented with glutamine, arginine, and omega-3 fatty acid in predicted acute severe pancreatitis.

CONTEXT: Current best evidence is in favour of early institution of enteral feeding in acute severe pancreatitis with promising results from trials in immunonutrition on other patient groups. OBJECTIVE: To identify which groups of patients and products are associated with benefit, we investigated immunonutrition in patients with predicted acute severe pancreatitis. DESIGN: A randomised trial of a study feed containing glutamine, arginine, tributyrin and antioxidants versus an isocaloric isonitrogenous control feed was undertaken. PATIENTS: Thirty-one patients with a diagnosis of acute pancreatitis predicted to develop severe disease: 15 study feeds and 16 control feeds. INTERVENTIONS: Enteral feeding via nasojejunal tube for 3 days. If patients required further feeding the study was continued up to 15 days. MAIN OUTCOME MEASURES: Reduction in C-reactive protein (CRP) by 40 mg/L after 3 days of enteral feeding was the primary endpoint. Carboxypeptidase B activation peptide (CAPAP) levels were taken at regular intervals. RESULTS: After 3 days of feeding, in the study group 2/15 (13%) of patients had reduced their CRP by 40 mg/L or more. In the control group 6/16 (38%) of patients had reduced their CRP by this amount. This difference was found to be near the statistical significant limit (P=0.220). CONCLUSIONS: The cause of the unexpectedly higher CRP values in the study group is unclear. The rise in CRP was without a commensurate rise in CAPAP or outcome measures so there was no evidence that this represented pancreatic necrosis. The contrast between the CRP and CAPAP results is of interest and we believe that specific pancreatic indices such as CAPAP should be considered in larger future studies.