They underwent a gastrectomy with standard lymphadenectomy. One day before surgery, 99mtechnetium-tin colloid was endoscopically injected into the submucosa around the tumor. After surgery, the uptake of radioisotope in dissected lymph nodes was measured using Navigator GPS. Then, all dissected lymph nodes were investigated by hematoxylin-eosin staining and immunohistochemistry using an antihuman cytokeratin monoclonal antibody. Hematoxylin-eosin staining demonstrated lymph node metastasis in two (12.5%) of 16 patients and in three (0.8%) of 382 nodes. However, immunohistochemistry Protease Inhibitor Library concentration showed that none of the patients had lymph node micrometastasis.

Sentinel nodes (SNs) were identified in all patients. The mean number of SNs was 3.1 (range, 1–6). Among two patients with lymph node metastasis, the SNs, at least, contained positive nodes. Accordingly, the false-negative and accuracy rates were 0% and 100%, respectively. Our results indicate that SNNS may have potential as a further minimally invasive surgery in early gastric cancer patients after noncurative endoscopic resection. “
“Chronic diseases of the biliary

system are common and may cause fibrosis and eventually progression to liver cirrhosis. The aim was to define a new mouse p38 MAPK inhibitor model of a cholangiopathy leading to liver fibrosis in fra-1tg mice. Liver pathology of fra-1tg mice was analyzed in detail by histology and flow cytometry. Transcript levels of fibrosis-related genes and matrix metalloproteinase (MMP) activities were quantified and immunohistochemical analysis additionally applied. The role of the immune system in this model was analyzed by crossing fra-1tg mice with rag2−/− mice. Furthermore, expression of Fra-1 in corresponding human liver diseases was investigated on transcription level and histologically. Fra-1tg mice spontaneously 上海皓元医药股份有限公司 develop biliary fibrosis preceded by ductular proliferation and infiltration of inflammatory cells. Fra-1 protein

is present in cholangiocytes and inflammatory cells within the liver. These findings were replicated in human biopsies of patients with advanced liver fibrosis. The inflammatory infiltrate showed a strong increase in activated T cells and decreased natural killer (NK), natural killer T cells (NKT), and B cells in fra-1tg mice as compared to wildtype mice. Moreover, fra-1tg mice develop biliary fibrosis with a time-dependent increase in hepatic collagen content and increase in relative messenger RNA (mRNA) expression of profibrotic genes. Attenuation but not complete prevention of collagen accumulation in liver was observed in the fra-1tg × rag2−/− mice. However, transplantation of fra-1tg bone marrow cells into wildtype mice could not induce disease. Conclusion:Fra-1tg mice spontaneously develop a progressive biliary disease.

In continuation of this idea, I calculated that, if the morphology of a taxon can be scored as a set of X binary characters, and morphological species boundaries are defined by a minimum of a one-character difference, the theoretical number of morphologically diagnosable species (N) increases exponentially with the number of characters available (N = 2X). Consequently, chances of encountering multiple species with identical morphologies increase quickly in taxa of lower morphological complexity (Verbruggen et al. 2009b). While such reasoning is useful conceptually, it is unlikely that all theoretically possible

morphologies will be produced in the course of the evolution of a lineage. To obtain a more realistic image of morphospace occupancy, I have now simulated character data using sensible models of character evolution.

buy PLX3397 buy Silmitasertib In summary, this approach consists of generating phylogenetic trees containing a number of species (between 10 and 400), and subsequently letting a set of traits (i.e., morphological characters) evolve along this phylogeny at a rate that corresponds to those measured for a real algal morphometric data set. The result of this exercise is a set of values for each trait for each species in the phylogeny. Those can then be compared with each other to evaluate how many of the species can be reliably distinguished from one another. For a more detailed description of the simulations, see the author’s blog at http://phycoweb.wordpress.com/. As could be expected, only a small subset of all possible

character combinations were produced during the evolution of the simulated 上海皓元 lineages. For example, when lineages of 400 species were simulated, only ~50 distinct morphologies were produced in lineages with 20 characters, and only ~20 morphologies in lineages with 10 characters (Fig. 2A). It is evident that more complex lineages (i.e., with more characters) reach higher actual numbers of diagnosable species than simpler lineages. Consequently, complex lineages have a higher fraction of species pairs that are distinguishable (Fig. 2B), and these fractions are not influenced by the number of species in the lineages. The same pattern returns if continuous rather than binary characters are used: 54.2% of species pairs could be distinguished for lineages with 10 characters, whereas this number increased to 72.5% for organisms with 20 characters (Fig. 3, 1st vs. 4th boxplot). In conclusion, it appears to be a general rule that species of more complex lineages (i.e., those having more characters) are more easily distinguishable from one another than species of simpler lineages. But how about selection? We know that habitat has a major influence on the morphology of organisms. For example, macroalgae from very different phylogenetic backgrounds (Rhodophyta, Ulvophyceae, and Phaeophyceae) have converged onto very similar body architectures in similar environments (e.g., Littler and Littler 1980, Steneck and Dethier 1994).

The sum of the six positive controls for a given lane was divided by the average sum across lanes to yield a normalization factor, which was then multiplied by the raw counts in each lane to give normalized

values. Raw mRNA and microRNA data are accessible through the accession numbers GSE32879 and GSE32957 at the NCBI Gene Expression Omnibus (GEO) database. Other statistical methods can be found in the Supporting Materials. Total RNA was subjected to qRT-PCR. Mature microRNAs and other mRNAs were analyzed using the TaqMan microRNA Assays and Gene Expression Assays, respectively, in accordance with manufacturer’s instructions (Applied http://www.selleckchem.com/products/dorsomorphin-2hcl.html Biosystems, Foster City, CA). All RT reactions were run in a GeneAmp PCR 9700 Thermocycler (Applied Biosystems). Probes used for the analyses were as follows: ZEB1, Hs00232783_m1; ZEB2, Hs00207691_m1; VIM, Hs00185584_m1; CDH1, Hs01023894_m1; CDH2, Hs00983056_m1; MYC, Hs00905030_m1; Adriamycin Hsa-miR-200c, 002300; Hsa-miR-141, 000463 (Applied Biosystems). The experiments were performed in triplicate. The TaqMan

gene assay for 18s and actin was used to normalize the relative abundance of mRNA. RNU6B RNA was used as a control for miR-200c. We performed transcriptomic analyses of 30 retrospectively collected ICC and CHC clinical

specimens from Chinese (n = 13) and Japanese (n = 10) patients with seven paired nontumor liver tissues from ICC patients using Affymetrix 上海皓元医药股份有限公司 GeneChip Human Gene-ST arrays. Five FNH cases and two adenomas were also included as benign tumors of the liver. Clinical features of these ICC and CHC cases are included in Supporting Table S1. Multidimensional scaling analysis revealed that malignant tumor samples were mainly different from benign tumors and nontumor tissues, suggesting that malignant tumors have a vastly different gene expression profile (Fig. S1). To determine tumor heterogeneity, unsupervised hierarchical clustering analysis of 23 ICC and CHC samples based on all genes was conducted. The result revealed that tumor samples can be divided into two main groups, i.e., cluster-A and cluster-B (Fig. 1A). Kaplan-Meier survival analysis revealed that ICC cases in cluster-A had a shorter survival than those in cluster-B (Fig. 1B). These results suggest that gene expression and tumor biology differ significantly among different ICC tumor samples. We previously identified two HCC subgroups, one resembling gene expression signatures of hepatic stem cells (referred to as HpSC-HCC) and the other similar to mature hepatocyte (referred to as MH-HCC).

Our data

suggest that MA has an increased volume of WMLs compared with MO. Disease duration does not seem to influence the WMLs load, while aging positively correlates with the increased number and volume of WMLs, suggesting that they increase over the time. At the same time, both the presence of cognitive dysfunctions and WMLs seem unrelated to the severity of migraine. On the basis of our results, we cannot confirm that the frontal lobe cognitive dysfunction in migraine patients is linked to WMLs. We cannot exclude the possibility that this could depend, at least in part, on some limitations in our study such as the small size of the sample and the CP-690550 purchase use of 1.5 T MRI to detect WMLs instead of 3 T or higher magnet which could have better visualized smaller lesions. Therefore, cognitive deficit could be due to other causes. It is possible to hypothesize different pathogenetic mechanisms to explain executive dysfunctions. A voxel-based

morphometry INCB024360 price study showed that migraine patients with brain T2-visible lesions had areas of reduced gray matter density, mainly located in the frontal and temporal lobes, and strongly related to age, disease duration, and T2-visible lesion load.[29] This is confirmed by the relationship between frontal atrophy and executive dysfunctions[30] and between frontal atrophy and clinical migraine features (attacks frequency and disease duration).[31] Our data suggest that the presence of executive deficits in migraine exists, but it is not related to the presence of WMLs, in disagreement with what previously hypothesized by Camarda et al.[6] MRI hyperintensities, accumulating over time in migraine patients, remain meaningless. The clinical medchemexpress relevance in migraine of this brain damage deserves further investigations. (a)  Conception and Design (a)  Drafting the Manuscript (a) 

Final Approval of the Completed Manuscript “
“To identify factors associated with triptan discontinuation among migraine patients. It is unclear why many migraine patients who are prescribed triptans discontinue this treatment. This study investigated correlates of triptan discontinuation with a focus on potentially modifiable factors to improve compliance. This multicenter cross-sectional survey (n = 276) was performed at US tertiary care headache clinics. Headache fellows who were members of the American Headache Society Headache Fellows Research Consortium recruited episodic and chronic migraine patients who were current triptan users (use within prior 3 months and for ≥1 year) or past triptan users (no use within 6 months; prior use within 2 years).

Previous articles have reported that Mcl-1 knockdown makes Gefitinib molecular weight some tumor cells sensitive to ABT-737.26, 27 The present study showed that ABT-737 up-regulation of Mcl-1 rather than Mcl-1

expression itself may be a mechanism of tumor cell resistance to this agent. A recent study demonstrated that long-term exposure to ABT-737 made initially sensitive lymphoma cell lines resistant to this agent via up-regulation of Mcl-1.28 In this study, Mcl-1 up-regulation in the ABT-737–resistant lymphoma cells were reported to be mediated by transcriptional up-regulation. In the present study, hepatoma cells showed immediate, posttranscriptional up-regulation of Mcl-1. This rapid response may contribute to the difficulty of treating hepatoma cells with ABT-737 compared with lymphoma cells in which ABT-737 is reported to be effective not only in vitro29 but also in vivo.30 The mechanism by which hepatoma cells posttranscriptionally up-regulate Mcl-1 upon ABT-737 exposure is not clear at present. However, our study has shown that Mcl-1 up-regulation was mediated by delayed degradation of Mcl-1 protein in ABT-737–treated cells without involving the USP9X deubiquitinase. ABT-737 is a Bad mimetic small molecule and preferentially binds with the BH3-binding

groove of Bcl-xL. This binding may release endogenous BH3-only proteins such as Bim and Bid and presumably Bak and Bax from Bcl-xL and these unleashed Bcl-2 proteins may MCE公司 then bind Mcl-1. The interaction between Mcl-1 and the unleashed Bcl-2 proteins may cause increased Mcl-1 stability. Because Bak/Bax and Bid/Bim function

as effectors and activators for Ixazomib the mitochondrial pathway of apoptosis, respectively, their binding with Mcl-1 may also cause apoptosis resistance to ABT-737. Not only efficacy but also safety is an important point when considering a therapeutic strategy for cancer. Tumor cells sometimes share similar mechanisms for survival with normal cells. Indeed, HCCs overexpress Bcl-xL, but this molecule also plays an important role in maintaining the integrity of normal hepatocytes.8 In the present study, we administered ABT-737 to Mcl-1 knockout mice and demonstrated that inactivation of both Bcl-xL and Mcl-1 could induce lethal hepatitis. We previously reported that Bcl-xL and Mcl-1 are required for liver development during embryogenesis,15 and the present study also revealed the critical importance of both molecules in the adult liver. Recently, the possibility of combination therapy for down-regulation of Bcl-xL and Mcl-1 has been reported in vitro.26, 27, 31 The present study, for the first time, focused on the in vivo safety of this strategy. Regarding safety concerns about the inactivation of both Mcl-1 and Bcl-xL, sorafenib is an attractive agent because as we have revealed in this study, it down-regulates Mcl-1 expression in a relatively specific manner in tumor cells.

EtOH resulted in a 5-fold increase in FOXO3 binding to the proapototic promoters (TRAIL and Bim), but not the antioxidant (SOD2 and PrxIII) promoters. The increased binding of FOXO3 to proapoptotic promoters was selleck products associated with an increase in mRNA and protein levels for TRAIL, activation of caspase 3, increased LDH release and cell death. FOXO3/ethanol induced caspase activation and cell death was completely prevented by either TRAIL receptor antagonists or caspase inhibitors. Ethanol caused rapid JNK dependent phosphorylation

of FOXO3 at serine 574 in both Huh7.5 cells and primary human hepatocytes. FOXO3-S574-P was found exclusively in the nucleus and ChIP studies with an S574-P specific antibody showed binding of this form exclusively to the pro-apoptotic promoters BIM and TRAIL. Blocking FOXO3 phosphorylation at this site with an S574A mutant abolished ethanol-induced apoptosis www.selleckchem.com/products/Cisplatin.html and TRAIL promoter binding. A phos-phomimetic FOXO3_S574D mutant induced

apoptosis even in the absence of ethanol. CONCLUSION: Ethanol causes a specific phosphorylation of FOXO3 that selectively activates binding to promoters for pro-apoptotic proteins and induces caspase and TRAIL-dependent cell death without activating antioxidant or cell cycle control genes. This novel mechanism may contribute to the phenotype of alcohol-induced liver disease and is a potential therapeutic target. Disclosures: The following people have nothing to disclose: Zhuan Li, Josiah Cox, Irina Tikhanovich, Sudhakiranmayi Kuravi, Kenneth Dorko, Steven A. Weinman Sirtuin-6 (SIRT6) is a member of the sirtuin family of NAD+-dependent deacetylases and has been implicated in a wide range of cellular processes including genomic stability, stress response, energy metabolism, inflammation, tumorigenesis and ageing. Recent studies have shown

that hepatocyte-specific deletion of SIRT6 results in fatty liver formation and that myeloid cell-specific SIRT6 knockout mice develop chronic liver inflammation. Given that chronic alcohol consumption is associated with decreased cellular NAD+ levels, we hypothesized that decreased SIRT6 activity may contribute to alcoholic liver disease. To investigate the cell-specific medchemexpress role of SIRT6 in the patho-genesis of alcoholic liver disease, hepatocyte-specific SIRT6 knockout (L-SIRT6 KO) mice, myeloid cell-specific SIRT6 knockout (M-SIRT6 KO) mice, hepatocyte- and myeloid cell-specific double knockout (d-SIRT6 KO) mice and their wild-type (WT) lit-termates were fed a Lieber-DeCarli liquid diet containing 5% ethanol for 10 days then gavaged with a single dose of ethanol (5g/kg body weight) and sacrificed 9 hours later (NIAAA model). As expected, chronic plus binge ethanol feeding caused substantial liver injury in WT mice, as indicated by elevated serum ALT and AST levels.

0001).

Logistic regression model demonstrated that FSSG (odds ratio [OR] 1.232, 95% confidence interval [CI]: 1.1221.352, p<0.0001) and 丫GT (OR: 1.011, 95%CI: 1.0031.019, p=0.00o) were independently associated with insomniacs. In treated-patients, AIS was significantly decreased with significant reductions of FSSG after the treatment with RPZ. Four patients of eleven insomnias (44%) were relieved after RPZ. Conclusions: In biopsy-proven NAFLD patients, insomnia was found in nearly thirty percent of cases, BTK inhibitor related to ۷GT and GERD symptoms, and can be relieved by RPZ. Disclosures: Kazuaki Chayama – Consulting: Abbvie; Grant/Research Support: Dainippon Sumitomo, Chugai, Mitsubishi Īanabe, DAIICHI SANKYO, Toray, BMS, MSD; Speaking and Teaching: Chugai, Mitsubishi Īanabe, DAIIcHi SANKYO, KYORIN, Nihon Medi-Physics, BMS, Dainippon Sumitomo, MSD, ASKA, Astellas, AstraZeneca, Eisai, Olympus, GlaxoSmithKline, ZERIA, Bayer, Minophagen, JANSSEN, JIMRO, TSUMURA, Otsuka, Taiho, Nippon Kayaku, Nippon Shinyaku, Takeda, AJINOMOTO, Meiji Seika, Toray The following people have nothing to disclose: Hiroyoshi Taketani, Yoshio Sumida, Saiyu Tanaka, Kazuyuki Kanemasa, Masato Yoneda, Kento Imajo, Atsushi Nakajima, Hideyuki Hyogo, Masafumi Ono, Toshiji Saibara, Hideki Fujii, Yuichiro Eguchi, Yoshito Itoh Background & Aims:

Patients with nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) often have metabolic disorders including insulin resistance and type diabetes mellitus (T2DM). We clarified the predictive factors in glucose metabolism for progression of hepatic fibrosis in patients with NAFLD by the SAHA HDAC in vivo 75-g oral glucose tolerance test (75gOGTT) and a continuous glucose monitoring system MCE (CGMS). Methods: One hundred sixty-nine patients (68 female and 101 male patients) with biopsy-proven NAFLD with performance with 75gOGTT were enrolled and divided into four groups according to the stage of hepatic fibrosis

(F0-3). Results: The proportion of patients with T2DM significantly gradually increased, HbA1c and the homeostasis model assessment of insulin resistance were significantly elevated, and 1, 5-anhydroglucitol (1, 5-AG) was remarkably decreased with the progression of fibrosis. In the 75gOGTT, both plasma glucose and insulin secretion were remarkably increased with the progression of fibrosis. The only factor significantly associated with advanced fibrosis was 1, 5-AG (P = 0.008) as determined by multivariate logistic regression analysis. We next evaluated the changes in blood glucose during 24 hours by monitoring with the CGMS to confirm the relationship between glycemic variability and progression of fibrosis. Variability of median glucose, standard deviation of median glucose (P = 0.0022), maximum blood glucose (P = 0.0019), and AMin-max blood glucose (P = 0.0029) were remarkably higher in severe fibrosis than in mild fibrosis.

1 This is an impressive study of 151 patients with refractory ascites in whom beta-blockers were shown to have deleterious effects on survival. Despite meticulous analyses of the data, the authors did not find any plausible explanation for the differences between patients treated with beta-blockers and patients not treated with beta-blockers, such as differences in the degree of portal hypertension, the presence of esophageal varices, or liver dysfunction. However, the arterial

blood pressure was lower in the beta-blocker group, and four characteristics—the presence of hepatocellular carcinoma, Child-Pugh score class C, refractory ascites as the etiology, and beta-blocker therapy—predicted death. Apart from the arterial blood pressure and heart rate, characteristics of cardiac function such as

the cardiac output were not measured in the study. We therefore propose a potential contributing explanation for the dramatic effect of beta-blockers Selleckchem Z-VAD-FMK on survival in patients with refractory ascites. Treatment with a nonselective beta-blocker decreases cardiac output by blockade of the beta-1-adrenergic receptors. We believe that the pronounced inhibitory effect of propranolol on cardiac function may explain the increased mortality. It is well known that in patients with refractory ascites and circulatory dysfunction, renal function often deteriorates further with the development of hepatorenal syndrome. There seems to be a complex and bidirectional interaction between selleck kinase inhibitor the heart and the kidneys, and different observations have suggested that a type of cardiac dysfunction known as cirrhotic cardiomyopathy significantly contributes to the pathophysiology of hepatorenal syndrome. A cardiorenal interaction may be a key element in the homeostasis of the extracellular fluid volume, arterial blood pressure, and effective/central blood volume. We believe that different observations point to impaired cardiac function in cirrhosis as part of the pathogenesis of hepatorenal syndrome.2-4 It has been demonstrated that patients with cirrhosis, before they develop 上海皓元医药股份有限公司 type 1 hepatorenal syndrome, have

decreased or relatively low cardiac output.2-4 In these patients, treatment by beta-blockers further reduces cardiac output, systemic perfusion, and peripheral oxygen delivery with potentially deleterious effects.2-4 We therefore propose an additional explanation for the reduced survival after beta-blocker treatment. We hypothesize that the reduction of the effective arterial blood volume and renal failure in patients with cirrhosis and refractory ascites are consequences of not only progressive arterial vasodilatation but also cardiac systolic dysfunction. The result of systolic dysfunction is relatively reduced cardiac output insufficient to maintain adequate arterial blood pressure and renal perfusion. These mechanisms are further hampered by treatment with beta-blockers and explain the deleterious effects in patients with refractory ascites, as described by Sersté et al.

Predictive models LBH589 molecular weight for liver fibrosis are generally derived from panels of direct and indirect continuous peripheral blood variables.9 Direct markers reflect extracellular matrix (ECM) turnover. These include matrix metalloproteinases (MMPs), which are involved in degrading collagens, and tissue inhibitors of metalloproteinases (TIMPs), which regulate MMP activity.10 MMPs,

TIMPs, collagen, hyaluronic acid and YKL-40 also mirror scarring in liver fibrosis10 but do not independently predict significant fibrosis. Indirect markers of hepatic synthetic dysfunction and portal hypertension include serum aminotransferase levels, coagulation profile, haptoglobin, albumin level and platelet count.9FibroTest11 and Hepascore12 are non-invasive tests of liver fibrosis that incorporate patient age, gender and both direct and indirect blood variables. FibroTest is a composite model based on serum alpha-2 macroglobulin, total bilirubin, gamma-glutamyltransferase (GGT), Selleck GSI-IX apolipoprotein A1 and haptoglobin. In contrast, Hepascore utilises total bilirubin, GGT, hyaluronic acid, and alpha-2 macroglobulin. FibroTest11 (and its offshoots) have been validated for staging fibrosis in various populations, including CHB but with variable area under the receiver-operating

characteristic curve (AUROC). Also, emerging data indicate that Hepascore is useful for identifying cirrhosis in a predominantly Asian CHB population.Transient elastography is increasingly reported to be a rapid, relatively accurate test for liver fibrosis and recently was compared against a new model called the APGA index (aspartate aminotransferase [AST], platelet 上海皓元 count, GGT and alphafetoprotein [AFP]).13 In the current edition of the Journal, Lee

and colleagues14 describe an alternative non-invasive predictor of liver cirrhosis in CHB, called the PAHA (platelet count, AST, Haptoglobin, and Apolipoprotein-A1) model, which compares favorably with existing noninvasive liver fibrosis models. Remarkably, the predictive accuracy of the PAHA model was superior to the previously described AST/ALT ratio, PGA (prothrombin time, GGT, Apo-A1), PGAA (prothrombin time, GGT, apolipoprotein A1, α2-macroglobulin), age platelet index (API), Forns fibrosis index (FFI), and AST to platelet ratio index (APRI). The PAHA model was derived in a prospectively selected, predominantly male, non-obese, treatment-naive, adult Korean population with CHB who had undergone percutaneous liver biopsy and had no demonstrable decompensation of cirrhosis. Liver histology on biopsy specimens of at least 15 mm length was used as the reference test forcomparison with the PAHA model. The PAHA model is derived from platelet count, serum AST, haptoglobin and apolipoprotein-A1, which were independent predictors of liver cirrhosis when considered as categorical variables in a multivariate logistic regression model.

Ph. U of lipase

per meal and 20 000–25 000 Eur. Ph. U of lipase together with snacks should be given. In cases of insufficient response, inhibition of gastric acid secretion should be attempted. Finally, bacterial overgrowth should be detected and treated in non-responders (Fig. 2). As mentioned above, a low intraduodenal pH may inactivate endogenous and uncoated exogenous lipase, prevent the release of active lipase from enteric-coated granules within the proximal intestine, and lead to bile salt precipitation. Inhibition of gastric acid secretion, by increasing the intragastric pH and thus decreasing the duodenal acid load, should improve the efficacy of the enzyme substitution selleck therapy. Combining enteric-coated pancreatin microspheres with either a H2-receptor antagonist or a proton pump inhibitor was reported to be beneficial in patients with cystic fibrosis.24,25 More recently, addition of a proton pump inhibitor has been shown to significantly improve and even normalize fat digestion in patients with pancreatic exocrine insufficiency and incomplete response to the enzyme substitution therapy in form Alvelestat of enteric-coated minimicrospheres.18 This combined therapy, however, should not be used in patients with an adequate response to the enzyme substitution monotherapy.18 Independently of the therapy prescribed,

evaluation of the therapeutic efficacy of pancreatic enzymes is generally based on clinical parameters like weight gain or absence of weight loss, and improvement of steatorrhea-related symptoms. This clinical evaluation has been recently shown to be inappropriate, and only normalization of fat digestion, demonstrated by means of objective methods like normalization of CFA, 13C-MTG breath test, or specific nutritional parameters,

ensures a normal nutritional status in patients with pancreatic exocrine insufficiency.6,8 Pancreatic exocrine insufficiency develops in most patients after partial or total gastrectomy and duodenopancreatectomy.26,27 Multiple factors have been implicated, including decreased postprandial stimulation of pancreatic secretion secondary to the disruption of neural reflexes and reduced cholecystokinin (CCK) release, primarily decreased MCE公司 pancreatic secretion, arrival of big, hard-to-digest nutrient particles to the jejunal lumen due to pylorus resection, and postprandial asynchrony between gastric emptying of nutrients and biliopancreatic secretion.26–28 Despite the relevance of pancreatic exocrine insufficiency in the nutritional status of operated patients, the number of studies evaluating the usefulness of pancreatic enzyme substitution therapy in this setting is limited, and data regarding the best preparation to be used are scarce.28 Enteric-coated enzyme microspheres have been shown to be associated with a higher body weight gain compared with uncoated preparations in patients after duodenopancreatectomy.