Although electronic momentary assessment methodology

Although electronic momentary assessment methodology Deforolimus concentration was found to be feasible in this population and to have the potential to identify specific headache triggers for children, it remains to be determined how best (or even whether) to incorporate this information into treatment recommendations. “
“(Headache 2010;50:1286-1295) Objective.— To describe 2 topographic facial pain conditions with the pain clearly localized in the eye (idiopathic ophthalmodynia) or in the nose (idiopathic rhinalgia), and to propose their distinction from persistent idiopathic

facial pain. Background.— Persistent idiopathic facial pain, burning mouth syndrome, atypical odontalgia, and facial arthromyalgia are idiopathic facial pain syndromes that have been separated according to topographical criteria. Still, some other facial pain syndromes might have been veiled under the broad term of persistent idiopathic facial pain. Methods.— Through a 10-year period we have studied all patients referred to our neurological clinic because of facial pain of unknown etiology that might deviate from all well-characterized facial pain syndromes. Results.— In a group of

patients we have identified 2 consistent clinical pictures with pain precisely located either in the eye (n = 11) or in the nose (n = 7). Clinical features resembled those KU-60019 purchase of other localized idiopathic facial syndromes, the key Cell press differences relying on the topographic distribution of the pain. Conclusions.— Both idiopathic ophthalmodynia and idiopathic rhinalgia seem specific pain syndromes with a distinctive location, and may deserve a nosologic status

just as other focal pain syndromes of the face. Whether all such focal syndromes are topographic variants of persistent idiopathic facial pain or independent disorders remains a controversial issue. “
“(Headache 2011;51:52-63) Objective.— To evaluate the efficacy, safety, and optimum dose of a highly purified Clostridium botulinum type A toxin-hemagglutinin complex (Dysport) for migraine prophylaxis. Background.— Botulinum toxin type-A has demonstrated good efficacy in several open-label studies of patients with migraine, involving either individualized or standardized protocols, although data from placebo-controlled trials have been conflicting. Methods.— A 12-week, double-blind, randomized trial of Dysport (120 or 240 units) vs placebo was conducted in 6 centers in Thailand to evaluate the efficacy, safety, and optimum dose of botulinum toxin type-A (Dysport) for migraine prophylaxis. A total of 128 patients with migraine without aura were enrolled. The primary end point was the change in the mean number of migraine attacks per 4-week period from the pre-treatment period to 8-12 weeks post injection.

Although electronic momentary assessment methodology

Although electronic momentary assessment methodology http://www.selleckchem.com/GSK-3.html was found to be feasible in this population and to have the potential to identify specific headache triggers for children, it remains to be determined how best (or even whether) to incorporate this information into treatment recommendations. “
“(Headache 2010;50:1286-1295) Objective.— To describe 2 topographic facial pain conditions with the pain clearly localized in the eye (idiopathic ophthalmodynia) or in the nose (idiopathic rhinalgia), and to propose their distinction from persistent idiopathic

facial pain. Background.— Persistent idiopathic facial pain, burning mouth syndrome, atypical odontalgia, and facial arthromyalgia are idiopathic facial pain syndromes that have been separated according to topographical criteria. Still, some other facial pain syndromes might have been veiled under the broad term of persistent idiopathic facial pain. Methods.— Through a 10-year period we have studied all patients referred to our neurological clinic because of facial pain of unknown etiology that might deviate from all well-characterized facial pain syndromes. Results.— In a group of

patients we have identified 2 consistent clinical pictures with pain precisely located either in the eye (n = 11) or in the nose (n = 7). Clinical features resembled those BYL719 datasheet of other localized idiopathic facial syndromes, the key Pregnenolone differences relying on the topographic distribution of the pain. Conclusions.— Both idiopathic ophthalmodynia and idiopathic rhinalgia seem specific pain syndromes with a distinctive location, and may deserve a nosologic status

just as other focal pain syndromes of the face. Whether all such focal syndromes are topographic variants of persistent idiopathic facial pain or independent disorders remains a controversial issue. “
“(Headache 2011;51:52-63) Objective.— To evaluate the efficacy, safety, and optimum dose of a highly purified Clostridium botulinum type A toxin-hemagglutinin complex (Dysport) for migraine prophylaxis. Background.— Botulinum toxin type-A has demonstrated good efficacy in several open-label studies of patients with migraine, involving either individualized or standardized protocols, although data from placebo-controlled trials have been conflicting. Methods.— A 12-week, double-blind, randomized trial of Dysport (120 or 240 units) vs placebo was conducted in 6 centers in Thailand to evaluate the efficacy, safety, and optimum dose of botulinum toxin type-A (Dysport) for migraine prophylaxis. A total of 128 patients with migraine without aura were enrolled. The primary end point was the change in the mean number of migraine attacks per 4-week period from the pre-treatment period to 8-12 weeks post injection.

In this compact review, we clarify the disease of IAC, summarize

In this compact review, we clarify the disease of IAC, summarize criteria for diagnosis of IAC, discuss the role of CA 19-9, and provide key information to differentiate diagnosis of IAC from CCA. IAC should be highly suspected in unexplained biliary stricture associated with increased IgG4 (in serum especially in bile) and other organ involvement (kidney, retroperitoneum etc. especially pancreas in which there are abundant IgG4-positive

plasmocytes infiltration). Correct diagnosis of IAC will avoid unnecessary surgery because IAC responds well to steroid therapy. In a word, increased IgG4 levels, other organ involvement and response to steroids are keys to distinguishing IAC from Sotrastaurin CCA. In recent decades, autoimmune cholangitis (to IgG4) or immunoglobulin G4-associated cholangitis (IAC) has been identified see more worldwide.[1] The clinical, biochemical and imaging features of IAC mimic cholangiocarcinoma (CCA), making diagnosis difficult. Currently, the reports of IAC are rare except for some cases.[2, 3] Most of these few cases were misdiagnosed as CCA, and notably, unnecessary surgical resections were performed.[3-11] Early reports document cases of histological diagnoses of IAC after surgical

resection. Increasing knowledge about IAC is necessary. According medroxyprogesterone to reports and our experiences, a typical encounter between an IAC patient and doctor was as follows: A 50- to 60-year-old male complained of abdominal pain and weight loss. Physical examination showed subxiphoid area mild tenderness with or without jaundice. Laboratory assessments showed elevated serum amylase, urine amylase, or/and importantly serum carbohydrate antigen 19-9 (CA19-9). A variety of imaging findings, such as ultrasound, computed tomography (CT) scan, and magnetic resonance imaging (MRI), presented bile duct stricture. These

all made straightforward diagnoses of chronic pancreatitis and malignant bile duct carcinoma. Furthermore, Whipple’s operation was performed. Surprisingly, there were no tumor cells found in specimens even in the most abnormal parts, which looked like carcinomas. Then immunostaining of IgG4 was completed. The result showed a large amount of IgG4-positive stained cells infiltration in the bile duct (or/and in other involved organs, especially the pancreas, which would not have been examined earlier). The final diagnosis of IAC would be confirmed (and/or accompanied by other IgG-related disease, corresponding as Ig4 related autoimmune pancreatitis etc.). The lesson from the above case is that IAC shares a number of clinical, biochemical, imaging features with CCA and is often misdiagnosed as CCA.

S7) p38α may inactivate GSK3β by direct phosphorylation of Ser38

S7). p38α may inactivate GSK3β by direct phosphorylation of Ser389 or indirectly through phosphorylation of Thr9 by Akt, leading to β-catenin accumulation.20 Thus, p38 modulates canonical Wnt-β-catenin signaling, which is critical for normal cell proliferation and homeostasis.21 Inactivation of GSK3β produces embryonic lethality caused by severe liver degeneration associated with hypersensitivity to TNF-α and reduced NF-κB function.22 Inhibition of GSK3β may sensitize rat hepatocytes to apoptosis by reducing p65 phosphorylation and down-regulating NF-κB transactivation.23 In p38α-deficient

livers, activation of GSK3β due to reduced phosphorylation (Fig. 3B) does not seem to be associated with changes in apoptosis or p65 phosphorylation upon

BDL (Fig. EX 527 concentration S4). The p38α pathway is also involved in the up-regulation of inflammatory cytokines. p38 may positively regulate NF-κB activity by different mechanisms, including chromatin remodeling through Ser10 phosphorylation of histone H3 at NF-κB-dependent promoters or by impinging on IκB kinase (IKK) or the p65 subunit.20 However, in chronic cholestasis p38α deficiency did not significantly affect NF-κB activation (Supporting Fig. RG7204 order S4) or the expression of TNF-α and interleukin-6 (see Fig. 4). Nevertheless, RANTES and receptor 1 of TNF-α Bay 11-7085 were up-regulated in the liver of p38α-deficient mice under basal conditions and remained high during the first 12 days after cholestasis (Fig. 4B). RANTES is one of the major adjacent cysteines motif (CC) chemokines that is produced by T-lymphocytes, monocytes, endothelial cells, and fibroblasts. It is worth noting that expression of antiinflammatory IL-10 was markedly up-regulated at 12 days after cholestasis induction only in p38α KO mice, which should provide protection restraining the inflammatory response,

but this protection was lost in the long term (i.e., at 28 days) leading to up-regulation of Icam-1 and chemokine (C-C motif) ligand 2 (Ccl2) (Fig. 4B). Although previous reports have associated p38α with the regulation of apoptosis and fibrogenesis, liver-specific p38α-deficient mice did not show a higher degree of apoptosis or fibrosis upon chronic cholestasis compared with WT mice (see Fig. 4 and Supporting Fig. S5). Hence, neither apoptosis nor fibrosis would contribute to the increased mortality of these animals. p38α controls the differentiation and proliferation of many cell types, including hepatocytes.4, 24, 25 p38α may negatively regulate cell cycle progression at the G1/S and the G2/M transitions triggering cell cycle arrest by down-regulation of cyclins, up-regulation of cyclin-dependent kinase inhibitors, and by inducing p53 phosphorylation and the up-regulation of p16.

1A) Interestingly, the core components of PRC2, including EZH2,

1A). Interestingly, the core components of PRC2, including EZH2, SUZ12, EED, and RBBP7, were simultaneously up-regulated in human HCCs (Fig. 1B; Supporting Fig. 1B). The primary function of PRC2 is to induce epigenetic transcriptional repression by way of H3K27me3.8 EZH2 is the H3K27 methyltransferase that functions as the catalytic subunit of PRC28 and the presence of other PRC2 protein

subunits is functionally essential for the enzymatic activity of EZH2.24 The expression of each individual PRC2 component was found to correlate positively with EZH2 (Supporting Fig. 1C), indicating that up-regulation of PRC2 may play a critical Decitabine purchase role in HCC development. Up-regulation of PRC2 in HCC prompted us to further investigate its implication in HCC development. Because EZH2 is the only histone methyltransferase of the complex, we reasoned that its contribution by way of its enzymatic activity should be more widespread than other PRC2 protein subunits. Thus, later parts of our study were concentrated on EZH2 to represent PRC2 dysregulation. Up-regulation of EZH2 in HCCs was confirmed by qRT-PCR in 59-paired primary HCCs and five normal human liver samples (Fig. 1C; Supporting Fig. 2A); and by immunohistochemistry in tissue microarrays consisted of 108-paired primary HCCs Selleckchem INK128 (Fig. 1D; Supporting

Fig. 2B). However, EZH1, a protein homolog of EZH2 that also promotes methylation of H3K27 in human embryonic stem (hES) cells,25 was not up-regulated in our HCC samples (Supporting Fig. 2C). This result further supports a specific function of EZH2 containing PRC2 in liver carcinogenesis. Hepatocarcinogenesis involves multiple stages where normal liver can develop background diseases such as chronic hepatitis and cirrhosis, then progresses to early HCC (pTNM stages I and II) and advanced HCC (pTNM stages III and IV). Interestingly,

EZH2 Teicoplanin expression increased gradually with disease progression from normal liver through chronic hepatitis and/or cirrhosis to early and then advanced HCC (Fig. 1E). Increased expression of EZH2 was also significantly associated with various metastatic features of HCC, including the presence of venous invasion (P = 0.043), direct liver invasion (P = 0.014), and the absence of tumor encapsulation (P = 0.043) (Fig. 1F; Supporting Table 5). These findings highlight the pathological significance of EZH2 up-regulation during liver cancer development. After revealing the positive correlation between EZH2 expression and HCC aggressiveness, we decided to investigate the cellular and molecular effects of EZH2 up-regulation in HCC cells. Differential EZH2 expression was detected across a panel of HCC cell lines (Supporting Fig. 2D). Ectopic overexpression of EZH2 increased the levels of H3K27me3 in PLC/PRF/5 cells, which had low endogenous EZH2 levels (Supporting Fig. 3A).

Cumali Efe MD*, Tugrul Purnak MD†, Ersan Ozaslan

MD

Cumali Efe M.D.*, Tugrul Purnak M.D.†, Ersan Ozaslan

M.D.†, Staffan Wahlin M.D.‡, * Department of Internal Medicine, Ankara Numune Research and Education Hospital, Ankara, Turkey, † Department of Gastroenterology, Ankara Numune Research and Education Hospital, Ankara, Turkey, ‡ Department of Gastroenterology and Hepatology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. “
“Cholestasis with normal gamma glutamyl transferase characterizes functional deficiencies in the gene ABCB11, which encodes the bile salt export pump (BSEP), a liver-specific adenosine triphosphate (ATP)-binding selleck chemicals cassette transporter. Here we report the case of a patient presenting with features of benign recurrent intrahepatic cholestasis associated with a heterozygous mutation in the ABCB11 gene. Immunohistochemistry showed a gradual decrease of BSEP from zone 1 to zone 3 of the liver lobule, suggesting that the mutation identified here may predispose patients to cholestasis through a delocalization process of BSEP at the lobular level. (HEPATOLOGY 2013;57:2539–2541) ALT, alanine aminotransferase; ATP, adenosine triphosphate; BSEP, bile salt export pump; CT, computed tomography. A 44-year-old woman presented to the hospital for evaluation of progressive jaundice and

generalized itching during the previous 6 weeks. On physical exam her temperature was 36.5°C (97.7°F), the pulse was 72/min, and blood pressure was 125/80 mmHg. The liver was normal and there was no ascites. Examination PF-01367338 cell line of the skin revealed scratch lesions with crusts and erythema over the entire body with areas of minor injury in the mid-dorsal region that cannot be reached by hands (Fig. 1, Panel 1, dotted line). The grandmother and an aunt of this patient had had similar symptoms at the age of 40 with spontaneous resolution after several weeks. The patient had had an uneventful pregnancy 6 years earlier. She reported having suffered from gastroenteritis and having taken 500 mg acetaminophen twice during a stay in Tunisia 2 weeks before the development of jaundice. Laboratory studies revealed

a total bilirubin Resminostat of 155 μmol/L (6.7 mg/dL), alanine aminotransferase (ALT) 226 U/L, alkaline phosphatase 231 U/L, and gamma glutamyl transferase 36 U/L. Serum bile acids were elevated at 120 μmol/L (normal values <30 μmol/L). Ultrasound showed a normal liver parenchyma with a common bile duct diameter of 6 mm. An extensive diagnostic work-up including viral, autoimmune, and metabolic markers was negative. A computed tomography (CT) scan showed normal bile ducts and a large number of stones in the gallbladder (Fig. 1, Panel 2, arrow). The patient was administered antihistamine medication (hydroxyzine), rifampicin, and naltrexone without a significant improvement of her symptoms. Liver biopsy showed a normal parenchyma with major intrahepatocytic and intracanalicular cholestasis (Fig.

Primary cultures of mouse HSC were activated in response to cultu

Primary cultures of mouse HSC were activated in response to culture on plastic, marked by increased expression of alpha smooth muscle actin (αSMA) and collagen 1A1 (Col1A1) mRNA. Expression of mRNA and protein for the C5aR also increased during HSC activation in culture. To study if C5aR expression also increased during in vivo activation of HSC, hepatic fibrosis was induced in mice expressing GFP under the control of the collagen promoter by exposure to carbon tetrachloride. FACS analysis of GFP expressing HSC revealed an increased expression of C5aR, similar to that observed

in HSC activated in culture. To understand the functional significance of C5aR expression in activated HSC activation, we next investigated whether C5a influenced HSC activation or migration. Challenge of HSCs with C5a during culture had no effect on expression of αSMA and Col1A1, suggesting that C5a did selleck chemicals llc not influence HSC activation. Another important characteristic of HSC is their migratory capacity, primarily mediated by the chemokine MCP-1 and platelet derived growth factor (PDGF). Since C5a is a potent chemokine, we hypothesized that C5a would Lumacaftor molecular weight stimulate HSC migration. To test this hypothesis, wound healing cell migration assay was carried out. C5a enhanced HSC migration almost as efficiently as PDGF. C5a also stimulated the expression of MCP-1. C5a-induced cell migration was slower, but not completely inhibited, in presence of 227016, an MCP-1

receptor antagonist, suggesting C5a-induced migration occurs via MCP-1 dependent and independent mechanisms. Furthermore, C5a did not increase Ki67 nuclear staining, indicating wound healing was independent of cell proliferation. Taken together, these data reveal a novel mechanism for the interaction between complement and hepatic fibrosis, and suggest that C5a and its receptors are possible therapeutic targets in the treatment of liver fibrosis. PAK6 Disclosures: The following people have nothing to disclose: Dola Das, Jazmine Danner, Mark A. Barnes, Laura E. Nagy Hepatic fibrosis represents

the most worrisome histopathologic feature in non-alcoholic steatohepatitis (NASH) and it suggests a more severe and progressive liver damage. Understanding the mechanisms linking NASH to fibrogenesis is essential for defining potential novel therapeutic strategies. We have recently demonstrated (EASL 2013) that hepatocyte-derived microparticles (MPs) are released in the bloodstream during experimental NASH and their levels strongly correlate with severity of liver fibrosis. Here we tested the hypothesis that MPs released by hepatocytes during lipotoxicity alters hepatic stellate cells (HSC) biology resulting in its activation. Methods. For induction of lipotoxicity, the human hepatoma cells (HepG2) were treated with a saturated free fatty acids (FFA) including palmitic acid, or stearic acid, for up to 24hrs with various concentrations (0.25 to 0.50 mM).

The primary end point was the avoidance of a platelet transfusion

The primary end point was the avoidance of a platelet transfusion before, during, and up to 7 days after the procedure. A key secondary end point was the occurrence of bleeding (World Health Organization [WHO] grade 2 or higher) during this period. Results: A platelet transfusion was avoided in 104 of 145 patients who received eltrombopag (72%) and in 28 of 147 who received placebo (19%) (P<0.0001). No significant difference between the eltrombopag and placebo Gefitinib in vitro groups was observed in bleeding episodes of WHO grade 2 or higher, which were reported in 17% and 23% of patients, respectively. Thrombotic events of the portal venous system

were observed in 6 patients who received eltrombopag, as compared with 1 who received placebo, resulting in the early termination of the study. The incidence and severity of other adverse events were similar in the eltrombopag and placebo groups. Conclusions: Eltrombopag

reduced Torin 1 supplier the need for platelet transfusions in patients with chronic liver disease who were undergoing elective invasive procedures, but it was associated with an increased incidence of portal-vein thrombosis, as compared with placebo. (Funded by GlaxoSmithKline; ELEVATE ClinicalTrials.gov number, NCT00678587.) Platelets contribute to hemostasis in three ways. First, they adhere to the subendothelial matrix at the site of vessel wall injury by means of membrane receptors and the adhesive multimeric protein von Willebrand factor (Fig. 1, left). Second, they aggregate one another by means of membrane receptors and von Willebrand factor or fibrinogen (Fig. 1, left). Third, activated platelets help assemble vitamin K-dependent coagulation factors (i.e., tenase and prothrombinase complexes) on their surface by means of negatively charged phospholipids (i.e., phosphatidylserine), thus speeding up thrombin generation (Fig. 1, right) and fibrinogen-to-fibrin conversion. Patients with chronic liver disease are variably thrombocytopenic[1] and possibly thrombocytopathic[2] and this is considered an index of the bleeding risk, especially during/after invasive procedures. The bleeding

time, which was the test of choice to investigate primary hemostasis, has been performed for many years in patients who were about to undergo invasive procedures despite the fact that results of this test were not good Resveratrol predictors of bleeding in these patients.[3] As far as we know the bleeding time test is no longer carried out before invasive procedures, but platelet counts are still assessed and patients with low counts are considered at increased risk of bleeding. Guidelines for liver biopsy suggest platelet transfusion whenever platelet counts are lower than 50 × 109/L[4] and a survey conducted to assess the variation of practice showed that 81% of the respondents would use platelet transfusion before liver biopsy in patients with thrombocytopenia.

4% for intention-to-treat (ITT) analysis and 877% for per-protoc

4% for intention-to-treat (ITT) analysis and 87.7% for per-protocol (PP) analysis. The rates were statistically

significantly higher than those in Group Lev (66.2% and 72.6%) (p < 0.05). There were no severe adverse effects found in these two groups. Conclusions:  Fourteen-day quadruple therapy with a combination of proton-pump inhibitor, bismuth citrate, furazolidone, and rufloxacin is considered an effective and safe rescue therapy for H. pylori eradication after failure of standard triple treatment. "
“Background and Aims:  Fluoroquinolone-containing regimens have been suggested as an alternate to standard triple therapy for the treatment of Helicobacter pylori infections. To determine the relationship between fluoroquinolone resistance and mutations of GyrA and GyrB in H. pylori, we selleck chemicals llc exchanged the mutations at positions 87and 91 of

Autophagy activator GyrA among fluoroquinolone-resistant clinical isolates. GyrB of a strain with no mutations in GyrA was also analyzed to identify mechanisms of resistance to norfloxacin. Materials & Methods:  Natural transformation was performed using the amplified fragment of the gyrA and gyrB gene as donor DNA. The amino acid sequences of GyrA and GyrB were determined by DNA sequencing of the gyrA and gyrB genes. Results:  Norfloxacin-resistant strains which had mutations at position 87 and 91 became susceptible when the mutations were converted to the wild type. When the mutation from Asp to Asn at position 91 was exchanged to the mutation from Asn to

Lys at position 87, the MIC to levofloxacin, gatifloxacin, and sitafloxacin increased. Norfloxacin-resistant strain TS132 with no mutations in GyrA but had a mutation at position 463 in GyrB. Transformants obtained by natural transformation using gyrB DNA of TS132 had a mutation at position 463 of GyrB and revealed resistant to norfloxacin and levofloxacin. Conclusion:  Mutation from Asn to Lys at position 87 of GyrA confers higher resistance to levofloxacin and gatifloxacin than does mutation Amylase from Asp to Asn at position 91. We propose that mutation at position 463 in GyrB as a novel mechanism of fluoroquinolone resistance in H. pylori. “
“Background:  The relationship between H. pylori infection and anemia in childhood is still unclear. The aim of the study was to examine the association between H. pylori infection and anemia or iron deficiency in school-age children and in infants. Materials and Methods:  Six- to 9- year-old Israeli Arab children (N = 202) and infants (N = 197) were examined for hemoglobin and ferritin levels. ELISA was used to detect H. pylori antigens in stool specimens collected from the participants. Household characteristics were obtained through personal interviews with the mothers. Results:  The prevalence of anemia was 15.5 versus 5.5% in H. pylori-positive and -negative school-age children, respectively and 34.5 versus 29.8% in H. pylori-positive and -negative infants, respectively.

A total of 60 patients were admitted for surgery, however, surger

A total of 60 patients were admitted for surgery, however, surgery was not performed in five due to medical reasons. Indications for surgery was pain in 51patients

, gastric outlet obstruction in 2 and bleeding in 2 patients. Results: 38/60 were males and mean age was 37(SD± 12.94).22 patients were alcoholics and 17 were smokers.47 patients were on oral and 10 patients were on intravenous analgesics while 3 did not require regular analgesics.10 patients had diabetes mellitus and 11 had steatorrhea preoperatively.39 patients underwent Frey’s procedure while Whipple’s procedure was done in 6 and Izbicki’s procedure was done in two. LPJ was done in two while BAY 80-6946 chemical structure bipolar ligation and distal pancreatectomy with splenectomy(for splenic artery pseudo aneurysm) was done in another two. Roux-en-y cystojejunostomyperformed in 2. Three patients underwent reoperationsfor poor pain control; 2patient with LPJ done previously underwent Frey’s procedure after 2 years while one patientwho had undergone Frey’s procedure underwent Whipple’s procedure after 4 years. There were no in hospital mortalities.4 patients died during follow up; cause being alcoholic PLX4032 clinical trial cirrhosis in 2, suicide in 1 and diabetic ketoacidosis with sepsis in another. Two patients had postoperative intraluminal bleed and one needed re-exploration.

After a mean follow up of 23.9 months ± SE 23.6 months (median: 13 months; range 1 to 84 months) ; 54 % of patients reported excellent pain relief, 20% patients reported good pain relief and 11.4%

patients had fair pain relief(on regular oral pain killers). Two patients developed new onset diabetes controlled by diet and medications, while in 4 patients diabetes worsened.5 patients had new onset stetorrhea which was transient in all and settled with dietarymodification in two and enzyme supplementation in Miconazole another three. Conclusion: Tailored surgery for chronic pancreatitis has excellent benefit in pain relief without significant increase in functional abnormalities. Frey’s procedure was the commonest surgery performed in the present study. Key Word(s): 1. Chronic ; 2. Pancreatitis; 3. Surgery; 4. Outcome; Presenting Author: RAKESH KOCHHAR Additional Authors: MANISH MANRAI, JAHANGEERBASHA MEDARAPALEM, SREEKANTH APPASANI, PRADEEPKUMAR SIDDAPPA, THAKURDEEN YADAV, NIRANJAN KHANDELWAL, KARTAR SINGH Corresponding Author: RAKESH KOCHHAR Affiliations: Post Graduate Institute of Medical Education and Research Objective: To evaluate whether the site of fluid collections alters the clinical course of acute pancreatitis. Methods: Consecutive patients of acute pancreatitis &gt12 yrs of age between July 2011 and December 2012 were subjected to complete demographic profile, clinical and laboratory evaluation.