This epidemiologic disparity between donor size and recipient needs led to the use of reduction hepatectomies/segment liver transplantation and the development of other innovative transplant surgical techniques based on reduced size grafts, including split liver transplantation and the

use of organs from living donors.[96-99] These advances allowed more widespread application of liver transplantation for children. During 2011-2012, 64 centers performed at least one liver transplant in a patient <18 years of age; 23 programs performed 20 or more transplants in this population during that time frame.[100] Pediatric pretransplant www.selleckchem.com/products/VX-809.html mortality has steadily decreased, most dramatically for candidates less than 1 year of age. The number of new pediatric candidates added to the liver transplant waiting

list was 704 in 2011.[100, 101] In 2011, there were 477 deceased donor pediatric liver transplants and 59 living donor transplants. Graft survival has continued to improve for pediatric recipients. Despite this high success rate, challenges remain, including the need for targeted preoperative management to address the problems of malnutrition, and improved methods to prevent graft loss while avoiding the consequences of immunosuppression, such as posttransplant lymphoproliferative disease (PTLD) and renal injury.[99] All elements were in place for expansion and validation of Pediatric Hepatology. In the mid-1990s centers that focused selleckchem on Pediatric Hepatology became a component of many divisions of Pediatric the Gastroenterology. Research flourished with the application of state-of-the-art cellular and molecular biology techniques and the emergence of molecular genetics, which enhanced our understanding and recognition of the pathophysiological and genetic basis of an increasing number of disorders of the liver

in children.[102] With clinical and research efforts converging, the field rapidly gained momentum. The next key ingredient to establishing the formal field was to create and sustain a critical mass and validate the concept of Pediatric Hepatology as an academic subspecialty. In a decision that reflected validation and maturity, “Hepatology” was added to the name of the major Pediatric Gastroenterology society—which became the North American Society of Pediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN). This is symmetrical with the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN). In 1993, perhaps as a measure of the growth of the field (or the verbosity of the author) the chapter on Liver Disease in Infancy and Childhood in the 7th Edition of Diseases of the Liver (Leon and Eugene Schiff; editors) was 104 pages long!103 A community of colleagues interested in Pediatric Hepatology was being built.

This study provided some of the first evidence to suggest

that radical surgery with lymphadenectomy was unnecessary for certain gastric cancers due to the extremely low incidence of spread to lymph nodes.43 Curative endoscopic resection of early intramucosal gastric cancers has since become a valid therapeutic option, but until recently was restricted to small lesions less than 2 cm in size with no MK-1775 ic50 evidence of surface ulceration. Although other publications suggested that certain lesions invading into the submucosa also carried a low risk of progression, these studies were limited by small patient cohorts.44–46 Gotoda and colleagues published extensive data in 2000 that provided a more robust evidence base for the expansion

of endoscopic resection criteria. They examined the presence of lymph node metastasis in 5265 patients who underwent gastrectomy with lymph node dissection for early gastric cancer from two centers. Only Smad inhibitor 2.2% (65/3016) of intramucosal cancers were associated with regional lymph node metastasis. Of these lesions, lymph node metastasis was associated with poor differentiation, signet ring histology, lymphovascular invasion and lesions greater than 3 cm with surface ulceration. Specifically, intramucosal lesions without ulceration did not demonstrate lymph node metastasis irrespective of size. Gotoda et al. also showed that 18% of cancers with deeper invasion into the submucosal layer were associated with lymph node metastasis. However, lesions less than 3 cm in size

with submucosal invasion less than 500 µm, well- or moderately differentiated histology and no evidence of lymphovascular involvement demonstrated no lymph node metastasis. Table 4 summarizes data from this study, showing the lesion types that displayed no evidence of lymph node metastasis.47 In 2004, the Japanese Gastric Cancer Association issued expanded criteria for the treatment of early gastric cancer based on this study.48 Hirasawa and colleagues have since explored undifferentiated early gastric cancers in a similar population eltoprazine of 3843 Japanese patients. Undifferentiated lesions confined to the mucosa, less than 20 mm in diameter, without lymphovascular involvement or ulcer presence showed no lymph node metastasis. They proposed that endoscopic resection should also be considered for these lesions, thus further expanding the criteria for endoscopic management of gastric cancer.49 Other studies of the risk of lymph node metastasis in poorly differentiated lesions have produced similar results, although they involved smaller patient numbers.50–53 Worldwide, colorectal cancer incidence ranks fourth in frequency in men and third in women. Despite a relatively good prognosis, rates of colorectal cancer are rising rapidly in countries such as Japan where the risk was previously low.

Methods: Immunohistochemistry and western blot was used to show the expression of NKX 6.1 in check details the gastric cancer tissues and cell lines. Results: In our study, expression

of Nkx 6.1 was examined by IHC in most of the fresh gastric cancer tissues. In addition, Nkx 6.1 expressed at high levels in gastric cell lines SGC 7901, MGC 803 and HGC 27. Conclusion: Our finds suggest that Nkx 6.1 is expressed in gastric cancer cell lines. Key Word(s): 1. Gastric cancer; 2. Nkx 6.1; 3. IHC; Presenting Author: NADIR ARBER Additional Authors: SHIRAN SHAPIRA, DINA KAZANOV, SARAH KRAUS, ITAI BENHAR Corresponding Author: SHIRAN SHAPIRA, DINA KAZANOV, SARAH KRAUS, NADIR ARBER Affiliations: Tel-Aviv Sourasky Medical Center; Tel Aviv University Objective: Background: CD24, a heavily glycosylated GPI-anchored protein,

was proven as a valid target in GI malignancies. Anti-CD24 mAb treatment induces a significant growth inhibition of cancer cells, in a time- and dose-dependent manner, and reduces tumor growth in vivo. Aim: Engineer anti-CD24 chimeric, humanized and matured full-length IgGs, smaller derivatives, and toxin-immunconjugates. Methods: Methods: Edman-degradation, cDNA synthesis, sequence and computational analysis were performed to reveal the entire DNA sequence of the murine Ab. Replacement of the Fc with human IgG1 resulted in a mouse-human Enzalutamide mouse chimera. A scaffold human Ab was chosen for grafting critical sequences of the murine antibody into it. The immunotoxins were constructed first by non-covalent linking via the ZZ-protein (derived from Staphylococcus aureus). Then a bacterial system allowed a covalent linkage between the toxic molecule and the Ab. Sophisticated and high-efficiency engineering-technologies were established to construct, express and purify 15 novel anti-CD24 derivatives in tissue or bacterial cultures. Their binding-affinity, selective-targeting and cytotoxic activities were confirmed in several CD24-expressing GI tumors cells. Results: Results: The chimeric and humanized forms

have high affinity and Org 27569 selectivity towards the CD24 antigen that work additively with standard chemotherapies. The immunotoxins were superior to the unarmed Ab with lower IC50 values. Antibody targeting and accumulation within the tumor and its excess clearance was clearly demonstrated using direct imaging (SWA11-ZZ-mCherry-HIS fluobody). The scFv-toxin killed CD24-expressing cells with an IC50 of 1 μg/ml, while the values for the IgG-ZZ-toxin were lower (0.02-0.05 μg/ml). The IC50 values of the humanized anti-CD24(di/tetra)-PE38 and the scFv were similar, suggesting that the absence of post-translational modifications, in the E.coli-producing IgG, affected reactivity. MTD studies confirmed no toxicity at high dose of 40 mg/kg. Conclusion: Conclusion: Targeting CD24 may be a promising treatment for GI malignancies.

12 As hypercholesterolemia and diabetes are strongly associated with major vascular events, a holistic approach to NAFLD treatment is needed, including adequate treatment of metabolic conditions (e.g., diabetes and dyslipidemia).18, 19 As well as the emerging relevance of NAFLD for cardiovascular Idasanutlin ic50 diseases,30 this collaborative study highlights the risk of liver-related events and mortality in NAFLD with advanced fibrosis. The risk factors we identified for liver-related complications are of relevance to the practicing clinician, including

progressive rises in serum bilirubin and fibrosis stage for liver-related mortality and a low platelet count for both ascites and varices (consistent with a portal hypertensive etiology). The MELD score did not predict outcomes in our NAFLD cohort, which can be explained by patients being Child-Pugh class A at enrollment rather than assessment for liver transplantation. Many of the factors that play a role in the MELD equation, such as age, were independent predictors (in this case, of overall mortality and encephalopathy). Interestingly, the AST/ALT ratio (commonly used to differentiate fatty liver clinically from other etiologies) also served as a predictor of overall mortality, having previously been shown to independently distinguish between patients with BIBW2992 order and without advanced

liver fibrosis.31 In summary, in this multicenter, collaborative study, there were independent risk factors for vascular, liver, and all-cause outcomes in patients with NAFLD with advanced fibrosis or cirrhosis who had no overt evidence of hepatic decompensation

at enrollment. At these histological stages, NAFLD appears to lead to lower rates of liver-related complications and lower rates of HCC than patients with HCV infection of a similar disease stage, albeit the overall mortality in both conditions seems to be similar. However, larger, prospective studies are necessary to shed further insights on the impact of NAFLD on liver- and vascular-related morbidity and mortality. Additional Supporting Information may be found in the online version of this article. “
“The ectodomain of major histocompatibility complex Thalidomide class I–related chain A (MICA) is shed from tumor cells, and may be an important means of evading antitumor immunity. This study investigated the roles of a disintegrin and metalloproteinase 9 (ADAM9) in the shedding of MICA in human hepatocellular carcinoma (HCC). Small interfering RNA–mediated knockdown (KD) of ADAM9 resulted in up-regulation of membrane-bound MICA expression on the HepG2 and PLC/PRF/5 cellular surfaces and down-regulation of soluble MICA levels in their culture supernatant. ADAM9 was cleaved at a site between Gln347 and Val348 of MICA in vitro.

In patients with the favorable IL28B genotype, IP-10 levels tended to be lower but correlated well with the level of HCV RNA, suggesting that in this setting IP-10 production, and possibly production of other ISGs, is driven by and thus proportionate to the amount of virus present. However, in patients with the unfavorable genotypes IP-10 Selleck NVP-LDE225 levels were on average higher and appeared to be entirely independent of the HCV RNA level. This might suggest that the fundamental problem in those with the unfavorable genotypes is a loss of regulation of ISG induction such that ISGs are produced independent of the stimulus and therefore lead

to a less coordinated viral response. Although speculative, further research on this relationship could help clarify the elusive role of the IL28B genotype.

Although IP-10 is an ISG, it is also an important chemotactic factor for cells of the adaptive immune response, which are very important for spontaneous clearance. Higher levels of IP-10 might be expected to drive more immune cells to the liver and thus promote viral clearance. However, recent evidence has shown that IP-10 can undergo cleavage to form an inactive version of the protein that may act as a dominant negative by binding the CXCR3 receptor without leading to chemotaxis.19 It is possible that the higher levels of IP-10 seen in patients without spontaneous clearance are due to the cleaved inactive form of IP-10. Lastly, an additional explanation is that very high IP-10 levels may lead Rucaparib solubility dmso to chemorepulsion inhibiting migration of

immune cells to the liver, leading to persistent HCV infection. Understanding the role of IP-10 cleavage in HCV and other infections is clearly a priority for future studies. The observation that individuals of Aboriginal ethnicity had a lower proportion with high plasma IP-10 levels compared to Caucasians is unexpected and notably independent of IL28B genotype. Black ethnicity has been associated with higher IP-1017, 24 and preactivated ISG expression profiles10 compared to Caucasians, which has been attributed to SNPs in interferon Selleck Afatinib signaling pathway genes and interferon-stimulated genes, but is not completely understood.11 Further research investigating the role of Aboriginal ethnicity and IP-10 levels would be interesting to clarify whether there are pathways for differential innate immune responses that might lead to lower IP-10 production and ultimately explain the higher rates of spontaneous clearance reported in Aboriginals.29 As previously reported in chronic HCV, associations between plasma IP-10 levels and IL28B genotype18, 25 and HCV genotype16, 26 were observed in unadjusted analyses, but these were not significant in adjusted analysis. An association was observed between higher ALT and IP-10 levels in acute HCV, which is consistent with previous data in chronic HCV.

To test whether DCs may contribute to HSC activation and liver fibrogenesis, we first performed selleck a coculture of DCs and HSCs. Similar to HMs, DCs did not activate HSCs but rather up-regulated the expression of NF-κB–dependent genes, and NF-κB–driven luciferase reporter activity through an IL-1– and TNF-dependent manner (Fig. 6B). However, activation of NF-κB was considerably lower than the induction we observed in HM coculture. Based on these

results, we next determined whether DC ablation may have contributed to the reduced fibrogenesis in clodronate-treated mice. In our first approach, we performed BDL in diphtheria toxin-treated or PBS-treated bone marrow–chimeric CD11c-DTR-eGFP mice. Bone marrow chimerism avoids the known side effects of diphtheria toxin treatment observed after long-term Cell Cycle inhibitor treatment in global CD11c-DTR-eGFP mice.[26] We did not observe a significant difference in BDL-induced fibrosis as determined by sirius red staining and qRT-PCR

for the fibrogenic genes α-SMA, Col1a1, and TIMP1 (Fig. 6C-D). We confirmed these data employing CCl4 injection for induction of liver fibrosis, again using bone marrow-chimeric CD11c-DTR-eGFP mice. Similar to the BDL model, we did not observe significant differences in liver fibrosis between PBS and diphtheria toxin-treated mice (Fig. 6E). As a third approach, we used antibody-mediated ablation of pDC. Again, we did not observe a reduction of CCl4-induced liver fibrosis (Fig. 6F). Importantly, we achieved considerable oxyclozanide depletion of cDC and pDC using the above methods (Supporting Fig. 8). Similar to previous studies,[27] we observed neutrophilia in CD11c-DTR mice (Supporting Fig. 9) but consider this unlikely to exert a profound effect on fibrosis based on previous studies.[28] Thus, our data suggest that neither class of DC significantly contributes to liver fibrogenesis in vivo. Hepatic fibrogenesis involves multiple resident and recruited cell populations. HSCs represent the center component of this wound healing response, but

other populations, including macrophages, are known positive modulators of fibrogenesis. Here, we uncover a novel function of macrophages, the promotion of HSC/myofibroblast survival. A second novel finding of our study lies in the discovery that DCs do not contribute to liver fibrosis. Employing microarray and pathway analysis, we discovered that NF-κB, the best-characterized antiapoptotic signaling pathway[29, 30] and an important regulator of liver injury and fibrosis,[31] was a key pathway activated in HSCs by HMs. The relevance and physiologic nature of the employed in vitro coculture system is validated by the finding that this system achieves HSC gene expression patterns highly similar to those found in in vivo–activated HSCs, and that all gene expression changes and functional consequences of NF-κB activation were confirmed in vivo.

855, p < 0.01). Computerized NCTs was able to diagnose

www.selleckchem.com/products/Adrucil(Fluorouracil).html MHE with 88.9% sensitivity and 87.5% specificity (Area under the curve = 0.958, p < 0.01). Conclusion: Computerized Number Connection Tests is established and preliminarily confirmed to be a valid and reliable method for screening of MHE. Key Word(s): 1. liver cirrhosis; 2. MHE; 3. NCT; Presenting Author: CHAO DU Additional Authors: DEMING JIANG Corresponding Author: CHAO DU Affiliations: Chengdu Military Command Objective: To explore the possibility and validity of differentiation of rat bone mesenchymal stem cells (BMSCs) into hepatocytes with a culture system containing salidroside and cholestatic rat serum in vitro. Methods: BMSCs were isolated by selleck compound plastic adherence from whole bone marrow of health SD rat at the age of 2–3 weeks, identifying

stem cell surface markers of CD45, CD14, CD34, CD79a, CD90, CD105 by the flow assay; cholestatic serum were prepared by common bile duct ligation from 10 health SD rats at the age of 10–13 weeks. the 3rd – passage BMSCs were divided into three groups for vitro induction by the different culture systems : Group A : basic growth medium plus 5% cholestatic serum; Group B : basic growth medium plus 5% cholestatic serum plus 30UM salidroside; group C : basic growth medium plus 5% cholestatic serum plus 20 ug / L Hepatocyte Growth Factor (HGF); observing changes of cell morphology during culture time in each group-induced, RT-PCR assay to detect mRNA expression of alpha-fetoprotein (AFP) and albumin (ALB); Western-Blot assay to detect protein expression levels of AFP and ALB. Results: The BMSCs highly express CD90, CD105, did not express CD45, CD14, CD34, CD79a, the cells of three groups appear polygonal and binucleate cells in the procedure of induction; The mRNA and protein expression of AFP and ALB emerged in the three groups on the 7th day; in the same period the lowest expression

ratio was in group A (p < 0.05), while there was no significant difference between group B and group C (p > 0.05). Conclusion: Salidroside and cholestatic serum can effectively induce BMSCs differentiated into hepatocytes. Key Word(s): 1. cholestatic serum; 2. salidroside; 3. induction; 4. HGF; Arachidonate 15-lipoxygenase Presenting Author: SU SHUAI Additional Authors: LIUWEN TIAN, WANGBANG MAO Corresponding Author: SU SHUAI Affiliations: TIANJIN MEIDICAL UNIVERSITY GENERAL HOSPITAL Objective: To investigate the clinical characteristics of Chinese patients with Peliosis hepatis. Methods: ReIevant data of Chinese Peliosis hepatis Patients were retrieved from PubMded and CNKI database and a meta–analysis was conducted Results: A total of 27 Peliosis hepatic cases had been reported by Chinese hospitals with obscure causes, mainly manifestied as abdominal distention and edema, accompanied with transudative ascites and maybe Hemorrhagic ascites. Liver rupture was reported in 4 patients and Liver dysfunction was in 44.44% patients..

Janssen – Consulting: Abbott, Bristol Myers Squibb, Debio, Gilead Sciences, Merck, Medtronic, Novartis, Roche, Santaris; Grant/Research Support: Anadys, Bristol Myers Squibb, Gilead Sciences, Innogenetics, Kirin, Merck, Medtronic, Novartis, Roche, Santaris Maria Buti – Advisory Committees or Review Panels: Gilead,

Janssen, Vertex, MSD; Grant/Research Support: Gilead, Janssen; Speaking and Teaching: Gilead, Janssen, Vertex, Novartis The following people have nothing to disclose: Iskren A. Kotzev Introduction: In patients with chronic hepatitis B (CHB) who failed on prior nucleos(t)ide (NUC) therapy, see more rescue therapy should involve an effective antiviral regimen that is active against any existing drug-resistant hepatitis B virus (HBV) variants. Combination therapy with entecavir (ETV) and tenofovir disoproxil fumarate (TDF), two potent agents with non-overlapping resistance profiles, may provide a single regimen suitable for all patients who failed on other NUC regimens. Here we present Week 96 results of the ENTEBE study assessing ETV+TDF for patients with prior failure on NUC therapy. Methods: In this single-arm, open-label, multicenter study, CHB patients with prior non-response, partial response, or virologic breakthrough on NUC therapy were treated with ETV (1 mg) plus TDF (300 mg) for 96 weeks. The primary endpoint was the proportion of patients with HBV DNA <50 IU/mL (Roche

COBAS TaqMan-HPS Assay) at Week 48 (non-completer=-failure). Secondary endpoints included proportions of patients

with antiviral responses at Ulixertinib Week 96, safety, and resistance to ETV or adefovir (ADV). Results: Overall, 92 patients were treated; 6 patients discontinued prior to Week 96. At baseline, 65% of patients were HBeAg(+), median HBV DNA was 3.7 log10 IU/mL. Prior NUC treatment included monotherapy with ETV (53%), lamivudine (LVD; 22%), TDF (12%), (ADV; 4%), or telbivudine (LdT; 2%), or combinations of these agents (7%); 58% of patients had evidence of single- or multidrug resistance mutations (LVD: 52%, ETV: 26%; ADV: 7%). At Week 48, 76% (70/92) of patients achieved Tenofovir mw the primary endpoint (HBV DNA <50 IU/mL). By Week 96, 85% (78/92) of patients had HBV DNA <50 IU/mL, including 80% (16/20) with prior failure on LVD, 100% (4/4) on ADV, 88% (42/48) on ETV, 82% (9/11) on TDF, 100% (2/2) on LdT, and 83% (5/6) on combination therapy. No treatment-emergent resistance to ETV or ADV was observed. Six patients had on-treatment serious adverse events, none of which were considered related to study treatment. One patient died from hepatocellular carcinoma. Conclusions: In patients who failed prior NUC therapy, 96 weeks of ETV+TDF combination therapy was well tolerated and achieved virologic suppression in the majority (85%) of patients, irrespective of the type of prior NUC, with no new resistance development. All data shown as % (n/N). *Primary endpoint.

pylori density and gastritis could be of help in reducing the risk of H. pylori-associated complication later in life [82]. Finally, as a perspective it is fascinating the hypothesis of using probiotics to inhibiting H. pylori adhesion to gastric epithelial cells thus preventing H. pylori colonization especially in young children or H. pylori re-infection in high-risk patients. Results so far are encouraging and further clinical trials are called for. The design of such studies should be such as to clarify which probiotic

strains are suitable, in what form, in what dose and for how long. No competing interests or financial support exist. “
“This review concerns important pediatric studies published from April 2013 to March 2014. New data on pathogenesis have demonstrated that Th1 type cytokine secretion at the gastric level is less intense in children compared with adults. They have learn more also shown that the most significant risk factor for Helicobacter pylori infection is the parents’ click here origin and frequency of childcare in settings with a high prevalence of infection. A new hypothesis on the positive relationship between childhood H. pylori

infection and the risk of gastric cancer in adults has been suggested which calls for an implementation of preventive programs to reduce the burden of childhood H. pylori infection in endemic areas. Several studies have investigated the role of H. pylori infection in iron-deficiency anemia, and results support the role of the bacterium in this condition. ZD1839 in vitro Antibiotic resistance is an area of intense research with data confirming an increase in antibiotic resistance, and the effect of CYP2C19 genetic polymorphism on proton-pump inhibitor metabolism should be further investigated as cure rates are lower in extensive metabolizers. Studies confirmed that probiotic supplementation may have beneficial effects on eradication and therapy-related

side effects, particularly diarrhea in children. In numerous studies, the influence of Helicobacter pylori virulence on the development of various diseases has been studied. Alvarez et al. [1, 2] studied methylation of some genes predisposing to gastric cancer. They observed that THBS1 and GATA-4 were methylated already in the early stage of infection and are downregulated. HIC-1 demonstrated the lowest level of methylation and therefore, the main mechanism of downregulation has to be different. On the other hand, methylation of promotor regions of MGMT and MLH 1 depended on the duration of the infection. Nodular gastritis was very frequently associated with H. pylori infection in childhood. Nodular gastritis associated with H. pylori infection can commonly occur in childhood and is regarded as benign with no clinical significance. Yang et al. [3] analyzed gastric mucosa-associated lymphoid tissue (MALT) to clarify the significance of nodular gastritis in 80 H.

Only through the endoscopists in cooperation with the ultrasound doctors to the integration of its advantages, the rational the use of medical resources, without increasing the the medical input, will be able

to www.selleckchem.com/products/KU-60019.html effective in reducing the of PEG surgery the complications of and for surgical risk. It can be perform more convenient in the primary hospitals in China with high clinical value in use. Key Word(s): 1. PEG; 2. abdominal ultrasound; 3. enteral nutrition; Presenting Author: RAVINDRA SATARASINGHE Additional Authors: JAYEWARDENE RATHNAYAKE, SATHYAJITH AMBAWATTE, NAYOMISHERMILA JAYASINGHE, RAVI WIJESINGHE, PUBUDU DE SILVA, NARTHANI RASENDRAN Corresponding Author: RAVINDRA SATARASINGHE, NAYOMISHERMILA JAYASINGHE Affiliations: Sri Jayewardenepura Hospital Objective: To endoscopically evaluate the aetiology of dysphagia in adult Sri Lankans presented to a tertiary care hospital. Methods: Case notes of 2728 patients who

had undergone upper gastrointestinal endoscopy from 15th of February 2002 to 15th February 2013 in the principle author’s unit at Sri Jayewardenepura General Hospital, Kotte, Sri Lanka were retrospectively analyzed. Results: There were 148 dysphagics (5.4%) in the sample. Age range was 11 years to 95 years. Mean age of presentation was 62.2 ± 17.0 SD years. Sex distribution male: female was 1 : 1.3 with

a slight female predominance. The endoscopic findings were hiatus hernia, normal appearance, EPZ-6438 cell line non erosive GORD, oesophagitis, oesophageal malignancies and oesophagial candidiasis of 50.6%, 54%, 22.9%, 19.5%, 20.3% and 2% instances respectively with overlaps. Barrett’s oesophagus was found only in one patient. A post cricoid web was found with Plummer Vinson syndrome in another. Mean age of hiatus hernia patients was 60.0 ± 16.4 SD years and Sex distribution male: female was 1 : 1.2. Mean age of endoscopically normal patients was 65.2 ± 16.0 SD years. Sex distribution male: female was 2: 3. Mean age of non erosive GORD patients was 59.4 ± 17.1 SD years and had a sex distribution male: female of 1.3: 1. Mean age of oesophagitis SDHB patients was 58.4 ± 18.0 SD years. Sex distribution male: female was 1: 1.3. Mean age of patients who has had oesophageal malignancies was 62.3 ± 11.8 SD years. Sex distribution male: female of 3: 2. Conclusion: Oesophageal malignancies as a cause of dysphagia were found in 1/5th in this cohort. The role of the hiatus hernia was unclear in the causation of dysphagia. Neuromuscular incordination could have played a major role in the endoscopically normal patients. Dysphagia as an indication for endoscopy was rare in this population. Key Word(s): 1. dysphagia; 2. endoscopy; 3.