8% HIV+ and3.8% post-transplant. Regimens were SPR 37.9%, SR 42.4% and SS/R 19.8%. Overall 5% of patients discontinued treatment by 4 weeks. Among 592 patients with week 4 data, HCV RNA was UD in 75.0%, <50 IU/mL in 15.0%, 50-99 in 3.5%, 100-999 in 5.1% and ≥1000 in 1.4%. ALD patients were less likely to have UD HCV RNA (68.3%

vs 84.5%, p<0.0001; OR 0.47 95%CI 0.30-0.73, p=0.001) as were those on SR (67.5% SR, 73.4% SS/R, 84.0% SPR, p=0.0002; OR 0.32 95%CI 0.18-0.55 compared to SPR, p<0.0001). No association was found between age, sex, race/ethnicity, GT, prior treatment, HIV or transplant status and UD week 4 HCV RNA. In 347 patients with ALD, prior treatment (OR 0.59 95%CI 0.36-0.95, p=0.03), age>65 years (OR 0.38 95%CI 0.15-0.94 compared to <55, p=0.04), and SR regimen (OR 0.37 95%CI 0.19-0.69 DAPT mouse compared to SPR, p=0.002) were independent predictors of reduced likelihood of UD week 4 HCV RNA. In 245 patients without ALD, GT1 or 4 (OR 0.22 95%CI 0.05-0.84 compared to GT2, p=0.03)

and SR regimen (OR 0.15 95%CI 0.04-0.53 compared to SPR, p=0.003) were independent predictors of reduced likelihood of UD week 4 HCV RNA. Conclusion: In a large real-world cohort of patients treated with SOF-based regimens, 90% had undetectable or very low level HCV RNA at week 4 of treatment. ALD and use of SR was associated with a greater likelihood of detectable week 4 HCV RNA. The impact of low level viremia at week 4 on sustained virologic response is yet to be determined. Disclosures: The following people have nothing to disclose: Lisa Luminespib chemical structure I. Backus, Pamela S. Belperio, Troy A. Shahoumian, Larry A. Mole Objectives: Sofosbuvir (SOF) is the first nucleotide polymerase inhibitor with pan-genotypic

activity and a high barrier to resistance. Efficacy and safety have been demonstrated in five phase III clinical trials of SOF administered with either ribavirin (R) or a combination of pegylated interferon alfa see more and ribavirin (PR). SOF is also the first all-oral 24-week option available for patients unsuitable for interferon (UI). This analysis evaluated the cost-effectiveness of SOF in treatment-naïve (TN) genotype (GT) 1/4/5/6 and GT 2 and 3 patients who are TN, treatment-experienced (TE), interferon eligible (IE) and UI, in the UK. Methods: A Markov model followed a cohort of 10,000 patients over lifetime, with approximately 20% initiating treatment at the compensated cirrhotic stage. SOF/PR for 12 weeks was compared to telaprevir, boceprevir, PR and no treatment (NT); SOF/PR achieved 90% cure rates with only 12 weeks of treatment with no adverse drug reactions above those for PR. For patients UI SOF/RBV for either 12 or 24 weeks was compared to NT. The analysis took the perspective of the National Health Service.

Overall 5% of patients discontinued treatment by 4 weeks. Among 592 patients with week 4 data, HCV RNA was UD in 75.0%, <50 IU/mL in 15.0%, 50-99 in 3.5%, 100-999 in 5.1% and ≥1000 in 1.4%. ALD patients were less likely to have UD HCV RNA (68.3%

vs 84.5%, p<0.0001; OR 0.47 95%CI 0.30-0.73, p=0.001) as were those on SR (67.5% SR, 73.4% SS/R, 84.0% SPR, p=0.0002; OR 0.32 95%CI 0.18-0.55 compared to SPR, p<0.0001). No association was found between age, sex, race/ethnicity, GT, prior treatment, HIV or transplant status and UD week 4 HCV RNA. In 347 patients with ALD, prior treatment (OR 0.59 95%CI 0.36-0.95, p=0.03), age>65 years (OR 0.38 95%CI 0.15-0.94 compared to <55, p=0.04), and SR regimen (OR 0.37 95%CI 0.19-0.69 PF 2341066 compared to SPR, p=0.002) were independent predictors of reduced likelihood of UD week 4 HCV RNA. In 245 patients without ALD, GT1 or 4 (OR 0.22 95%CI 0.05-0.84 compared to GT2, p=0.03)

and SR regimen (OR 0.15 95%CI 0.04-0.53 compared to SPR, p=0.003) were independent predictors of reduced likelihood of UD week 4 HCV RNA. Conclusion: In a large real-world cohort of patients treated with SOF-based regimens, 90% had undetectable or very low level HCV RNA at week 4 of treatment. ALD and use of SR was associated with a greater likelihood of detectable week 4 HCV RNA. The impact of low level viremia at week 4 on sustained virologic response is yet to be determined. Disclosures: The following people have nothing to disclose: Lisa PS341 I. Backus, Pamela S. Belperio, Troy A. Shahoumian, Larry A. Mole Objectives: Sofosbuvir (SOF) is the first nucleotide polymerase inhibitor with pan-genotypic

activity and a high barrier to resistance. Efficacy and safety have been demonstrated in five phase III clinical trials of SOF administered with either ribavirin (R) or a combination of pegylated interferon alfa selleck chemical and ribavirin (PR). SOF is also the first all-oral 24-week option available for patients unsuitable for interferon (UI). This analysis evaluated the cost-effectiveness of SOF in treatment-naïve (TN) genotype (GT) 1/4/5/6 and GT 2 and 3 patients who are TN, treatment-experienced (TE), interferon eligible (IE) and UI, in the UK. Methods: A Markov model followed a cohort of 10,000 patients over lifetime, with approximately 20% initiating treatment at the compensated cirrhotic stage. SOF/PR for 12 weeks was compared to telaprevir, boceprevir, PR and no treatment (NT); SOF/PR achieved 90% cure rates with only 12 weeks of treatment with no adverse drug reactions above those for PR. For patients UI SOF/RBV for either 12 or 24 weeks was compared to NT. The analysis took the perspective of the National Health Service. Results: SOF, including interferon-free regimens, was shown to be cost-effective across all genotypes (£17,981/ QALY).

Among the 3,027 patients included in the Italian Liver Cancer study group database, we selected 205 Child-Pugh class A and Eastern Cooperative Group Performance Status 0 patients with cirrhosis with a single HCC ≤3 cm of diameter diagnosed during surveillance who were treated with curative intent (hepatic

resection, liver transplantation, percutaneous ethanol injection, radiofrequency thermal ablation). this website Patients were subdivided according to alpha-fetoprotein serum levels (i.e., normal ≤20 ng/mL; mildly elevated 21-200 ng/mL; markedly elevated >200 ng/mL). Patient survival, as assessed by the Kaplan-Meier method, was not significantly different among the three alpha-fetoprotein classes (P = 0.493). The same result was obtained in the subgroup of patients with a single HCC ≤2 cm (P = 0.714). An alpha-fetoprotein serum level of 100 ng/mL identified by receiver operating characteristic curve had inadequate accuracy (area under the curve = 0.536, 95% confidence interval = 0.465-0.606) to discriminate between survivors and deceased patients. Conclusion: Alpha-fetoprotein Selleckchem Gefitinib serum levels have no prognostic meaning in well-compensated cirrhosis patients with single, small HCC treated with curative intent. (HEPATOLOGY 2012) Hepatocellular carcinoma (HCC) is the third cause of cancer death and the leading cause of mortality among patients with cirrhosis.1 Liver

cirrhosis is in fact the main risk factor for HCC, and the annual incidence learn more of HCC in cirrhosis patients is 3%-7%.2, 3 Detecting HCC at an early stage is the main objective of screening and surveillance programs.3 Indeed, the utility of surveillance for HCC in patients with cirrhosis is supported by the results of a randomized trial carried out in patients with chronic hepatitis B virus (HBV) infection and several cohort studies performed in patients with cirrhosis.4-7 Surveillance of patients at risk of HCC with liver ultrasound, with or without serum alpha-fetoprotein assessment, is recommended by European, American, and Asiatic HCC

management guidelines with the aim to identify HCC at an early stage in those patients who, in the event of cancer detection, are amenable to curative therapies able to improve their prognosis.8-10 The American Association for the Study of Liver Diseases (AASLD) guidelines for HCC diagnosis and treatment, however, recently dropped alpha-fetoprotein assessment from the surveillance armamentarium due to poor sensitivity for early diagnosis of HCC and unacceptable specificity of this tumoral marker.10 Nonetheless, the use of alpha-fetoprotein as a prognostic indicator when HCC is diagnosed in the most favorable setting—patients with compensated cirrhosis, optimal performance status, single, small HCC, and as such amenable to curative treatment—has not been sufficiently addressed so far.

Among the 3,027 patients included in the Italian Liver Cancer study group database, we selected 205 Child-Pugh class A and Eastern Cooperative Group Performance Status 0 patients with cirrhosis with a single HCC ≤3 cm of diameter diagnosed during surveillance who were treated with curative intent (hepatic

resection, liver transplantation, percutaneous ethanol injection, radiofrequency thermal ablation). selleck screening library Patients were subdivided according to alpha-fetoprotein serum levels (i.e., normal ≤20 ng/mL; mildly elevated 21-200 ng/mL; markedly elevated >200 ng/mL). Patient survival, as assessed by the Kaplan-Meier method, was not significantly different among the three alpha-fetoprotein classes (P = 0.493). The same result was obtained in the subgroup of patients with a single HCC ≤2 cm (P = 0.714). An alpha-fetoprotein serum level of 100 ng/mL identified by receiver operating characteristic curve had inadequate accuracy (area under the curve = 0.536, 95% confidence interval = 0.465-0.606) to discriminate between survivors and deceased patients. Conclusion: Alpha-fetoprotein selleck kinase inhibitor serum levels have no prognostic meaning in well-compensated cirrhosis patients with single, small HCC treated with curative intent. (HEPATOLOGY 2012) Hepatocellular carcinoma (HCC) is the third cause of cancer death and the leading cause of mortality among patients with cirrhosis.1 Liver

cirrhosis is in fact the main risk factor for HCC, and the annual incidence see more of HCC in cirrhosis patients is 3%-7%.2, 3 Detecting HCC at an early stage is the main objective of screening and surveillance programs.3 Indeed, the utility of surveillance for HCC in patients with cirrhosis is supported by the results of a randomized trial carried out in patients with chronic hepatitis B virus (HBV) infection and several cohort studies performed in patients with cirrhosis.4-7 Surveillance of patients at risk of HCC with liver ultrasound, with or without serum alpha-fetoprotein assessment, is recommended by European, American, and Asiatic HCC

management guidelines with the aim to identify HCC at an early stage in those patients who, in the event of cancer detection, are amenable to curative therapies able to improve their prognosis.8-10 The American Association for the Study of Liver Diseases (AASLD) guidelines for HCC diagnosis and treatment, however, recently dropped alpha-fetoprotein assessment from the surveillance armamentarium due to poor sensitivity for early diagnosis of HCC and unacceptable specificity of this tumoral marker.10 Nonetheless, the use of alpha-fetoprotein as a prognostic indicator when HCC is diagnosed in the most favorable setting—patients with compensated cirrhosis, optimal performance status, single, small HCC, and as such amenable to curative treatment—has not been sufficiently addressed so far.

After reviewing the title or abstract for evidence of the use of US for the diagnosis of musculo-skeletal lesions in haemophilia, we selected 24 of these references. We added data collected from our experience to the most important data found in the references. Our main conclusion is that US is highly valuable for the diagnosis of musculo-skeletal diseases in haemophilia. It is a fast, effective, safe, available, comparative, real-time technique that can help us confirm the clinical examination. It is particularly important in acute haemarthrosis, as it can be used to objectively identify the presence of blood in the joints, measure its

size, pinpoint its location, assess its evolution and this website confirm its complete disappearance. “
“Children with active Rucaparib bleeding or a history of excessive bleeding need a structured evaluation to determine if they suffer from a bleeding disorder and, if so, the etiology of the bleeding disorder. A structured evaluation should

begin with a comprehensive medical history focusing on the child’s history of bleeding. The bleeding history is optimally obtained using validated bleeding questionnaires. This is followed by a thorough family history taking note of abnormal bleeding in close relatives, and any history of parental consanguinity. The physical examination should look for clues to possible underlying bleeding disorders. In general, laboratory testing commences with screening tests. These are able, in most cases, to point toward possible underlying disorders that can be confirmed by specific laboratory tests. Unfortunately,

mild bleeding disorders are often not detected in screening tests and, in children with clinically significant bleeding, additional specific tests are warranted. “
“Summary.  von Willebrand’s disease (VWD) is regarded as the most common congenital bleeding disorder, and although not available in all laboratories von Willebrand factor (VWF) activity is most frequently assessed as ristocetin cofactor (VWF:RCo). This test can be technically challenging, is subject to poor sensitivity (∼20 IU dL−1 VWF:RCo) click here and has a high degree of inter- and intra-assay imprecision [coefficient of variation (cv) > 25%]. We studied an automated assay using a combined fixed platelet/ristocetin reagent (BC von Willebrand reagent, Siemens Healthcare Diagnostics) on the CS-2000i analyser (Sysmex UK Ltd). Initially inter- and intra-assay imprecision was assessed. The automated method showed good day-to-day reproducibility and linearity of standard curves. This technique, also gave low intra- and inter-assay imprecision using commercial normal (cv < 4.5%) and pathological (cv < 8.1%) control plasmas.

After reviewing the title or abstract for evidence of the use of US for the diagnosis of musculo-skeletal lesions in haemophilia, we selected 24 of these references. We added data collected from our experience to the most important data found in the references. Our main conclusion is that US is highly valuable for the diagnosis of musculo-skeletal diseases in haemophilia. It is a fast, effective, safe, available, comparative, real-time technique that can help us confirm the clinical examination. It is particularly important in acute haemarthrosis, as it can be used to objectively identify the presence of blood in the joints, measure its

size, pinpoint its location, assess its evolution and GSK-3 activity confirm its complete disappearance. “
“Children with active find more bleeding or a history of excessive bleeding need a structured evaluation to determine if they suffer from a bleeding disorder and, if so, the etiology of the bleeding disorder. A structured evaluation should

begin with a comprehensive medical history focusing on the child’s history of bleeding. The bleeding history is optimally obtained using validated bleeding questionnaires. This is followed by a thorough family history taking note of abnormal bleeding in close relatives, and any history of parental consanguinity. The physical examination should look for clues to possible underlying bleeding disorders. In general, laboratory testing commences with screening tests. These are able, in most cases, to point toward possible underlying disorders that can be confirmed by specific laboratory tests. Unfortunately,

mild bleeding disorders are often not detected in screening tests and, in children with clinically significant bleeding, additional specific tests are warranted. “
“Summary.  von Willebrand’s disease (VWD) is regarded as the most common congenital bleeding disorder, and although not available in all laboratories von Willebrand factor (VWF) activity is most frequently assessed as ristocetin cofactor (VWF:RCo). This test can be technically challenging, is subject to poor sensitivity (∼20 IU dL−1 VWF:RCo) selleck compound and has a high degree of inter- and intra-assay imprecision [coefficient of variation (cv) > 25%]. We studied an automated assay using a combined fixed platelet/ristocetin reagent (BC von Willebrand reagent, Siemens Healthcare Diagnostics) on the CS-2000i analyser (Sysmex UK Ltd). Initially inter- and intra-assay imprecision was assessed. The automated method showed good day-to-day reproducibility and linearity of standard curves. This technique, also gave low intra- and inter-assay imprecision using commercial normal (cv < 4.5%) and pathological (cv < 8.1%) control plasmas.

In this model, passenger leukocytes, which are donor-derived hepatic resident leukocytes, appear to mediate much of the injury. CD39tg livers were more resistant to IRI and were deficient in both CD4+ T cells and iNKT cells. Reconstitution of these livers with a WT immune system (restoring resident T-cell number and function) abolished resistance. Furthermore, WT donor livers depleted of CD4+ T cell showed similar protection

to CD39tg donor livers. Although CD4+ iNKT cells represent 20% to 40% of hepatic T cells,27 conventional http://www.selleckchem.com/products/MK-1775.html CD4+ T cells appeared to be the prime orchestrators of early hepatic injury, as livers from iNKT KO mice were not protected. The role of CD4+ T-cell subsets in warm hepatic IRI has been defined.28 T-cell activation occurring through antigen-dependent and -independent mechanisms mediates liver injury through neutrophil recruitment and activation.

Further, NKT cell activation can cause direct liver injury in partial hepatic warm IRI.28 Our data are in accordance with recent observations in a similar mouse liver transplantation model using CD1d KO donors and WT recipients,29 but is at odds with data from a warm model of hepatic IRI where systemic blocking of NKT cells was protective and adoptive transfer of NKT cells in T-cell-deficient mice restored injury.14 This discrepancy suggests that warm and cold IRI have two distinct pathophysiologies and that the immune Selleck AZD1208 response against the transplanted organ differs from the response to local ischemia. Further, NK and NKT cells mediate phase-specific responses in IRI: depletion of NK1.1 cells, which encompass both NK and NKT cells, failed to moderate

IRI at early timepoints17 but significantly reduced later hepatocellular damage.14 NK and NKT cells are a prime source of IFN-γ, which becomes critically important at 24 hours of reperfusion. Our data confirm selleck chemical that CD4+ iNKT cells of donor origin have minimal effect during the early phase (within 6 hours) of IRI. We have previously shown that the overexpression of CD39 on the renal parenchyma mitigates IRI up to 72 hours following transplantation.15 However, overexpression of CD39 within the hepatic parenchyma appears to play a minor role, if any, in this model of liver transplantation. Recipient circulating T cells, particularly CD4+ T cells, are recruited to the liver within hours of perfusion.16 It was anticipated that the adenosine-rich milieu created by CD39 overexpression would modify the inflammatory response. However, there was no significant difference in the susceptibility to IRI of WT or CD39tg donor livers following reconstitution with WT bone marrow, suggesting minimal if any effect of tissue restricted overexpression of CD39. This was unexpected, given the potent antiinflammatory effects of adenosine, but may be accounted for by the very short half-life of adenosine in the circulation.

In this model, passenger leukocytes, which are donor-derived hepatic resident leukocytes, appear to mediate much of the injury. CD39tg livers were more resistant to IRI and were deficient in both CD4+ T cells and iNKT cells. Reconstitution of these livers with a WT immune system (restoring resident T-cell number and function) abolished resistance. Furthermore, WT donor livers depleted of CD4+ T cell showed similar protection

to CD39tg donor livers. Although CD4+ iNKT cells represent 20% to 40% of hepatic T cells,27 conventional click here CD4+ T cells appeared to be the prime orchestrators of early hepatic injury, as livers from iNKT KO mice were not protected. The role of CD4+ T-cell subsets in warm hepatic IRI has been defined.28 T-cell activation occurring through antigen-dependent and -independent mechanisms mediates liver injury through neutrophil recruitment and activation.

Further, NKT cell activation can cause direct liver injury in partial hepatic warm IRI.28 Our data are in accordance with recent observations in a similar mouse liver transplantation model using CD1d KO donors and WT recipients,29 but is at odds with data from a warm model of hepatic IRI where systemic blocking of NKT cells was protective and adoptive transfer of NKT cells in T-cell-deficient mice restored injury.14 This discrepancy suggests that warm and cold IRI have two distinct pathophysiologies and that the immune Selleck BMS-354825 response against the transplanted organ differs from the response to local ischemia. Further, NK and NKT cells mediate phase-specific responses in IRI: depletion of NK1.1 cells, which encompass both NK and NKT cells, failed to moderate

IRI at early timepoints17 but significantly reduced later hepatocellular damage.14 NK and NKT cells are a prime source of IFN-γ, which becomes critically important at 24 hours of reperfusion. Our data confirm selleck products that CD4+ iNKT cells of donor origin have minimal effect during the early phase (within 6 hours) of IRI. We have previously shown that the overexpression of CD39 on the renal parenchyma mitigates IRI up to 72 hours following transplantation.15 However, overexpression of CD39 within the hepatic parenchyma appears to play a minor role, if any, in this model of liver transplantation. Recipient circulating T cells, particularly CD4+ T cells, are recruited to the liver within hours of perfusion.16 It was anticipated that the adenosine-rich milieu created by CD39 overexpression would modify the inflammatory response. However, there was no significant difference in the susceptibility to IRI of WT or CD39tg donor livers following reconstitution with WT bone marrow, suggesting minimal if any effect of tissue restricted overexpression of CD39. This was unexpected, given the potent antiinflammatory effects of adenosine, but may be accounted for by the very short half-life of adenosine in the circulation.

Subsequently, praziquantel 2400 mg/day and predonisolone 30 mg/day were administered for 28 days to treat NCC, and the brain cystic lesions was completely disappeared. Results: In this case, mitochondrial DNA analysis confirmed the diagnosis of NCC as the Asian genotype of Taenia solium. The route

of infection was presumed to be infected pork meat ingested in west Asia. Conclusion: Capsule endoscopy for detecting GI lesion is a very useful tool as a decision of treatment strategy for NCC. Key Word(s): 1. Capsule endoscopy neurocysticercosis Presenting Author: TOSHIFUMI MITANI Additional Authors: HOTEYA SHU, MITSURU KAISE Corresponding Author: TOSHIFUMI MITANI Affiliations: Toranomon Hospital, Toranomon Hospital Objective: Endoscopic submucosal dissection (ESD) is also useful therapy for colorectal tumors because AUY-922 price large and difficult lesions can be resected in an en bloc fashion. However, the Methods: This study

enrolled 958 consecutive colorectal epithelial neoplasms, conducted by ESD procedures in Toranomon Hospital from June 2005 to December 2013 and retrospectively examined. Rates of en bloc resection, R0 resection, and major complications were analyzed as short-term outcomes. As long-term outcomes, over-all survival were assessed in 508 patients followed up more BMS-777607 in vivo than 1 year in our hospital. Results: Total results of this study was shown that male: female was 518: 328, mean age 65.4 years (range 34–91 years), mean tumor size 30.7 mm (range 4–209 mm), procedure time 67.9 minutes (range: 5–500 minutes), Rates of en bloc resection and R0 resection 98.5% and 91.0%, respectively. Perforation occurred in 3.4% and 8 cases of perforation were managed with surgical treatment.

Postoperative bleeding occurred in 3.0% and endoscopically managed, 3 cases were required with blood transfusion. Additional colectomy was undergone for 45 patients and 3 cases were proven lymph node metastasis. Local recurrence was detected in 4 lesions. There were no patients died of primary colorectal cancer but 7 patients died of other diseases and over-all survival rate was 96.2%. Conclusion: Excellent short-term and long-term outcomes revealed that ESD showed acceptable resectability for colorectal tumor although our data was single-center retrospective study. Key Word(s): 1. selleck kinase inhibitor Colorectal ESD; 2. outcomes Presenting Author: HEE SEOK MOON Additional Authors: SE WOONG HWANG, HYUN YONG JEONG Corresponding Author: HEE SEOK MOON Affiliations: Department of Internal Medicine, Department of Internal Medicine Objective: Hyperplastic polyps are the most common type of gastric polyps that constitute 30–93% of all benign epithelial gastric polyps. The overall prevalence of dysplasia in patients with hyperplastic polyps is believed to be <2%, and higher in patients with large polyps (>2 cm). We aimed to identify the clinical features of hyperplastic polyps that undergo neoplastic transformation.

Subsequently, praziquantel 2400 mg/day and predonisolone 30 mg/day were administered for 28 days to treat NCC, and the brain cystic lesions was completely disappeared. Results: In this case, mitochondrial DNA analysis confirmed the diagnosis of NCC as the Asian genotype of Taenia solium. The route

of infection was presumed to be infected pork meat ingested in west Asia. Conclusion: Capsule endoscopy for detecting GI lesion is a very useful tool as a decision of treatment strategy for NCC. Key Word(s): 1. Capsule endoscopy neurocysticercosis Presenting Author: TOSHIFUMI MITANI Additional Authors: HOTEYA SHU, MITSURU KAISE Corresponding Author: TOSHIFUMI MITANI Affiliations: Toranomon Hospital, Toranomon Hospital Objective: Endoscopic submucosal dissection (ESD) is also useful therapy for colorectal tumors because BVD-523 nmr large and difficult lesions can be resected in an en bloc fashion. However, the Methods: This study

enrolled 958 consecutive colorectal epithelial neoplasms, conducted by ESD procedures in Toranomon Hospital from June 2005 to December 2013 and retrospectively examined. Rates of en bloc resection, R0 resection, and major complications were analyzed as short-term outcomes. As long-term outcomes, over-all survival were assessed in 508 patients followed up more selleck chemical than 1 year in our hospital. Results: Total results of this study was shown that male: female was 518: 328, mean age 65.4 years (range 34–91 years), mean tumor size 30.7 mm (range 4–209 mm), procedure time 67.9 minutes (range: 5–500 minutes), Rates of en bloc resection and R0 resection 98.5% and 91.0%, respectively. Perforation occurred in 3.4% and 8 cases of perforation were managed with surgical treatment.

Postoperative bleeding occurred in 3.0% and endoscopically managed, 3 cases were required with blood transfusion. Additional colectomy was undergone for 45 patients and 3 cases were proven lymph node metastasis. Local recurrence was detected in 4 lesions. There were no patients died of primary colorectal cancer but 7 patients died of other diseases and over-all survival rate was 96.2%. Conclusion: Excellent short-term and long-term outcomes revealed that ESD showed acceptable resectability for colorectal tumor although our data was single-center retrospective study. Key Word(s): 1. selleck Colorectal ESD; 2. outcomes Presenting Author: HEE SEOK MOON Additional Authors: SE WOONG HWANG, HYUN YONG JEONG Corresponding Author: HEE SEOK MOON Affiliations: Department of Internal Medicine, Department of Internal Medicine Objective: Hyperplastic polyps are the most common type of gastric polyps that constitute 30–93% of all benign epithelial gastric polyps. The overall prevalence of dysplasia in patients with hyperplastic polyps is believed to be <2%, and higher in patients with large polyps (>2 cm). We aimed to identify the clinical features of hyperplastic polyps that undergo neoplastic transformation.