Most patients suffer a severe bleeding diathesis that includes postnatal umbilical cord bleeding, cutaneous bruising and haematomas, intramuscular and joint haemorrhage, postoperative haemorrhage, impaired wound healing, spontaneous abortions in early pregnancy and intracranial haemorrhage, which is the major cause

of death [40]. Typically, bleeding Volasertib research buy symptoms occur hours or days after trauma as the initially formed uncrosslinked fibrin clot is not stable. The possible diagnosis of congenital FXIII deficiency should not be delayed in any child with an unidentified bleeding disorder. Prolonged umbilical bleeding with a normal coagulation profile mandates FXIII analysis. Congenital FXIII deficiency can be caused by mutations in both FXIII genes. More than 70 causative mutations in the FXIII-A gene have been published, but only five mutations in the FXIII-B gene (see online databases www.f13-database.de, and those held by the ISTH at www.isth.org/and www.hgmd.cf.ac.uk). Most mutations code for a single amino acid exchange resulting in defective folding and instability of the mutant protein [40]. Acquired FXIII deficiency has been

reported in several conditions. FXIII A-subunit levels fall to 20–70% from decreased synthesis or consumption. Over 30 cases of severe FXIII deficiency caused by autoantibodies against FXIII-A have also been reported (∼30% in association with systemic lupus erythematosus [SLE]). These may inhibit FXIII activation or FXIIIa activity [41]. Clinical symptoms in congenital selleck chemicals medroxyprogesterone FXIII deficiency may be suggestive, but the diagnosis must be based on appropriate laboratory tests. Unless there is another concomitant coagulation disorder, typical coagulation screening tests are normal. Traditionally, solubility of fibrin clots in urea, acetic acid or monochloroacetic acid solution (clot solubility test)

has been used for screening. This qualitative method detects only very severe FXIII deficiency, is not standardized, and its sensitivity depends on the fibrinogen level, the clotting reagent (thrombin and/or Ca2+) and the solubilizing agent and its concentration. The detection limit varies between <0.5% and 5% FXIII activity. The high number of undiagnosed or late-diagnosed FXIII deficiencies is partly attributable to the use of this test and it is therefore no longer recommended. Diagnosis and classification of FXIII deficiencies require a quantitative functional FXIII activity assay that detects all forms of FXIII deficiency as a first-line screening test. Quantitative FXIII activity assays are based on two assay principles: (i) Measurement of ammonia released during the transglutaminase reaction and (ii) measurement of labelled amine incorporated into a protein substrate.

No study has examined the role of EGF genotype, and only one study has examined the role of PNPLA3 genotype in LT recipients. IL28B genotype is associated with IFN-based treatment response in LT recipients, although data differ regarding its association with allograft disease course. We

sought to determine whether these SNPs predict cirrhosis development and graft survival in a multicenter population. Methods: HCV Erlotinib patients who underwent LT at MGH, Beth Israel Deaconess, and Lahey Clinic between 1990 and 2008 were studied. Genotypes were determined from donor wedge or allograft biopsies and recipient explants. Cox proportional hazards regression model was used to assess time to cirrhosis, liver-related death, and re-LT, adjusting for donor age and sustained virologic response (SVR) as a time-dependent covariate. Logistic regression was used to assess SVR in patients receiving antiviral therapy. Results: The cohort comprised 257 LT recipients followed for a median of 6.9 years. We observed a trend towards a higher rate of progression

to cirrhosis among recipients with an EGF non-AA vs. AA donor genotype (adjusted HR 2.02; 95%CI 0.93–4.37; p=0.07). No association was observed between recipient EGF, IL28B, and PNPLA3 or donor IL28B and PNPLA3 genotypes and cirrhosis. Additionally, no association was observed between these genotypes and graft survival. Among treated patients, the presence of

the CC IL28B variant in either the recipient (R) or donor (D) liver was associated with increased rate of SVR Maraviroc cost (R-CC/D-CC 8/12 [67%], R-non-CC/ D-CC 19/42 [45%], R-CC/D-non-CC 3/9 [33%], R-non-CC/D-non-CC 12/45 [27%], p=0.07). Conclusions: Recipient EGF, IL28B, and PNPLA3 and donor IL28B and PNPLA3 genotypes do not predict adverse outcomes in LT recipients with HCV. www.selleck.co.jp/products/Romidepsin-FK228.html A potential association exists between donor EGF genotype and cirrhosis. Since the EGF GG genotype produces higher serum and liver levels of EGF than the non-GG genotype, and since the EGF receptor is involved in HCV entry, this finding is biologically plausible. Future efforts will be directed at investigating this relationship in larger cohorts. The results also suggest that IL28B and PNPLA3 genotypes do not play a major role in determining the natural history of allograft hepatitis C. Disclosures: Jessica L. Mueller – Employment: NIDDK Kathleen E. Corey – Advisory Committees or Review Panels: Gilead; Speaking and Teaching: Synageva Kenneth K. Tanabe – Patent Held/Filed: EGF SNP and risk for HCC, EGFR inhibition and HCC, gene signature for prognosis in cirrhosis Michael P. Curry – Grant/Research Support: Gilead Sciences, Mass Biologics, Merck, Salix, Conatus; Stock Shareholder: Achilion, Idenix Raymond T.

Patients were censored at the date of the last follow-up, death, or liver retransplantation. The multivariate Cox proportional hazards regression analysis was used to evaluate the independence of the MBL2, FCN2, and MASP2 SNPs or the quantity of gene polymorphisms. The forced entry method, including all variables, as well as the backward elimination regression method (Wald statistic) was applied. Results were considered statistically significant

when P values were <0.05. Bonferroni correction for multiple comparison see more tests was not performed because SNPs were selected on the basis of a deducible hypothesis. All analyses were performed with the SPSS statistical software package (version 16.02; SPSS, Inc., Chicago, IL). The principal study

consisted of 143 patients who received OLT (Table 1) of which 59 (41%) encountered a CSI within the selleck kinase inhibitor first year after transplantation. The MBL2, FCN2, and MASP2 genotype distribution of recipients and donors were analyzed in relation to the cumulative incidence of CSI in the first year after OLT (Supporting Table 2). Patients receiving a liver from an MBL-deficient donor (XA/O or O/O) had an increased cumulative incidence of CSI compared to those receiving a wild-type liver (Table 2). In addition, patients receiving a donor liver with at least one copy of the minor T-allele of FCN2 SNP rs17549193 (+6359CT) also had an increased cumulative CSI incidence. Interestingly, the absence of the minor C-allele (homozygosity for the major A-allele) of MASP2 SNP rs12711521 (+371AC) in the donor liver was also accompanied with an increased incidence

of CSI. The joint genetic effect of risk-conferring variants of MBL2, FCN2, and/or MASP2 present within the donor liver were clustered as the lectin pathway gene very profile (Table 2). This profile, including the number of risk-conferring gene variants, showed an ever-increasing cumulative risk for developing CSI with increasing numbers of variants: 18% CSI with no genetic variant, 33% in those with one, 50% in those with two, and 75% in those with three variants (P = 0.002; Table 2 and Fig. 1). The genotype distribution in OLT recipients (Supporting Table 2) showed no significant association with the occurrence of CSI either for the independent SNPs or for the number of risk-conferring variants (not shown). However, some remarkable interactions between the genotype of the donor and the recipient with the occurrence of CSI were found. Recipients with an MBL-sufficient or wild-type MBL genotype (A/A and YA/O) receiving an MBL-insufficient (XA/O and O/O) donor liver developed significantly more CSI than the other patients (61% [17/28] versus 37% [42/115], respectively, P < 0.006).

Patients were censored at the date of the last follow-up, death, or liver retransplantation. The multivariate Cox proportional hazards regression analysis was used to evaluate the independence of the MBL2, FCN2, and MASP2 SNPs or the quantity of gene polymorphisms. The forced entry method, including all variables, as well as the backward elimination regression method (Wald statistic) was applied. Results were considered statistically significant

when P values were <0.05. Bonferroni correction for multiple comparison Selleckchem SCH727965 tests was not performed because SNPs were selected on the basis of a deducible hypothesis. All analyses were performed with the SPSS statistical software package (version 16.02; SPSS, Inc., Chicago, IL). The principal study

consisted of 143 patients who received OLT (Table 1) of which 59 (41%) encountered a CSI within the this website first year after transplantation. The MBL2, FCN2, and MASP2 genotype distribution of recipients and donors were analyzed in relation to the cumulative incidence of CSI in the first year after OLT (Supporting Table 2). Patients receiving a liver from an MBL-deficient donor (XA/O or O/O) had an increased cumulative incidence of CSI compared to those receiving a wild-type liver (Table 2). In addition, patients receiving a donor liver with at least one copy of the minor T-allele of FCN2 SNP rs17549193 (+6359CT) also had an increased cumulative CSI incidence. Interestingly, the absence of the minor C-allele (homozygosity for the major A-allele) of MASP2 SNP rs12711521 (+371AC) in the donor liver was also accompanied with an increased incidence

of CSI. The joint genetic effect of risk-conferring variants of MBL2, FCN2, and/or MASP2 present within the donor liver were clustered as the lectin pathway gene nearly profile (Table 2). This profile, including the number of risk-conferring gene variants, showed an ever-increasing cumulative risk for developing CSI with increasing numbers of variants: 18% CSI with no genetic variant, 33% in those with one, 50% in those with two, and 75% in those with three variants (P = 0.002; Table 2 and Fig. 1). The genotype distribution in OLT recipients (Supporting Table 2) showed no significant association with the occurrence of CSI either for the independent SNPs or for the number of risk-conferring variants (not shown). However, some remarkable interactions between the genotype of the donor and the recipient with the occurrence of CSI were found. Recipients with an MBL-sufficient or wild-type MBL genotype (A/A and YA/O) receiving an MBL-insufficient (XA/O and O/O) donor liver developed significantly more CSI than the other patients (61% [17/28] versus 37% [42/115], respectively, P < 0.006).

Patients were censored at the date of the last follow-up, death, or liver retransplantation. The multivariate Cox proportional hazards regression analysis was used to evaluate the independence of the MBL2, FCN2, and MASP2 SNPs or the quantity of gene polymorphisms. The forced entry method, including all variables, as well as the backward elimination regression method (Wald statistic) was applied. Results were considered statistically significant

when P values were <0.05. Bonferroni correction for multiple comparison learn more tests was not performed because SNPs were selected on the basis of a deducible hypothesis. All analyses were performed with the SPSS statistical software package (version 16.02; SPSS, Inc., Chicago, IL). The principal study

consisted of 143 patients who received OLT (Table 1) of which 59 (41%) encountered a CSI within the Selleck Atezolizumab first year after transplantation. The MBL2, FCN2, and MASP2 genotype distribution of recipients and donors were analyzed in relation to the cumulative incidence of CSI in the first year after OLT (Supporting Table 2). Patients receiving a liver from an MBL-deficient donor (XA/O or O/O) had an increased cumulative incidence of CSI compared to those receiving a wild-type liver (Table 2). In addition, patients receiving a donor liver with at least one copy of the minor T-allele of FCN2 SNP rs17549193 (+6359CT) also had an increased cumulative CSI incidence. Interestingly, the absence of the minor C-allele (homozygosity for the major A-allele) of MASP2 SNP rs12711521 (+371AC) in the donor liver was also accompanied with an increased incidence

of CSI. The joint genetic effect of risk-conferring variants of MBL2, FCN2, and/or MASP2 present within the donor liver were clustered as the lectin pathway gene Galactosylceramidase profile (Table 2). This profile, including the number of risk-conferring gene variants, showed an ever-increasing cumulative risk for developing CSI with increasing numbers of variants: 18% CSI with no genetic variant, 33% in those with one, 50% in those with two, and 75% in those with three variants (P = 0.002; Table 2 and Fig. 1). The genotype distribution in OLT recipients (Supporting Table 2) showed no significant association with the occurrence of CSI either for the independent SNPs or for the number of risk-conferring variants (not shown). However, some remarkable interactions between the genotype of the donor and the recipient with the occurrence of CSI were found. Recipients with an MBL-sufficient or wild-type MBL genotype (A/A and YA/O) receiving an MBL-insufficient (XA/O and O/O) donor liver developed significantly more CSI than the other patients (61% [17/28] versus 37% [42/115], respectively, P < 0.006).

In all CR patients after eradication treatment, the TLA finding had disappeared (100%); see more however, in the non-CR patients, TLA remained the same as before the eradication therapy (p = 0.002). Conclusion: These results suggest that NBI magnifying endoscopy may be useful not only in the diagnosis but also in the evaluation of response to eradication therapy of MALT lymphoma of the stomach. Key Word(s): 1. NBI; 2. malt Presenting Author: KOUICHI NONAKA Additional Authors: KEN OHATA, MAIKO TAKITA, YASUSHI MATSUYAMA, TOMOAKI TASHIMA, YOHEI MINATO, NOBUYUKI MATSUHASHI Corresponding Author: KOUICHI NONAKA Affiliations: Ntt Medical Center Tokyo, Ntt Medical Center

Tokyo, Ntt Medical Center Tokyo, Ntt Medical Center Tokyo, Ntt Medical Center Tokyo, Ntt Medical Center Tokyo Objective: Probe-based confocal laser endomicroscopy (pCLE) is a new imaging modality that enables the in vivo histological Luminespib mw evaluation of gastrointestinal mucosa during ongoing endoscopy. As confocal imaging is possible by fluorescein of the tissue, fluorescein contrast is necessary for pCLE. Fluorescein is intravenously administered. The side effects of fluorescein include yellow-colored urine, nausea, and exanthema. However, these symptoms resolve over time. Other severe adverse effects are extremely rare. However, some studies indicated that the intravenous administration of fluorescein caused shock or arterial ischaemia. To promote the widespread application of pCLE,

an alternative method in which pCLE can be more safely performed compared

to the intravenous administration of fluorescein should be developed. We successfully obtained Fludarabine an image quality similar to that on intravenous administration by dripping fluorescein in the duodenal mucosa, and not by intravenous administration, and reported it as a first in the world (Digestive Endoscopy, 2014). Methods: In 3 subjects, crystal violet, indigo carmine, Lugol’s iodine, and 10% fluorescein were dripped on the upper gastrointestinal mucosa (esophagus, gastric body, and duodenum) in this order. Finally, 2.5 mL of 10% fluorescein was intravenously injected, and the image with this was used as a control. Results: In the stomach and duodenum, images could be acquired only with the dripping and intravenous injection of fluorescein in all subjects, and the images were favorable for histological evaluation. In the esophagus, images could also be acquired only with the dripping and intravenous injection of fluorescein, but the images were insufficient to evaluate the histology. Conclusion: Confocal laser endomicroscopy was suggested to be inappropriate for histological evaluation of the esophageal mucosa. For the stomach and duodenum, it was suggested that dripping a very small amount of fluorescein is an alternative to intravenous administration, being a clue to promoting the widespread of confocal laser endomicroscopy. We also report on the preparation and skills for the fluorescein dripping method. Key Word(s): 1.

10 The objectives of this article are (1) to provide a description of all adult patients enrolled in NASH CRN studies; (2) to determine the associations of basic clinical variables with the diagnosis of definite NASH, stage of fibrosis, grade of inflammation and presence of hepatocellular ballooning injury; and (3) to determine the overall accuracy of models using only demographic and basic clinical variables to predict the presence find more of NASH,

and the activity grade and fibrosis stage of NASH. A similar analysis of the clinical and histological features of NAFLD in children enrolled in the NASH CRN studies has been published.11 ANA, antinuclear antibody; ASMA, anti-smooth muscle antibody; ANA, antimitochondrial antibody; ALT, alanine aminotransferase; AST, aspartate aminotransferase; AUROC, area under the receiver operator characteristic curve; BMI, body mass index; CI, confidence interval; GGT, gamma glutamyl transpeptidase; HDL, high-density lipoprotein; HOMA-IR, homeostasis model of assessment of insulin resistance; LDL, low-density lipoprotein; NAFLD, nonalcoholic fatty

liver disease; NASH, nonalcoholic steatohepatitis; NASH CRN, NASH Clinical Research Network; NAS, NAFLD activity score; NCEP, National Cholesterol Depsipeptide clinical trial Education Program; NIDDK, National Institute of Diabetes and Digestive and Kidney Diseases. Patients with suspected or histologically proven NAFLD were enrolled into the Database observational study at nine U.S. medical centers: Case Western Reserve (Cleveland, OH); Duke University (Durham, NC); Indiana University (Indianapolis, IN); Johns Hopkins University (Baltimore, MD); Saint

Louis University (St. Louis, MO); University of California, San Diego (San Diego, CA); University of California, San Francisco (San Francisco, CA); University of Washington (Seattle, WA); and Virginia Commonwealth University (Richmond, VA). The data were stored, monitored, Adenosine and analyzed at the Data Coordinating Center at the Johns Hopkins Bloomberg School of Public Health. The NASH CRN enrolled into the Database patients who were at least 2 years of age who met any one of the following criteria: (1) a histologic diagnosis of NAFLD; (2) a histologic diagnosis of cryptogenic cirrhosis; (3) suspected NAFLD based on imaging studies; (4) clinical evidence of cryptogenic cirrhosis. Patients were excluded if they had clinical or histological evidence of alcoholic liver disease or alcohol consumption during the 2 years before entry of more than 20 g daily for men and 10 g daily for women.

Conclusion: Chest CT scan for achalasia patients undergoing a POEM procedure can be used to detect early signs of postoperative bleeding, but routine

application is probably not warranted. The role in guiding the management of post-POEM pneumothorax who need intervention has to be studied further. Key Word(s): 1. POEM; 2. esophageal achalasia; 3. chest CT scan; Presenting Author: AKRAM POURSHAMS Additional Authors: ELHAM JAFARI Corresponding Author: AKRAM POURSHAMS Affiliations: Tehran University of Medical Sciences; Tehran University of Medical Sciences Objective: The incidence of esophageal squamous cell carcinoma (ESCC) shows geographic variation. Northeastern Iran (Golestan province) Quizartinib cost has one of the highest incidences of ESCC in the world, over 50 per 100,000 person-years. Aim: to identify host and environmental risk factors associated with ESCC in northeastern Iran. Methods: we included published data of all ecologic, case-control studies, and the Golestan Cohort Study, (50,000 members) that conducted by the Digestive Disease Research Center of Tehran University of Medical Sciences (with collaboration of national DAPT cell line and international cancer research centers) in the area during the last 13 years. Results: Socio-economic status was inversely

related to ESCC. The strongest inverse association was found with education. Poor oral health was also correlated to ESCC. A total of 16.7%, 13.7% and 0.7% of cohort members were current tobacco, opium and alcohol consumers respectively. Tobacco and opium use was strongly associated with ESCC in the case-control study but alcohol consumption was not. About 98% of the cohort participants drank black tea regularly, (mean volume >1 L/d), 39.0% drank their tea at temperatures less than 60°C, 38.9% at 60–64°C, and 22.0% at 65°C or higher. Drinking very hot tea was associated with increased risk of ESCC (OR: 8.16, 3.93–16.9). Fresh vegetable, fruit and Vitamin A intake were low especially in ESCC cases and rural dwellers.

Two cross sectional studies have confirmed high exposure of the general population to polycyclic aromatic hydrocarbons (PAHs). An ecologic study suggests that certain foods and cooking methods increase exposure to PAHs. In addition, levels Non-specific serine/threonine protein kinase of PAH DNA adducts was significantly higher in ESCC tissues than in normal tissues of cases and healthy controls. The highest rate of TP53 mutations ever reported in any cancer was observed. Also a high rate of p16 hyper methylation was reported in ESCC tissues. A nonsense variant of BRCA2 was associated with higher ESCC risk with a frequency of 4.6% among cases and 0.8% among controls. No selenium deficiency was observed among cohort members. Contamination with carcinogenic mycotoxins was not found in raw rice, sorghum and wheat samples. The prevalence of the gluten-sensitive enteropathy was about 1%, so this disease is unlikely to be a risk for ESCC in the area.

We assessed the usefulness of capsule endoscopy (CE) for detecting small-bowel lesions in such patients. Methods: Seventy-seven patients who underwent CE for investigation of chronic abdominal symptoms lasting >3 months were classified into four groups according to

their symptoms: (A) chronic abdominal pain (n = 39), (B) chronic Sotrastaurin molecular weight diarrhea (n = 20), (C) chronic abdominal pain and diarrhea (n = 10), (D) chronic abdominal discomfort (n = 8). Overall and per-group total enteroscopy rates, mean small-bowel transit times, small-bowel lesion detection rates, and types of lesions detected were examined. Results: The total enteroscopy rate was 83% (64/77), with per-group rates of (A) 71% (28/39), (B) 90% (18/20), (C) 100% (10/10) and (D) 100% (8/8). Among the 64 total enteroscopies, mean small-bowel transit time was 268 minutes;

per-group times were (A) 268 minutes, (B) 262 minutes, (C) 277 minutes and (D) 265 minutes. The small-bowel lesion detection rate was 29% (22/77); per-group rates Hydroxychloroquine were (A) 15% (6/39), (B) 40% (8/20), (C) 70% (7/10) and (D) 13% (1/8), being significantly high in group C versus groups A and D. Small-bowel lesions detected by CE were non-specific enteritis (n = 9), NSAID ulcer (n = 3), non-specific ulcer (n = 3), Schönlein-Henoch purpura (n = 2), eosinophilic enteritis (n = 2), Crohn disease (n = 1), jejunum

adenoma (n = 1) and lupus enteritis (n = 1). Of the 22 patients in whom small-bowel lesions were detected, 9 (41%) were treated successfully by medication. Conclusion: CE is useful medroxyprogesterone when upper and lower gastrointestinal endoscopy don’t identify the cause of chronic abdominal symptoms. Key Word(s): 1. capsule endoscopy; 2. small-bowel; 3. abdominal symptom; Presenting Author: CRISTIANO SPADA Additional Authors: CESARE HASSAN, LEONARDO MINELLI GRAZIOLI, SAMUEL ADLER, PAOLA CESARO, LUCIO PETRUZZIELLO, GUIDO COSTAMAGNA Corresponding Author: CRISTIANO SPADA Affiliations: Catholic University; Bikur Holim Hospital Objective: Flat lesions gained special attention because were noted to have a higher risk than polypoid lesions. Studies indicate a prevalence ranging between 5%–25%. These lesions are difficult to detect and may be easily missed at optical colonoscopy (OC). Colon Capsule Endoscopy (CCE) was proven to be accurate for significant findings (polyps ≥6 mm) with a sensitivity and specificity for polyps ≥10 mm of 88% and 89–95%, respectively. The ability of CCE to detect flat colonic lesions is unknown. Aims: To primarily evaluate the ability of CCE in diagnosing flat colonic lesions. Methods: This is a retrospective evaluation of patients enrolled in prospective comparative trials that used OC as gold standard.

We assessed the usefulness of capsule endoscopy (CE) for detecting small-bowel lesions in such patients. Methods: Seventy-seven patients who underwent CE for investigation of chronic abdominal symptoms lasting >3 months were classified into four groups according to

their symptoms: (A) chronic abdominal pain (n = 39), (B) chronic Selleckchem Roxadustat diarrhea (n = 20), (C) chronic abdominal pain and diarrhea (n = 10), (D) chronic abdominal discomfort (n = 8). Overall and per-group total enteroscopy rates, mean small-bowel transit times, small-bowel lesion detection rates, and types of lesions detected were examined. Results: The total enteroscopy rate was 83% (64/77), with per-group rates of (A) 71% (28/39), (B) 90% (18/20), (C) 100% (10/10) and (D) 100% (8/8). Among the 64 total enteroscopies, mean small-bowel transit time was 268 minutes;

per-group times were (A) 268 minutes, (B) 262 minutes, (C) 277 minutes and (D) 265 minutes. The small-bowel lesion detection rate was 29% (22/77); per-group rates Selleckchem Palbociclib were (A) 15% (6/39), (B) 40% (8/20), (C) 70% (7/10) and (D) 13% (1/8), being significantly high in group C versus groups A and D. Small-bowel lesions detected by CE were non-specific enteritis (n = 9), NSAID ulcer (n = 3), non-specific ulcer (n = 3), Schönlein-Henoch purpura (n = 2), eosinophilic enteritis (n = 2), Crohn disease (n = 1), jejunum

adenoma (n = 1) and lupus enteritis (n = 1). Of the 22 patients in whom small-bowel lesions were detected, 9 (41%) were treated successfully by medication. Conclusion: CE is useful Bcl-w when upper and lower gastrointestinal endoscopy don’t identify the cause of chronic abdominal symptoms. Key Word(s): 1. capsule endoscopy; 2. small-bowel; 3. abdominal symptom; Presenting Author: CRISTIANO SPADA Additional Authors: CESARE HASSAN, LEONARDO MINELLI GRAZIOLI, SAMUEL ADLER, PAOLA CESARO, LUCIO PETRUZZIELLO, GUIDO COSTAMAGNA Corresponding Author: CRISTIANO SPADA Affiliations: Catholic University; Bikur Holim Hospital Objective: Flat lesions gained special attention because were noted to have a higher risk than polypoid lesions. Studies indicate a prevalence ranging between 5%–25%. These lesions are difficult to detect and may be easily missed at optical colonoscopy (OC). Colon Capsule Endoscopy (CCE) was proven to be accurate for significant findings (polyps ≥6 mm) with a sensitivity and specificity for polyps ≥10 mm of 88% and 89–95%, respectively. The ability of CCE to detect flat colonic lesions is unknown. Aims: To primarily evaluate the ability of CCE in diagnosing flat colonic lesions. Methods: This is a retrospective evaluation of patients enrolled in prospective comparative trials that used OC as gold standard.