Luis Viola

Implementation of a program to improve the quality of colonoscopy increases the neoplasia detection rate: a prospective study

Background and study aims: Endoscopists worldwide have been encouraged to report quality indicators in order to evaluate their performance. We aimed to determine whether a program to improve the quality of colonoscopy results in better rates of neoplasia detection. Patients and methods: This is a prospective study set in a private endoscopy center. From May 2009 to March 2010, we evaluated 1573 consecutive colonoscopies (group 1). After the implementation of a quality program, from February 2011 to January 2012, we prospectively evaluated 1583 colonoscopies (group 2). Our quality-enhancing intervention consisted of instructing both patients and endoscopists. We measured the cecal intubation rate and the neoplasia detection rate. Overall neoplasias, high-risk adenomas, carcinomas, right colon adenomas, and adenomas detected in screening studies were analyzed. Results: Cecal intubation was documented in 1384 cases from group 1 (88 %) and 1534 from group 2 (96.9 %) (P < 0.0001). The neoplasia detection rates in groups 1 and 2 were, respectively: neoplasias 288 (18.3 %) and 427 (27 %) (P < 0.0001), high-risk adenomas 76 (4.8 %) and 142 (9 %) (P < 0.0001), carcinomas 16 (1 %) and 21 (1.3 %) (P = 0.52), right colon adenomas 112 (7.1 %) and 154 (9.7 %) (P = 0.01), and adenomas 141 (16.5 %) and 233 (28 %) (P < 0.0001). Conclusions: Implementation of a quality program improves the neoplasia detection rate. Because of the small number of cancerous lesions found in both groups, we were unable to identify differences in the carcinoma detection rate.

Prevalence and risk factors of acute-on-chronic liver failure in a single center from Argentina

AIM To study the prevalence, characteristics, risk factors and mortality at 28 d of acute-on-chronic liver failure (ACLF). METHODS A total of 100 cirrhotic patients admitted to our hospital for more than one day were included during the period between June 2013 and December 2015. We used the European Association for the Study of the Liver-Chronic Liver Failure-Consortium diagnostic criteria for ACLF, considering it as the acute decompensation of cirrhosis associated with the presence of one or more organ failure. For the diagnosis of organic failure the Chronic Liver Failure-Sequential Organ Failure Assessment score was used. Our population was divided into patients with and without ACLF. Clinical characteristics, presence of precipitating events, potential risk factors for developing ACLF and causes of mortality were analyzed. Mortality at 28 d was evaluated. RESULTS Twenty-nine patients (29%) developed ACLF criteria. Alcoholism, detected in 58 patients (58%), was the major etiological agent of cirrhosis. Bacterial infections were recognized as a precipitating event in 41.3% of cases and gastrointestinal bleeding in 27.5%. No precipitating event was identifiable in 27.5% of patients with ACLF. Comparing patients with and without ACLF, statistically significant risk factors were: Child Pugh score 10.2 ± 2.1 vs 8.4 ± 1.6 (P ˂ 0.0001), MELD score 20.7 ± 8.5 vs 12.3 ± 4 (P ˂ 0.0001), presence of ascites 27 (93%) vs 43 (60.5%) (P = 0.001), leukocytosis 15300 ± 8033 per cubic millimeter vs 10770 ± 5601 per cubic millimeter (P ˂ 0.0001), and high plasma levels of C reactive protein values 50.9 ± 46.4 mg/L vs 28.6 ± 23.4 mg/L (P ˂ 0.0019). Mortality rate was 62% (18 patients) vs 5.6% (4 patients), respectively (P < 0.0001). CONCLUSION We observed that the ACLF is a frequent entity in this group of patients and has a significantly higher mortality rate.

S1082 Fundic Gland Polyps and Association with Proton Pump Inhibitor Intake: A Prospective Study in 1,780 Upper Gastroduodenal Endoscopies

Background: The duodenal adenomas as seen in familial adenomatous polyposis (FAP) are likely to develop through the classical adenoma-carcinoma pathway as they exhibit mutations in the APC gene, KRAS mutations, p53 dysfunction, and loss of E-cadherin expression. However, it is unknown whether sporadic duodenal adenomas also develop into duodenal carcinoma through the classical adenoma carcinoma sequence. Limited data suggest that sporadic adenomas show similar molecular features as colorectal adenomas, harboring APC and KRAS mutations. Therefore, the aim of the present study was to evaluate the molecular changes of sporadic duodenal adenomas. Methods: Tissue samples of 64 sporadic duodenal adenomas were available from the pathology archives of two academic hospitals. Tissue samples of patients with duodenal carcinoma or patients with FAP were excluded. None of the patients belonged to a known Lynch syndrome family. DNA was extracted from paraffin sections of the adenoma and analyzed for the presence of microsatellite instability. Also, mutation analysis using polymerase chain reaction followed by direct-sequencing was performed. The mutation analysis included mutational hotspots of the Wnt signaling pathway (APC, β-catenin), the MAP kinase pathway (KRAS and BRAF) and the del1100c mutation within the CHK2 gene. Results: Two (3%) of the 64 adenomas showed a high level of MSI (MSI-H). APC mutation analysis was possible in 52 adenomas and revealed a mutation in thirteen (24%), including seven duodenal adenomas with a recurrent 4684insA (K1555fsX1557)mutation. KRASmutation analysis was possible in 52 adenomas and revealed one (2%) mutation (34GGT>TGT (G12C)). β-catenin mutation analysis was possible in 48 adenomas and revealed one (2%) mutation (121ACC>GCC(T41A)). BRAF (58 adenomas) and CHK2 (53 adenomas) mutation analysis did not reveal any mutation. Conclusions: In our cohort of sporadic duodenal adenomas the frequency of Wnt signaling pathway abnormalities is low, most adenomas are microsatellite stable and the number of MAP kinase pathway abnormalities is negligible. In addition, CHK2 mutations seem not to be present in sporadic duodenal adenomas. These findings suggest that a proportion of sporadic duodenal adenomas develop via the same mechanisms (the adenoma-carcinoma sequence) as colorectal adenomas, but it is possible that other molecular changes may also underlie the development of sporadic duodenal adenomas.