Gastric Intestinal Metaplasia: Demographic and Epidemiological Characterization in Puerto Rican Hispanics (2012-2014).

BACKGROUND AND AIMS: Gastric cancer is the 5th leading cause of cancer mortality worldwide and the leading infection-associated cancer. Helicobacter pylori is the most common chronic bacterial infection in humans and the major predisposing factor for the development of gastric intestinal metaplasia (GIM), the principal preneoplastic lesion in the gastric carcinogenesis pathway. GIM surveillance is now recommended for individuals among high-risk subgroups by three major gastroenterology societies in Europe, England, and U.S. Our objective was to provide the initial epidemiologic data for GIM among Hispanics in Puerto Rico. METHODS: Using a cross-sectional study design, we analyzed an extensive pathology database (n = 43,993) that captured approximately 50% of all endoscopy biopsies taken during 2012-2014 at academic, public, and private sectors in Puerto Rico. Prevalence estimates of GIM, GIM subgroups, and H. pylori status were estimated using logistic regression models. RESULTS: A total of 4,707 GIM cases were identified during the study period for a prevalence rate of 10.7%. H. pylori was detected in 26.9% (95% CI: 25.7-28.2) of the GIM cases. The majority of the pathology reports lacked information regarding the high-risk subtypes (99.6%) and extension (71.2%). CONCLUSIONS: The prevalence of GIM among Hispanics living in Puerto Rico may be higher than in U.S. mainland non-Hispanic populations. The prevalence of H. pylori detected in our study population was comparable to the rates reported in the mainland U.S. Standardization of the endoscopy biopsy protocol and pathology reporting is needed to characterize and risk stratify GIM surveillance programs in Puerto Rico.

Implementation of Universal Colorectal Cancer Screening for Lynch Syndrome in Hispanics Living in Puerto Rico.

OBJECTIVE: Colorectal cancer is the leading cause of cancer death in Puerto Rico and third among Hispanics in the USA. Up to 2-4% of colorectal cancer cases are a result of Lynch syndrome (LS), a hereditary cancer syndrome caused by a germline mutation in at least one of the DNA mismatch repair genes. The objective of this study was to determine the prevalence of LS in colorectal tumors during the first 15-months after the implementation of universal tumor-based screening for LS in Puerto Rico. METHODS: A total of 317 colorectal tumors were evaluated in a large private pathology laboratory from September 2014 to December 2015. Clinical characteristics were obtained from the pathology reports. Unadjusted and adjusted logistic regression models were used to estimate the magnitude of association (odds ratio [OR] with 95% confidence intervals [CI]) between absent MMR protein expression and patient characteristics. RESULTS: Most cases (93.4%) were analyzed by immunohistochemistry; 11.8% (35 of 296) had deficient mismatch repair protein expression. While 29 of the 317 cases were subjected to PCR-based microsatellite instability analysis of which 10.3% (3 of 317) had microsatellite instability. In total, 11.0% of the tumors were reported MMR deficient. These tumors were more likely from females and more likely localized in the proximal colon compared to those with proficient MMR expression. CONCLUSIONS: Our data is consistent with the results from other studies including US Hispanics, where approximately 10% of Hispanic individuals with colorectal cancer have microsatellite instability. Our results support universal tumor-based screening for LS among Hispanics in accordance with National Comprehensive Cancer Network guidelines.

A Comparison of Brunt's Criteria, the Non-Alcoholic Fatty Liver Disease Activity Score (NAS), and a Proposed NAS Scoring that Includes Fibrosis in Non-Alcoholic Fatty Liver Disease Staging.

OBJECTIVE: The aim of this study was to determine the prevalence of NASH in veterans with metabolic syndrome and compare histologic grading using the Brunt criteria, the NAFLD activity score (NAS), and a proposed NAS scoring system that has been modified to include fibrosis staging. METHODS: Veterans with metabolic syndrome, hepatic steatosis, and elevated ALT and AST levels and who underwent liver biopsies from 2004 through 2010 were included in this study. Biopsies were evaluated by a single hepatopathologist. Each biopsy was analyzed using the Brunt criteria, the NAS system, and the NAS system plus fibrosis staging. RESULTS: Sixty patients having a mean age of 50.4 (±12.8 years) were included in the study; 88.3% were men. Fifty percent met criteria according to the Brunt system. When biopsies were classified using the NAS system, only 30.0% (18/60) were found to have a score of 5 or more, while, when adding fibrosis staging, the number of patients with a score of 5 or more increased to 33 (55.0%). Upon evaluating the predictive ability of the NAS scoring system, we found that when including fibrosis staging we obtained a higher sensitivity (86.7% vs. 40.0%) and a lower specificity (76.7% vs. 80.0%). CONCLUSION: In our population of patients with metabolic syndrome about 50 to 55% had steatohepatitis. There were significant differences between the scoring systems. When our NAS plus fibrosis system was used, more patients were recognized and the sensitivity increased. Further validation studies are required to evaluate this proposed modified NAS scoring system.

Surveillance for dysplasia in patients with ileal pouch-anal anastomosis for ulcerative colitis: an interim analysis.

BACKGROUND: The risk of developing cancer in the ileal pouch of patients with surgery for ulcerative colitis has not been defined. Dysplasia in the pouch is quite rare. Although some suggest pouch surveillance based on previous histological assessments, there are no guidelines for surveillance of these patients. The aim of our study was to investigate that risk and identify time intervals for ileoanal pouch surveillance. METHODS: Endoscopy and biopsies of the ileal pouch were performed at 3, 6, and/or 12 months after ileal pouch-anal anastomosis (IPAA) became functional. Biopsies were evaluated by two pathologists using Riddel's criteria. Interim data analysis using descriptive statistics is reported. RESULTS: Thirty-eight patients have entered the study. Average patient age at 3, 6, and 12 months of surveillance was 39.1, 36.8, and 39.1 years, respectively. Average disease duration was 8.2 years. Ten of 38 cases (26%) had colonic dysplasia prior to surgery. Dysplasia within the pouch was reported in one patient 6 months after IPAA became functional. This patient demonstrated no dysplasia at 12 months or statistical divergence by age, duration of disease or history of colonic dysplasia prior to IPAA. No subgroup of patients with dysplasia was identified to calculate cumulative risk or perform comparative statistical analysis. CONCLUSION: A study with longer follow-up after IPAA should precede any attempt to recommend routine surveillance. However, the finding of dysplasia early after surgery underscores the importance of early pouch surveillance in our population, at least until definite predisposing variables are identified.

Distribution of the H+/peptide transporter PepT1 in human intestine: up-regulated expression in the colonic mucosa of patients with short-bowel syndrome.

BACKGROUND: Intestinal adaptation after massive bowel resection in animal models is characterized by increased gut-mucosal growth and expression of nutrient transporters. Few data about these indexes exist in humans with short-bowel syndrome (SBS). OBJECTIVE: The objective was to compare small-bowel and colonic mucosal growth and expression of the peptide transporter PepT1 in adults with or without SBS. DESIGN: Mucosal biopsy specimens were obtained from the small bowel and colon of 33 control subjects with intact intestine and from 13 SBS patients dependent on parenteral nutrition because of chronic malabsorption. Gut-mucosal crypt depth, villus height, and villus width were measured, and expression of PepT1 was determined by Northern blotting, in situ hybridization, and immunohistochemistry. RESULTS: The indexes of small-bowel and colonic mucosal growth were not significantly different between the 2 groups. PepT1 expression was high in the apical region of duodenal, jejunal, and ileal villus epithelial cells; low in absorptive colonocytes; and not significantly different in the distal small intestine of the 2 groups. However, the abundance of PepT1 mRNA in the colon of SBS patients was more than 5-fold that in control subjects (P < 0.01). CONCLUSIONS: Gut adaptation in SBS patients does not appear to involve an increase in gut-mucosal crypt depth or villus size. PepT1 is abundant along the small-bowel brush border in humans; expression in the colon indicates that the large intestine has a mechanism for luminal di- and tripeptide transport. Up-regulation of colonic PepT1 in SBS may adaptively improve accrual of malabsorbed di- and tripeptides, independent of changes in the mucosal surface area.