Subacute distal ileitis in a healthy young adult.

A previously healthy 36-year-old male presented with pain in the right lower abdomen associated with weight loss, diarrhea and fever, after suffering blunt abdominal trauma during a vehicular collision 4 weeks earlier. An explorative laparoscopy was performed. A plastron composed of the appendix, caecum and 30 cm of small bowel loops was found.

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.

Helicobacter pylori heterogeneity in patients with gastritis and peptic ulcer disease.

Genetic diversification allows Helicobacter pylori to persist during chronic colonization/infection. We investigated the intra-host variation of several markers that suggested microevolution in patients with chonic gastritis (CG) and peptic ulcer disease (PUD). One-hundred twenty-six isolates recovered from 14 patients with CG and 13 patients with PUD were analysed. cag pathogenicity island (cagPAI), oipA, vacA, bab gene status and the presence of jhp0926, jhp0945, jhp0947, jhp0949 and jhp0940 genes from the genomic Plasticity Zone (PZ) were taken into accout to investigate intra-host variation. lspA-glmM-RFLP was performed to identify mixed infections. Only one patient was colonised/infected by two ancestrally unrelated strains. Among the 126 isolates, a significant association among cagPAI genotypes, oipA status and vacA alleles was indicated. Complete cagPAI, oipA "on", and vacA s1-m1 variants were significantly found in patients with PUD, without intra-host variations. Isolates from 7/14 patients with CG lacked babA in all chromosomal loci. In contrast, isolates from all or several biopsies of PUD patients carried babA, but in one patient only, the isolates showed positive Lewis b (Leb) binding assay. Considering cagPAI, vacA, oipA, bab genotypes, intra-host variation was also significantly higher in patients with CG. Conversely, a similarly high intra-host variation in almost PZ genes was observed in isolates from patients with CG and PUD. In conclusion, the lowest intra-host variation in cagPAI, oipA, vacA, and bab genes found in patients with PUD suggests the selection of a particular variant along the bacteria-host environment interplay during ulceration development. However, the predominance of this variant may be a refletion of the multifactorial etiology of the disease rather than the cause, as it was also found in patients with CG. The intra-host variation in PZ genes may predict that this genomic region and the other markers of microevolution studied evolve under diverse pressure(s).

Fundic gland polyps and association with proton pump inhibitor intake: a prospective study in 1,780 endoscopies.

BACKGROUND AND AIMS: Fundic gland polyps (FGPs) are incidentally found when an endoscopy is performed for a non-related indication. Some authors suggested a relationship with proton pump inhibitor (PPI) intake. We aimed to determine their prevalence and association with PPI intake. METHODS: We prospectively studied 1,780 patients who underwent a gastroduodenal endoscopy at our ambulatory care center between June 2007 and August 2008. PPI intake during a period of at least 12 months, female gender and age were statistically evaluated as risk factors for the presence of FGPs. Then, a multiple logistic regression analysis was applied to these variables. RESULTS: Gastric polyps were found in 129 patients (7.2%) and 77 (4.33%) were FGPs. Five patients with no available histology were excluded for the assessment of risk factors. PPI intake was detected in 49 patients with FGPs (63.6%) and 264 without FGPs (15.5%) (P < 0.0001). Fifty-nine patients with FGPs (76.7%) and 987 without FGPs (58.1%) were women (P < 0.001). The mean age was 58.91 ± 11.82 years in patients with FGPs and 50.34 ± 15.04 years in patients without FGPs (P < 0.0001). The three variables remained significant in the multiple model: PPI intake: P < 0.0001, OR 9.00 (95% CI 5.44-14.89); female gender: P = 0.0001, OR 2.95 (95% CI 1.69-5.15); age: P = 0.001, OR 1.03 (95% CI 1.01-1.05). CONCLUSIONS: In our population, the prevalence of FGPs was high. Although female gender and age were also significant, PPI intake was the strongest risk factor associated with the presence of FGPs.