Citations

ObjectiveOur aim was to identify patient and procedure characteristics that correlate with increased likelihood of bleeding during and after endoscopic mucosal resection (EMR), and thus anticipate the need for preventative therapy.MethodsThis was a retrospective, observational, descriptive study using a prospective EMR database, performed in a tertiary‐care center. A total of 935 EMR of various locations within the gastrointestinal tract were collected. The main outcome measurement was early bleeding (occurring during the procedure) and delayed bleeding (occurring after the completion of the procedure and up to 30 days after).ResultsEarly bleeding occurred in 5.3% (50/935) of the procedures. In multivariate logistic regression analysis, esophageal EMR (OR 2.5, 95% CI 1.2–5, P = 0.0009) and increase in lesion size (OR 1.24, 95% CI 1.1–1.5, P = 0.003) were both associated with higher odds of early bleeding in EMR when controlling for age, gender and non‐steroidal anti‐inflammatory drugs (NSAIDs)/clopidogrel use. Delayed bleeding occurred after 3.1% (n = 29) of the procedures. Of these, 86.2% (25/29) required hospital admission and endoscopic intervention to confirm and/or treat bleeding site. In multivariate logistic regression analysis, increased lesion size (OR 1.3, 95% CI 1.1–1.5, P = 0.004) was associated with higher incidence of delayed bleeding post‐EMR.ConclusionsIn experienced hands bleeding during and after EMR appears to be uncommon. Larger lesions are at increased risk of early and delayed bleeding.

We executed a genome-wide association scan for age-related macular degeneration (AMD) in 2,157 cases and 1,150 controls. Our results validate AMD susceptibility loci near CFH ( P < 10 −75 ), ARMS2 ( P < 10 −59 ), C2/CFB ( P < 10 −20 ), C3 ( P < 10 −9 ), and CFI ( P < 10 −6 ). We compared our top findings with the Tufts/Massachusetts General Hospital genome-wide association study of advanced AMD (821 cases, 1,709 controls) and genotyped 30 promising markers in additional individuals (up to 7,749 cases and 4,625 controls). With these data, we identified a susceptibility locus near TIMP3 (overall P = 1.1 × 10 −11 ), a metalloproteinase involved in degradation of the extracellular matrix and previously implicated in early-onset maculopathy. In addition, our data revealed strong association signals with alleles at two loci ( LIPC , P = 1.3 × 10 −7 ; CETP , P = 7.4 × 10 −7 ) that were previously associated with high-density lipoprotein cholesterol (HDL-c) levels in blood. Consistent with the hypothesis that HDL metabolism is associated with AMD pathogenesis, we also observed association with AMD of HDL-c—associated alleles near LPL ( P = 3.0 × 10 −3 ) and ABCA1 ( P = 5.6 × 10 −4 ). Multilocus analysis including all susceptibility loci showed that 329 of 331 individuals (99%) with the highest-risk genotypes were cases, and 85% of these had advanced AMD. Our studies extend the catalog of AMD associated loci, help identify individuals at high risk of disease, and provide clues about underlying cellular pathways that should eventually lead to new therapies.