The Answer to "When to Clip" After Colorectal Endoscopic Mucosal Resection Based on a Cost-Effectiveness Analysis.

INTRODUCTION: Delayed bleeding (DB) is the most common major complication of endoscopic mucosal resection (EMR). Two randomized clinical trials recently demonstrated that clip closure after EMR of large nonpedunculated colorectal polyps (LNPCPs) reduces the risk of DB. We analyzed the cost-effectiveness of this prophylactic measure. METHODS: EMRs of LNCPCPs were consecutively registered in the ongoing prospective multicenter database of the Spanish EMR Group from May 2013 until July 2017. Patients were classified according to the Spanish Endoscopy Society EMR group (GSEED-RE2) DB risk score. Cost-effectiveness analysis was performed for both Spanish and US economic contexts. The average incremental cost-effectiveness ratio (ICER) thresholds were set at 54,000 € or $100,000 per quality-adjusted life year, respectively. RESULTS: We registered 2,263 EMRs in 2,130 patients. Applying their respective DB relative risk reductions after clip closure (51% and 59%), the DB rate decreased from 4.5% to 2.2% in the total cohort and from 13.7% to 5.7% in the high risk of the DB GSEED-RE2 subgroup. The ICERs for the universal clipping strategy in Spain and the United States, 469,706 € and $1,258,641, respectively, were not cost effective. By contrast, selective clipping in the high-risk of DB GSEED-RE2 subgroup was cost saving, with a negative ICER of -2,194 € in the Spanish context and cost effective with an ICER of $87,796 in the United States. DISCUSSION: Clip closure after EMR of large colorectal lesions is cost effective in patients with a high risk of bleeding. The GSEED-RE2 DB risk score may be a useful tool to identify that high-risk population.

Guía práctica para el diagnóstico de displasia y de carcinoma colorrectal en la enfermedad inflamatoria intestinal / Practical guidelines for the diagnosis of dysplasia and colorectal carcinoma in idiopathic inflammatory bowel disease

El importante y significativo incremento de la incidencia de la enfermedad inflamatoria intestinal (EII) en la población europea ha supuesto la creación de unidades clínicas multidisciplinarias y guías prácticas de manejo y estandarización de los informes anatomopatológicos. Recientemente hemos publicado una guía interpretativa de biopsias endoscópicas con sospecha de EII. Sin embargo, el apartado de diagnóstico de lesiones preneoplásicas quedó pendiente y lo abordamos en este documento. El riesgo de carcinoma de colon se halla aumentado en la EII, en la que la displasia epitelial (DE) constituye la manifestación histológica inicial del proceso neoplásico. Su diagnóstico, la gradación y el control determinan las pautas de cribado y manejo del paciente. En este artículo procedemos a revisar: las definiciones de DE, las clasificaciones macroscópicas y microscópicas así como su repercusión en el establecimiento del tratamiento, la distinción entre DE secundaria a EII y adenoma esporádico, la utilidad de la inmunohistoquímica en los estudios histopatológicos además de los protocolos de estudio macroscópico de piezas de colectomía y de disección submucosa endoscópica provenientes del tratamiento quirúrgico de la DE o del carcinoma asociado a EII (AU)

The important, significant increase in the incidence of inflammatory bowel disease (IBD) in the European population has led to the creation of multidisciplinary clinical units and guidelines for specific aspects of Pathology reporting. Recently we published guidelines for the interpretation of endoscopy biopsies in which there was a suspicion of IBD. However, pre-neoplastic diagnosis was not included and is explained here. The risk of colon carcinoma increases in IBD and epithelial dysplasia (ED) is the initial histological manifestation of neoplasia. Diagnosis, grading and control determine guidelines for screening and patient management. We have revised the following: definition of ED, macroscopic and microscopic classifications and their significance in the choice of treatment, the distinction between ED secondary to IBD and sporadic adenoma, the usefulness of immunohistochemistry in histological studies and the protocols for macroscopic examination of submucosal dissection specimens from endoscopy and colectomy during the surgical treatment of ED or carcinoma associated with IBD (AU)

Cirugía de la poliposis adenomatosa familiar atendiendo a sus bases moleculares / Surgical options for familial adenomatous polyposis depending on genetic factors

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Simplifying the detection of MUTYH mutations by high resolution melting analysis.

BACKGROUND: MUTYH-associated polyposis (MAP) is a disorder caused by bi-allelic germline MUTYH mutation, characterized by multiple colorectal adenomas. In order to identify mutations in MUTYH gene we applied High Resolution Melting (HRM) genotyping. HRM analysis is extensively employed as a scanning method for the detection of heterozygous mutations. Therefore, we applied HRM to show effectiveness in detecting homozygous mutations for these clinically important and frequent patients. METHODS: In this study, we analyzed phenotype and genotype data from 82 patients, with multiple (> or = 10) synchronous (19/82) or metachronous (63/82) adenomas and negative APC study (except one case). Analysis was performed by HRM-PCR and direct sequencing, in order to identify mutations in MUTYH exons 7, 12 and 13, where the most prevalent mutations are located. In monoallelic mutation carriers, we evaluated entire MUTYH gene in search of another possible alteration. HRM-PCR was performed with strict conditions in several rounds: the first one to discriminate the heteroduplex patterns and homoduplex patterns and the next ones, in order to refine and confirm parameters. The genotypes obtained were correlated to phenotypic features (number of adenomas (synchronous or metachronous), colorectal cancer (CRC) and family history). RESULTS: MUTYH germline mutations were found in 15.8% (13/82) of patients. The hot spots, Y179C (exon 7) and G396D (exon 13), were readily identified and other mutations were also detected. Each mutation had a reproducible melting profile by HRM, both heterozygous mutations and homozygous mutations. In our study of 82 patients, biallelic mutation is associated with being a carrier of >/=10 synchronous polyps (p = 0.05) and there is no association between biallelic mutation and CRC (p = 0.39) nor family history (p = 0.63). G338H non-pathogenic polymorphism (exon 12) was found in 23.1% (19/82) of patients. In all cases there was concordance between HRM (first and subsequent rounds) and sequencing data. CONCLUSIONS: Here, we describe a screening method, HRM, for the detection of both heterozygous and homozygous mutations in the gene encoding MUTYH in selected samples of patients with phenotype of MAP. We refine the capabilities of HRM-PCR and apply it to a gene not yet analyzed by this tool. As clinical decisions will increasingly rely on molecular medicine, the power of identifying germline mutations must be continuously evaluated and improved.