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Aliment Pharmacol Ther 2011; 33: 585–591 Summary Background Temporal changes in the incidence of cause-specific gastrointestinal (GI) complications may be one of the factors underlying changing medical practice patterns. Aim To report temporal changes in the incidence of five major causes of specific gastrointestinal (GI) complication events. Methodology Population-based study of patients hospitalised due to GI bleeding and perforation from 1996 to 2005 in Spain. We report crude rates, and estimate regression coefficients of temporal trends, severity and recorded drug use for five frequent GI events. GI hospitalisation charts were validated by independent review of large random samples. Results The incidence per 100 000 person-years of hospitalisations due to upper GI ulcer bleeding and perforation decreased over time [from 54.6 and 3.9 in 1996 (R2 = 0.944) to 25.8 and 2.9 in 2005 (R2 = 0.410) respectively]. On the contrary, the incidence per 100 000 person-years of colonic diverticular and angiodysplasia bleeding increased over time [3.3 and 0.9 in 1996 (R2 = 0.443) and 8.0 and 2.6 in 2005 (R2 = 0.715) respectively]. A small increasing trend was observed for the incidence per 100 000 person-years of intestinal perforations (from 1.5 to 2.3 events). Based on data extracted from the validation process, recent recorded drug intake showed an increased frequency of anticoagulants with colonic diverticular and angiodysplasia bleeding, whereas NSAID and low-dose aspirin use were more prevalent in peptic ulcer bleeding and colonic diverticular bleeding respectively. Conclusions From 1996 to 2005, hospitalisations due to peptic ulcer bleeding and perforation have decreased significantly, whereas the number of cases of colonic diverticular and angiodysplasia bleeding have increased.

The worst outcome of gastrointestinal complications is death. Data regarding those associated with nonsteroidal antiinflammatory drug (NSAID) or aspirin use are scarce.To determine mortality associated with hospital admission due to major gastrointestinal (GI) events and NSAID/aspirin use.The study was based on actual count of deaths from two different data sets from 2001. Study 1 was carried out in 26 general hospitals serving 7,901,198 people. Study 2 used a database from 197 general hospitals, representative of the 269 hospitals in the Spanish National Health System. Information regarding gastrointestinal complications and deaths was obtained throughout the Minimum Basic Data Set (CIE-9-MC) provided by participating hospitals. Deaths attributed to NSAID/aspirin use were estimated on the basis of prospectively collected data from hospitals of study 1.The incidence of hospital admission due to major GI events of the entire (upper and lower) gastrointestinal tract was 121.9 events/100,000 persons/year, but those related to the upper GI tract were six times more frequent. Mortality rate was 5.57% (95% CI = 4.9-6.7), and 5.62% (95% CI = 4.8-6.8) in study 1 and study 2, respectively. Death rate attributed to NSAID/aspirin use was between 21.0 and 24.8 cases/million people, respectively, or 15.3 deaths/100,000 NSAID/aspirin users. Up to one-third of all NSAID/aspirin deaths can be attributed to low-dose aspirin use.Mortality rates associated with either major upper or lower GI events are similar but upper GI events were more frequent. Deaths attributed to NSAID/ASA use were high but previous reports may have provided an overestimate and one-third of them can be due to low-dose aspirin use.

Changing patterns in medical practice may contribute to temporal changes in the incidence of upper and lower gastrointestinal (GI) complications. There are limited data on the incidence of lower GI complications in clinical practice and most studies that have been done have serious methodological limitations to inferring the actual burden of this problem. The aims of this study were to analyze time trends of hospitalizations resulting from GI complications originating both from the upper and lower GI tract in the general population, and to determine the risk factors, severity, and clinical impact of these GI events.This was a population-based study of patients hospitalized because of GI complications in 10 general hospitals between 1996 and 2005 in Spain. We report the age- and gender-specific rates, estimate the regression coefficients of the upper and lower GI event trends, and evaluate the severity and associated risk factors. GI hospitalization charts were validated by an independent review of large random samples of unspecific and specific codes distributed among all hospitals and study years.Upper GI complications fell from 87/100,000 persons in 1996 to 47/100,000 persons in 2005, whereas lower GI complications increased from 20/100,000 to 33/100,000. Overall, mortality rates decreased, but the case fatality remained constant over time. Lower GI events had a higher mortality rate (8.8 vs. 5.5%), a longer hospitalization (11.6+/-13.9 vs. 7.9+/-8.8 days), and higher resource utilization than did upper GI events. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) without concomitant proton pump inhibitor was more frequently recorded among upper GI complications than among lower GI complications. When comparing upper GI events with lower GI events, we found that male gender (adjusted odds ratio (OR): 1.94; 95% confidence interval (CI): 1.70-2.21), and recorded NSAID use (OR: 1.92; 95% CI: 1.60-2.30) were associated to a greater extent with upper GI events, whereas older age (OR: 0.83; 95% CI: 0.77-0.89), number of comorbidities (OR: 0.91; 95% CI: 0.86-0.96), and having a diagnosis in recent years (OR: 0.92; 95% CI: 0.90-0.94) were all associated to a greater extent with lower GI events than with upper GI events after adjusting for age, sex, hospitalization, and discharge year.Over the past decade, there has been a progressive change in the overall picture of GI events leading to hospitalization, with a clear decreasing trend in upper GI events and a significant increase in lower GI events, causing the rates of these two GI complications to converge. Overall, mortality has also decreased, but the in-hospital case fatality of upper or lower GI complication events has remained constant. It will be a challenge to improve future care in this area unless we develop new strategies to reduce the number of events originating in the lower GI tract, as well as reducing their associated mortality.

Las glutation S-transferasas son una familia de enzimas involucradas en mecanismos de detoxificacion celular, eliminando xenobioticos y substancias nocivas para las celulas. Los genes que codifican la sintesis de las isoformas GSTM(mu)1, GSTT(theta)1 y GSTP(pi) son altamente polimorficos. Existen 2 polimorfismos caracterizados por una delecion de los genes GSTM1 y GST1 que conllevan un perdida total de la activad enzimatica correspondiente y cuya presencia se ha asociado con un mayor riesgo de desarrollar ciertos tipos de cancer. Ademas, el gen GSTP1 presenta dos polimorfismos relativamente frecuentes (Ile105Val y Val114Ala) relacionados con una disminucion de la actividad enzimatica. Puesto que el status GST de un individuo podria ser determinante en el proceso de carcinogenesis, el objetivo de nuestro estudio fue analizar el papel de dichos polimorfismos en el desarrollo del cancer gastrico (CG). Metodos ADN genomico procedente de 515 pacientes con CG y 515 individuos sanos fue tipado mediante RFL-PCR para el analisis de los polimorfismos GSTP1 Val105Ile (rs1695) y GSTP1 Val114Ala (rs1138272) y mediante PCR multiple para el estudio de las deleciones de los genes GSTM1 y GSTT1. El estatus de infeccion por H. pylori y de anticuerpos CagA/VacA se realizo mediante Western blot. Resultados La infeccion por cepas cagA de H. pylori (OR: 2,33; 95% IC: 1,78–3,06), el tabaco (OR: 2,26; 95% IC: 1,39–3,08) y la existencia de antecedentes familiares de CG (OR: 3,1; 95% IC: 1,83–5,14) fueron factores de riesgo asociados al desarrollo de CG. El porcentaje de individuos homozigotos para la delecion de los genes GSTM1 y GSTT1 fue similar en pacientes y controles (52% vs 49%, OR: 1,57; 95% IC: 0,89–1,49 para GSTM1 y 22% vs 21%, OR: 1,07; 95% IC: 0,78–1,46 para GSTT1). Igualmente, el porcentaje de individuos homozigotos para ambas deleciones fue casi identico en ambos grupos (10,8% en CG vs 10,7% en controles; OR: 1,14; 95% IC: 0,73–1,78). Tampoco se observaron diferencias significativas en la distribucion de genotipos y frecuencias alelicas de los polimorfismos GSTP1 Val105Ile y GSTP1 Val114Ala entre pacientes y controles. Por ultimo, no se encontraron diferencias significativas en los genotipos cuando los pacientes fueron clasificados en funcion del sexo, edad, tabaquismo, status de infeccion por H. pylori, presencia de anticuerpos anti CagA/VacA, tipo histologico tumoral, localizaron del tumor o antecedentes familiares de cancer gastrico. Conclusion Nuestros resultados sugieren que los polimorfismos geneticos de GTSM1, GTST1 y GTSP1 analizados en nuestro estudio no estan implicados en la susceptibilidad al desarrollo de CG.

Relevance of GSTM1, GSTT1, and GSTP1 Gene Polymorphisms On Gastric Cancer Susceptibility Maria Asuncion Garcia-Gonzalez, Enrique Quintero, Rafael Benito, Mark Strunk, David Nicolas-Perez, Adolfo Parra-Blanco, Santos Santolaria, Federico Sopena, Elena Piazuelo, Pilar Jimenez, Maria Badia, Jesus Espinel, Rafael Campo, Marisa Manzano, Fernando Geijo, Maria Pellise, Ferran Gonzalez-Huix, Miguel Nieto, Jorge C. Espinos, LLucia Tito, Luis Bujanda, Manuel Zaballa, Maria Angeles Perez-Aisa, Isabel Maria Mendez-Sanchez, Angel Lanas