Low-grade dysplasia in Barrett's esophagus: A problematic diagnosis / Displasia de bajo grado en el esófago de Barrett: un diagnóstico problemático

Although low-grade dysplasia (LGD) in Barrett's esophagus (BE) is a histopathological diagnosis based on different histological abnormalities, it is still problematic for different reasons. Patients without confirmed diagnosis of LGD undergo unnecessary and intensified follow-up where the risk of progression is low in the majority of cases. In contrast, the presence of confirmed LGD indicates a high risk of progression. In this article we try to address these reasons focusing on re-confirmation of LGD diagnosis, interobserver agreement, and persistent confirmed LGD. The progression risk of LGD to high-grade dysplasia and esophageal adenocarcinoma will also be reviewed. (AU)

Aunque la displasia de bajo grado (DBG) en el esófago de Barrett (EB) es un diagnóstico histopatológico basado en diferentes anomalías histológicas, este no deja de ser problemático por diferentes razones. Los pacientes sin diagnóstico confirmado de DBG se someten a un seguimiento innecesario e intensificado donde el riesgo de progresión es bajo en la mayoría de los casos. Por el contrario, la presencia de DBG confirmada indica un alto riesgo de progresión. En este artículo tratamos de abordar estas razones centrándonos en la reconfirmación del diagnóstico de la DBG, la concordancia entre observadores y la DBG confirmada y persistente. También se revisará el riesgo de progresión de la DBG a displasia de alto grado y adenocarcinoma esofágico. (AU)

Low-grade dysplasia in Barrett's esophagus: A problematic diagnosis.

Although low-grade dysplasia (LGD) in Barrett's esophagus (BE) is a histopathological diagnosis based on different histological abnormalities, it is still problematic for different reasons. Patients without confirmed diagnosis of LGD undergo unnecessary and intensified follow-up where the risk of progression is low in the majority of cases. In contrast, the presence of confirmed LGD indicates a high risk of progression. In this article we try to address these reasons focusing on re-confirmation of LGD diagnosis, interobserver agreement, and persistent confirmed LGD. The progression risk of LGD to high-grade dysplasia and esophageal adenocarcinoma will also be reviewed.

[Why is it important to detect atrophic gastritis and gastric intestinal metaplasia? What is the proper way to do it?] / ¿Por qué es importante detectar la gastritis atrófica y la metaplasia intestinal gástrica? ¿Cuál es la forma adecuada de hacerlo?

Gastric intestinal metaplasia and atrophic gastritis are a known precancerous condition (PCC) of the stomach, meaning that patients with PCC are at risk for gastric cancer and so, diagnosis and risk categorization for these patients is relevant. The aim of this review is to provide an update regarding the problem, diagnosis, and management of PCCs with an emphasis on the role of appropriate endoscopic detection.

¿Por qué es importante detectar la gastritis atrófica y la metaplasia intestinal gástrica? ¿Cuál es la forma adecuada de hacerlo? / Why is it important to detect atrophic gastritis and gastric intestinal metaplasia? What is the proper way to do it?

RESUMEN La metaplasia intestinal gástrica y la gastritis atrófica son condiciones precancerosas conocidas (CPCs) del estómago, lo que significa que los pacientes con CPCs están en riesgo de desarrollar cáncer gástrico y, por lo tanto, el diagnóstico y la categorización de riesgo para estos pacientes es un tema relevante. El objetivo de esta revisión es proporcionar una actualización sobre el problema, el diagnóstico y el manejo de las CPCs con énfasis en el papel de la detección endoscópica adecuada.

ABSTRACT Gastric intestinal metaplasia and atrophic gastritis are a known precancerous condition (PCC) of the stomach, meaning that patients with PCC are at risk for gastric cancer and so, diagnosis and risk categorization for these patients is relevant. The aim of this review is to provide an update regarding the problem, diagnosis, and management of PCCs with an emphasis on the role of appropriate endoscopic detection.

Helicobacter pylori and corpus gastric pathology are associated with lower serum ghrelin.

AIM: To evaluate the association of Helicobacter pylori (H. pylori), cagA genotype, and type of gastric pathology with ghrelin, leptin and nutritional status. METHODS: Fasted dyspeptic adults (18-70 years) referred for an upper digestive endoscopy were enrolled in this cross-sectional study. Height and weight were assessed for body mass index (BMI) calculation. A sociodemographic survey was administered and nutrient intake was evaluated with 24 h dietary recalls. Serum total ghrelin and leptin levels were analyzed by enzyme-linked immunosorbent assay. 13C-Urea Breath Test was performed and four gastric biopsies were obtained during endoscopy for histopathology and H. pylori DNA amplification and genotyping. Data analysis was performed using χ2, Mann-Whitney U, Kruskal-Wallis tests, Spearman's correlation and linear regression. RESULTS: One hundred and sixty-three patients (40.8 ± 14.0 years), 98/65 females/males, were included. Overall, persistent H. pylori prevalence was 53.4% (95%CI: 45.7%-65.8%). Neither nutrient intake nor BMI differed significantly between H. pylori positive and negative groups. Serum ghrelin was significantly lower in infected patients [median 311.0 pg/mL (IQR 230.0-385.5)] than in uninfected ones [median 355.0 pg/mL (IQR 253.8-547.8)] (P = 0.025), even after adjusting for BMI and gender (P = 0.03). Ghrelin levels tended to be lower in patients carrying cagA positive strains both in the antrum and the corpus; however, differences with those carrying cagA negative strains did not reach statistical significance (P = 0.50 and P = 0.49, respectively). In addition, the type and severity of gastric pathology in the corpus was associated with lower serum ghrelin (P = 0.04), independently of H. pylori status. Conversely, leptin levels did not differ significantly between infected and uninfected patients [median 1.84 ng/mL (0.80-4.85) vs 1.84 ng/mL (0.50-5.09), (P = 0.51)]. CONCLUSION: H. pylori infection and severity of gastric corpus pathology are associated with lower serum ghrelin. Further studies could confirm a lower ghrelin prevalence in cagA-positive patients.

Occurrence of Mutations in the Antimicrobial Target Genes Related to Levofloxacin, Clarithromycin, and Amoxicillin Resistance in Helicobacter pylori Isolates from Buenos Aires City.

Domain V of 23S rRNA, gyrA and gyrB Quinolones Resistance-Determining Region (QRDR), and pbp-1A gene point mutations were investigated in Helicobacter pylori-resistant isolates from three centres of Buenos Aires. Minimal inhibitory concentrations (MICs) were performed in 197 isolates from 52 H. pylori-positive naive patients by agar dilution method. Point mutations were achieved by amplification and sequencing of the target genes, and their association with resistance was determined by natural transformation assays. Resistance rates were as follows: metronidazole 28.8%, clarithromycin (CLA) 26.9%, levofloxacin (LEV) 32.7%, and amoxicillin (AMX) 7.6%. Nearly one-third of patients carried multidrug-resistant isolates. A2143G or A2142G in domain V of 23S-rRNA was found in all isolates showing high level of resistance to CLA (MIC >2 mg/L), accounting for 76.0% (38/50) of those with the resistant phenotype. The mutations A2267G or T1861C carried by 8/12 isolates with MIC 1-2 mg/L (low level) did not confer resistance by transformation. Substitutions at GyrA position 87 or 91, mainly N87K and D91G, were found in 92.8% (52/56) of the LEV-resistant isolates: 48 isolates with MIC 4-64 mg/L and 4/8 isolates with MIC 2 mg/L. The remaining four harboured K133N, also present in susceptible isolates. None of the substitutions in GyrB demonstrated to confer resistance. Transformation proved that PBP-1A N562Y and/or T556S substitutions confer the AMX resistance in our isolates, showing an additive effect. In conclusion, the usually reported mutations related to CLA, LEV, and AMX resistance were found in our isolates. However, low-level CLA resistance seems not to be due to mutations in Domain V of 23S rRNA gene.

Rol de las formas cocoides de Helicobacter pylori en la infección y la recrudescencia / Role of Helicobacter pylori coccoid forms in infection and recrudescenc

Helicobacter pylori es un bacilo espiral gramnegativo que coloniza el estómago humano y desempeña un papel clave en la patogénesis de diferentes enfermedades gastroduodenales. Sin embargo, cuando se expone a condiciones de estrés ambientales, tales como el aumento de la tensión de oxígeno, la incubación prolongada o la exposición a antibióticos, Helicobacter pylori entra en un estado viable pero no cultivable, en el cual la bacteria modifica su morfología de una forma bacilar a una cocoide como manifestación de adaptación celular a estas condiciones adversas. En el tejido gástrico, las formas cocoides viables pueden permanecer latentes durante mucho tiempo y retener factores de virulencia, por lo que estas formas posiblemente puedan contribuir a los fracasos del tratamiento y la recurrencia de la infección y de las enfermedades gastroduodenales también. En esta revisión se discutirán varios aspectos de la adaptación celular y supervivencia de Helicobacter pylori, la susceptibilidad a los antibióticos y la virulencia de las formas cocoides y su participación en la recrudescencia

Helicobacter pylori is a spiral Gram-negative bacillus, which colonizes the human stomach and plays a key role in the pathogenesis of a number of gastroduodenal diseases. However, when expose to environmental stressed conditions, such as increased oxygen tension, extended incubation and exposure to antibiotics, Helicobacter pylori is able to entering the viable but nonculturable state, in which the bacterium modifies its morphology from a spiral to coccoid form, as a manifestation of cell adaptation to these adverse conditions. In gastric tissues, viable coccoid forms may remain latent for long time and retain virulence factors, so these forms possibly contribute to the treatment failures and recurrence of Helicobacter pylori infection and gastroduodenal diseases as well. In this review, we will discuss several aspects of cellular adaptation and survival of Helicobacter pylori, antibiotic susceptibility and virulence of coccoid forms and its involvement with recrudescence

[Role of Helicobacter pylori coccoid forms in infection and recrudescence]. / Rol de las formas cocoides de Helicobacter pylori en la infección y la recrudescencia.

Helicobacter pylori is a spiral Gram-negative bacillus, which colonizes the human stomach and plays a key role in the pathogenesis of a number of gastroduodenal diseases. However, when expose to environmental stressed conditions, such as increased oxygen tension, extended incubation and exposure to antibiotics, Helicobacter pylori is able to entering the viable but nonculturable state, in which the bacterium modifies its morphology from a spiral to coccoid form, as a manifestation of cell adaptation to these adverse conditions. In gastric tissues, viable coccoid forms may remain latent for long time and retain virulence factors, so these forms possibly contribute to the treatment failures and recurrence of Helicobacter pylori infection and gastroduodenal diseases as well. In this review, we will discuss several aspects of cellular adaptation and survival of Helicobacter pylori, antibiotic susceptibility and virulence of coccoid forms and its involvement with recrudescence.

Transmisión de la bacteria Helicobacter pylori a partir del agua en animales de laboratorio / Transmission of the bacterium Helicobacter Pylori from water in laboratory animals

Introducción y objetivo: El Helicobacter pylori (Hp) es una bacteria que coloniza el estómago humano y desempeña un papel clave en la patogénesis de diferentes enfermedades gastroduodenales. Aunque se ha propuesto que la transmisión del Hp se da vía oral-oral, fecal-oral o gastro-oral, las vías de transmisión aún no están del todo claras, lo que dificulta implementar medidas de salud pública para prevenir la infección. El objetivo de este trabajo es observar en animales de laboratorio la posible transmisión del Hp a través del agua de consumo, procedentes de dos zonas diferentes del conurbano. Materiales y métodos: Se utilizaron 21 ratas de la cepa Albinas, de 20 días de edad y al destete, que se dividieron en tres grupos: grupo A: 7 ratas a las que se les administró agua de pozo proveniente de la zona sur del conurbano; grupo B: 7 ratas a las que se les administró agua corriente proveniente de la zona oeste del conurbano; grupo C: 7 ratas a las que se les administró agua biodestilada de laboratorio. A todos los grupos se les suministró el agua y un alimento comercial balanceado seco en forma ad libitum. El período de administración de agua fue de dos meses para todos los grupos. Finalizado este período, los animales fueron sacrificados para obtener biopsias del estómago, las cuales fueron procesadas y coloreadas con Hematoxilina-Eosina. Resultados: Tanto en el grupo A como en el grupo B se observaron signos de inflamación en la lámina propia en diferentes grados: leve, moderado y severo. En algunos animales, se identificaron linfocitos intraepiteliales y folículos linfoides. En ambos grupos se observaron elementos compatibles con la bacteria Hp. Estos hallazgos microscópicos no fueron encontrados en muestras de ratas del grupo C. Conclusiones: Existe una relación entre el consumo de agua y la infección por el Hp, que debe ser confirmada por medio de otros estudios y métodos de investigación...

[Mediastinis related to esophagogastric disease and injury. Warning clinical signs and independent predictors of intrahospitalary survival]. / Mediastinitis vinculada a enfermedad y lesión esofagogástrica. Signos de alerta diagnóstica y predictores independientes de sobrevida.

OBJECTIVE: To identify clinical warning signs and independent predictors of survival in mediastinitis related to esophagogastric diseases and injuries. METHODS: From March 1998 to February 2009, 36 patients with a mean age of 55.7 +/- 12.3 years old, with mediastinitis due to esophagogastric diseases and injuries were treated. Signs present before diagnosis of mediastinitis were identified. Several presentation and evolutive variables were confronted with mortality and survival. RESULTS: Mortality was 41.7%. Three etiological groups were discriminated: 1) 21 postoperatives of esophagogastric surgery with 57.1% mortality, 2) 14 instrumental and foreign bodies perforations of esophagus with 14.3% mortality, 3) 1 esophageal cancer perforation with no survival. Warning signs in group 1 were: bad postoperative evolution with sepsis and no other septic focus, septic pleural effusion, neumothorax, and supraventricular tachyarrhythmia. Warning signs in group 2 were: thorax pain usually retrosternal, pneumomediastinum, prevertebral cervical and subcutaneous emphysema, pleural effusion, sepsis, and odynophagia. Independent predictors of survival were: surgical procedure tactics that prioritizes debridement with mediastinal, pleural and neck drainage, esophagostomy and gastrostomy in opposition to less aggressive surgical tactics [OR 12.6 (95% CI: 1.7-66.5)], and surgery within the 24 hs of noticing the warning signs [OR 10.6 (95% CI: 1.7-96.7)]. These survival predictors were at the expense of group 1. Group 2 did not show any predictor of survival. CONCLUSIONS: In mediastinitis involving esophagogastric surgery, we recommend to apply the surgical tactics delineated previously and perform surgery within the 24 hs of noticing the warning signs. In mediastinitis involving instrumental and foreign bodies esophageal perforation, we can not recommend any particular surgical tactic.

[Image-guided percutaneous biopsy of gastric lesions with suspicion of malignancy and negative endoscopic biopsies: report of our experience and revision of the literature]. / Biopsia percutánea guiada por imágenes de lesiones gástricas sospechosas de malignidad y biopsias endoscópicas negativas: reporte de nuestra experiencia y revisión de la literatura.

BACKGROUND: Endoscopic biopsy is the most efficient way to obtain a biopsy specimen from neoplastic lesions located in the stomach. Therefore, it is the procedure of choice to obtain a histologic diagnosis of gastric cancer. Image guided percutaneous biopsy is an alternative method to obtain histologic material for definitive diagnosis when the biopsies are negative for neoplastic cells in several endoscopies. OBJECTIVE: The purpose of this study was to evaluate the efficacy, complications, and histologic results of image guided percutaneous biopsies of gastric lesions in our center. MATERIALS AND METHODS: Between March 2004 and March 2007, 6 patients with strong suspicion of gastric cancer and negative endoscopic biopsies were referred for image guided percutaneous biopsy of gastric lesions (5 were guided by ultrasonography and 1 by CT scan). RESULTS: A histologic diagnosis was made in 5 patients: poorly differentated signet-ring cell carcinoma 3, B-cell non-Hodgkin's lymphoma 2. One patient suffered a perforation during the procedure and the final histologic diagnosis was obtained after the consequent surgery (B-cell non-Hodgkin's lymphoma). CONCLUSION: Despite of the scant published series, image guided percutaneous biopsy of gastric lesions is an useful, safe and effective technique to obtain a histologic diagnosis in patients with strong suspicion of gastric cancer and negative endoscopic biopsies.

Dispepsia funcional. Utilidad de las drogas procinéticas en su tratamiento en el año 2008 / Functional dyspepsia: Prokinetic drugs utility in your treatment in year 2008

En pacientes con dispepsia funcional pueden demostrarse anormalidades motoras en aproximadamente el 30-45 por ciento de los casos. Pacientes con retardo en el vaciado gástrico, electrogastrografía anormal (disritmias gástricas), alteraciones en la acomodación fúndica o distensión antral, podrían tener mejor respuesta a la terapéutica con drogas procinéticas que aquellos con vaciamiento gástrico normal. En este trabajo nosotros evaluamos nuevos agentes con targets específicos sobre anormalidades motoras especialmente agentes procinéticos. Los agentes procinéticos incluidos son: agentes antidopaminérgicos D1-D2; agonistas de receptores 5HT1-5HT3-5HT4; agonistas de receptores a la motilina y agentes opioides.

[Predictors of intrahospitalary mortality in the upper gastrointestinal variceal bleeding due to chronic liver disease treated endoscopically]. / Predictores de mortalidad hospitalaria en la hemorragia digestiva alta variceal por hepatopatía crónica tratada endoscópicamente.

UNLABELLED: Upper gastrointestinal variceal bleeding is one of the most serious complications in patients with chronic liver disease. The aim of this trial is to identify in hospital mortality predictors in this illness. MATERIAL AND METHODS: 106 hospitalizations due to this disease from October 2001 to April 2006 in cohort design. In hospital mortality was confronted with age, sex, liver disease etiology, Apache II score at admission, variceal severity, severity of the hepatic failure evaluated according to the Child Pugh's classes, a history of variceal bleeding, initial endoscopic treatment failure, haemostatic failure within the first 48 hours, and rebleeding after 48 hours from admission. In order to identify independent mortality predictors, all the variables correlated significantly with hospital mortality were selected. For the quantitative variable APACHE II score at admission, the best mortality discrimination value was chosen. RESULTS: independent in hospital mortality predictors were: initial endoscopic treatment failure (p = 0.005), haemostatic failure in the first 48 hours (p = 0.012), and Child Pugh C class (p = 0.024). Although male sex, Apache II score at admission and rebleeding after 48 hours were also significantly related to mortality by univaried model, they did not qualify as independent predictors. CONCLUSIONS: the independent predictors of intrahospitalary mortality in patients with variceal bleeding due to chronic liver disease, and first-line of endoscopic treatment were: 1) Initial haemostatic endoscopic treatment failure, 2) Haemostatic failure in the first 48 hs, and 3) Child Pugh C class hepatic failure at admission.

¿Cómo adaptan su alimentación los pacientes con acalasia? / How do patients with achalasia adapt their feeding habits?

La acalasia es un trastorno motor del esófago con una incidencia de 2 personas cada 200.000 por año. Al Hospital Udaondo, centro de referencia, concurren 80 pacientes al año. Los antecedentes describen que los pacientes no adaptan la dieta pero utilizan otras estrategias para aliviar los síntomas. Nos preguntamos cuáles son las características nutricionales de estos pacientes, refiriéndonos no sólo a su estado nutricional, sino también a las características de la ingesta y a las diferentes adaptaciones y estrategias utilizadas, en forma empírica, para mejorar sus síntomas. Objetivos: Describir el Status Nutricional, los factores clínicos, la alimentación y la relación entre ellos, en los pacientes que padecen acalasia. Materiales y métodos: Estudio prospectivo, transversal, descriptivo. Se estudió a los pacientes con diagnóstico de acalasia que concurrieron a la sección Esófago y Estómago del Htal Udaondo durante Octubre 2006 a Marzo 2007. Resultados: Se estudiaron 16 pacientes. Sólo 2 presentaron desnutrición. Sin embargo todos mostraron pérdida de (pérdida ponderal máxima de 41%). La mayor parte de los pacientes utilizaba bebidas y maniobras posturales para mejorar los síntomas. Sólo 3 pacientes suplementaban su dieta. La misma demostró ser subóptima en todos los casos. Existió baja tolerancia para todas las consistencias. No se halló relación entre factores clínicos y la pérdida de peso. Tampoco influyó en el mismo el uso de estrategias (bebidas, maniobras o suplementos). Conclusiones: Predominó el estado nutricional normal, con riesgo elevado por pérdida ponderal grave. La dieta fue subóptima en la totalidad de la muestra. Se observó un alto grado de intolerancia para todas las consistencias, siendo aún mayor en el caso de los sólidos y menor para jugos y licuados. Todos los pacientes utilizaron algún tipo de estrategia especialmente maniobras posturales. El riesgo nutricional no se relaciona con factores clínicos ni con el uso de estrategias.

Predictores de mortalidad hospitalaria en la hemorragia digestiva alta variceal por hepatopatía crónica tratada endoscópicamente / Predictors of intrahospitalary mortality in the upper gastrointestinal variceal bleeding due to chronic liver disease treated endoscopically

La hemorragia digestiva alta variceal es una de las complicaciones más graves en la hepatopatía crónica. El objetivo de este trabajo es identificar variables que predicen mortalidad hospitalaria. Material y métodos: 106 internaciones por esta patología desde octubre de 2001 hasta abril de 2006 en diseño de cohortes. Se confrontó mortalidad hospitalaria con edad, sexo, etiología de la hepatopatía, score APACHE II al ingreso, imensión de las várices evaluada endoscópicamente, severidad de la insuficiencia hepática evaluada por clases de Child Pugh, antecedente de hemorragia variceal, fracaso de la terapia endoscópica inicial, fracaso hemostático en las primeras 48hs y resangrado posterior a 48hs. Para identificar predictores independientes de mortalidad se seleccionaron todas las variables que correlacionaron significativamente con muerte hospitalaria. Para la variable cuantitativa score APACHE II de ingreso se consideró el valor que mejor discriminó mortalidad. Resultados: los predictores independientes de muerte hospitalaria fueron: el fracaso de la terapia endoscópica inicial (p=0,005), el fracaso hemostático en las primeras 48hs (p=0,012) y la clase C de Child Pugh (p=0,024). Si bien en el sexo masculino el score APACHE II al ingreso y el resangrado con posterioridad a las 48hs también correlacionaron con mortalimortalidad, no calificaron como predictores independientes. Conclusión: en portadores de hepatopatía crónica con hemorragia digestiva alta variceal y primera línea de tratamiento endoscópico, resultaron predictores independientes de muerte hospitalaria: 1) el fracaso de la terapia endoscópica hemostática inicial, 2) el fracaso hemostático en las primeras 48hs, y 3) la clase C de Child Pugh al ingreso.

Upper gastrointestinal variceal bleeding is one of the most serious complications in patients with chronic liver disease. The aim of this trial is to identify in hospital mortality predictors in this illness. Material and methods: 106 hospitalizations due to this disease from October 2001 to April 2006 in cohort design. In hospital mortality was confronted with age, sex, liver disease etiology, Apache II score at admission, variceal severity, severity of the hepatic failure evaluated according to the Child Pugh’s classes, a history of variceal bleeding, initial endoscopic treatment failure, haemostatic failure within the first 48 hours, and rebleeding after 48 hours from admission. In order to identify independent mortality predictors, all the variables correlated significantly with hospital mortality were selected. For the quantitative variable APACHE II score at admission, the best mortality discrimination value was chosen. Results: independent in hospital mortality predictors were: initial endoscopic treatment failure (p = 0,005), haemostatic failure in the first 48 hours (p = 0,012), and Child Pugh C class (p = 0,024). Although male sex, Apache II score at admission and rebleeding after 48 hours were also significantly related to mortality by univaried model, they did not qualify as independent predictors. Conclusions: the independent predictors of intrahospitalary mortality in patients with variceal bleeding due to chronic liver disease, and firstline of endoscopic treatment were: 1) Initial haemostatic endoscopic treatment failure, 2) Haemostatic failure in the first 48hs, and 3) Child Pugh C class hepatic failure at admission.

[Therapeutics of infection by Helicobacter pylori in 2008]. / Terapéutica de la infección por Helicobacter pylori en el 2008.

Eradication therapy for Helicobacter pylori is recommended in a number of clinical conditions as developed in Maastricht Consensus (I, II, III). In this state of art we discuss the results of current eradication therapies, the new approaches to the management of infection (new antibiotics and eradication schemes) and antimicrobial resistance.