Scielo RSS <![CDATA[Revista Española de Enfermedades Digestivas]]> http://scielo.isciii.es/rss.php?pid=1130-010820100011&lang=es vol. 102 num. 1 lang. es <![CDATA[SciELO Logo]]> http://scielo.isciii.es/img/en/fbpelogp.gif http://scielo.isciii.es <![CDATA[<B>Un ecógrafo en la consulta de proctología</B>: <B>la ayuda al "dedo ilustrado"</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100001&lng=es&nrm=iso&tlng=es <![CDATA[<B>¿Se debe incluir la ecografía rectoanal como prueba diagnóstica del dolor anal crónico?</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100002&lng=es&nrm=iso&tlng=es Objective: to assess the efficiency of endorectal ultrasound (ERUS) in the study of chronic idiopathic anal pain (CIAP). Material and method: this is a prospective and descriptive study in which 40 patients, 18 men and 22 women with an average of 47 years, were included. They had chronic anal pain of at least 3 months' duration. A complete colonoscopy was performed in all patients, which found no abnormalities to explain clinical symptoms. Patients with anal fissure and internal hemorrhoids of any degree, perianal suppurative processes, and pelvic surgery were excluded from the study. An ALOKA ProSound SSD-4000 ultrasound console attached to a multifrequency radial transductor ASU-67 (7.5 and 10 MHz) was used. Results: one patient could not tolerate the examination. In 8 patients (20% of cases) alterations were detected during ultrasonography: in 4 patients (10% of the cases; 1 man and 3 women) internal anal sphincter (IAS) hypertrophy, and in 5 patients (4 women and 1 man) a torn sphincter complex. A tear in the upper IAS canal and hypertrophy of the middle anal canal were observed in one patient (1 woman). Conclusions: ERUS is a simple, economic and useful test to study anorectal pathologies. Although in most studied cases no damage to the anal canal or rectal wall was detected, in a considerable number of patients we observed a thickening of the IAS, a probable cause of anal pain. Therefore, we understand that ERUS should be included in the study of CIAP.<hr/>Objetivo: evaluar el rendimiento de la ecografía rectoanal (ERA) en el estudio del dolor anal crónico idiopático (DACI). Material y método: se trata de un estudio prospectivo y descriptivo en el que se han incluido 40 pacientes, 18 hombres y 22 mujeres, con edad media de 47 años, con clínica de dolor anal crónico de al menos 3 meses de evolución. A todos los pacientes se les había realizado una colonoscopia completa, en la que no se encontró anomalía que justificara la clínica. Se excluyeron del estudio pacientes con fisura anal y con hemorroides internas de cualquier grado, enfermedad supurativa perianal y cirugía pélvica. Se utilizó un ecógrafo ALOKA ProSound SSD-4000 al que se conectó un transductor radial multifrecuencia ASU-67 (7,5 y 10 MHz). Resultados: un paciente no toleró la exploración. En 8 pacientes (20% de los casos estudiados) se detectaron alteraciones en el estudio ecográfico: en 4 pacientes, 10% de los casos (1 hombre y 3 mujeres), hipertrofia del esfínter anal interno (EAI) y en 5 pacientes (4 mujeres y 1 hombre) rotura del complejo esfinteriano. En una mujer se observó rotura de EAI en canal alto e hipertrofia del mismo en el canal medio. Conclusiones: la ecografía rectoanal es una prueba sencilla, económica y útil para el estudio de la patología rectoanal. Si bien, en la mayoría de los casos estudiados no se han detectado lesiones en el canal anal ni en la pared rectal, en un porcentaje no desdeñable de pacientes hemos observado engrosamiento del EAI, que podría considerarse posible causa del dolor anal. Por tanto, consideramos que la ecografía rectoanal debe ser incluida en el estudio del dolor anal crónico idiopático. <![CDATA[<B>Esofagitis eosinofílica</B>: <B>una experiencia italiana</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100003&lng=es&nrm=iso&tlng=es Background: eosinophilic esophagitis is an esophageal disorder characterized by esophageal and/or upper gastrointestinal tract symptoms, and by dense esophageal eosinophilia associated with a normal gastric and duodenal mucosa. Prevalently reported in children, eosinophilic esophagitis has recently been reported with increased frequency also in adults. Aims: the purpose of this study was to report our experience with eosinophilic esophagitis in Italy, since there are only very few series of such patients in our country. Patients and methods: we retrospectively reviewed the histological data of consecutive patients with a diagnosis of esophagitis or reflux disease in the period September 2004-September 2008. Eosinophils were counted where they appeared most numerous in the biopsy, with a cutoff > 15 eosinophils in more than one high-power field as diagnostic of eosinophilic esophagitis. Patients were excluded if gastric or duodenal biopsies showed a prominent eosinophilic infiltrate. Results: twenty two patients (14 adults, 8 children, age range 2-59 years) were identified according to the above criteria. The average eosinophil count was 86/ high-power field (range 31-150), associated with other pathologic features (eosinophilic microabscesses eosinophil degranulation, basal zone hyperplasia, papillary elongation). The main clinical complaints were dysphagia, food impaction, and heartburn, and endoscopic findings consisted of mucosal thickening and inelasticity, longitudinal shearing, rings, and white specks, without difference between adults and children for both clinical and endoscopic variables. Conclusions: eosinophilic esophagitis is not rare in Italy, and displays clinical, endoscopic, and pathologic features similar to those described in other countries. <![CDATA[<B>Polimorfismos del gen del factor de crecimiento vascular endotelial en pacientes con cáncer colorrectal</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100004&lng=es&nrm=iso&tlng=es Background: angiogenesis plays an important role in tumor progression. The vascular endothelial growth factor (VEGF) is an important regulator of angiogenesis. In the present study we evaluated single nucleotide polymorphisms (SNPs) -2578C > A, -1154G > A, and +936C > T in the VEGF gene, and their prognostic value for patients operated on for colorectal cancer (CRC). Patients and method: VEGF polymorphisms have been analyzed in 177 patients who had undergone surgical resection at Hospital Clínico San Carlos. The analysis of these polymorphisms was performed with specific probes for each nucleotide in a multiplex reaction using real-time PCR. Results: we only found a statistically significant relationship for one of these three polymorphisms, +936C > T, with gender and tumor location; 10.7% of patients heterozygotes for this SNP had tumors located in proximal colon, 35.2% in distal segment and 54.1% in rectum (p = 0.03). Patients with the +936T/T genotype had 100% overall survival (OS). Conclusion: patients with a +936T/T genotype showed increased survival, therefore the +936C > T SNP could be a useful marker in the follow-up and clinical management of patients with colorectal cancer.<hr/>Introducción: la angiogénesis juega un papel importante en la progresión de los tumores. El factor de crecimiento endotelial vascular (VEGF) es un importante regulador de la angiogénesis. En este trabajo se han analizado los polimorfismos de único nucleó-tido (SNP) -2578C > A, -1154G > A y +936C > T del gen VEGF en pacientes intervenidos de carcinoma colorrectal, así como su posible implicación pronóstica. Pacientes y método: el estudio de estos SNP se ha realizado en 177 pacientes intervenidos quirúrgicamente de carcinoma colorrectal (CCR) en el Hospital Clínico San Carlos. El análisis de los polimorfismos se realizó con sondas específicas para cada nucleótido y se determinó mediante una reacción multiplex mediante real time PCR. Resultados: de los 3 polimorfismos estudiados sólo encontramos relación estadísticamente significativa del SNP +936C > T con el sexo y la localización. El 10,7% de los pacientes heterocigotos para este SNP tenían como localización el tumor en colon proximal, el 35,2% en colon distal y el resto en recto (p = 0,03). La supervivencia global (SG) de los pacientes con el genotipo +936T/T fue del 100%. Conclusión: los pacientes con el genotipo +936T/T presentan mayor supervivencia y el polimorfismo +936C > T podría ser una herramienta de ayuda en el seguimiento y terapéutica de este grupo de pacientes. <![CDATA[<B>Intususcepción en el adulto</B>: <B>Revisión de 14 casos y su seguimiento</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100005&lng=es&nrm=iso&tlng=es Aims: to analyze diagnostic and therapeutic options depending on the clinical symptoms, location, and lesions associated with intussusception, together with their follow-up and complications. Patients and methods: patients admitted to the Morales Meseguer General University Hospital (Murcia) between January 1995 and January 2009, and diagnosed with intestinal invagination. Data related to demographic and clinical features, complementary explorations, presumptive diagnosis, treatment, follow-up, and complications were collected. Results: there were 14 patients (7 males and 7 females; mean age: 41.9 years-range: 17-77) who presented with abdominal pain. The most reliable diagnostic technique was computed tomography (8 diagnoses from 10 CT scans). A preoperative diagnosis was established in 12 cases. Invaginations were ileocolic in 8 cases (the most common), enteric in 5, and colocolic in 2 (coexistence of 2 lesions in one patient). The etiology of these intussusceptions was idiopathic or secondary to a lesion acting as the lead point for invagination. Depending on the nature of this lead point, the cause of the enteric intussusceptions was benign in 3 cases and malignant in 2. Ileocolic invaginations were divided equally (4 benign and 4 malignant), and colocolic lesions were benign (2 cases). Conservative treatment was implemented for 4 patients and surgery for 10 (7 in emergency). Five right hemicolectomies, 3 small-bowel resections, 2 left hemicolectomies, and 1 ileocecal resection were performed. Surgical complications: 3 minor and 1 major (with malignant etiology and subsequent death). The lesion disappeared after 3 days to 6 weeks in patients with conservative management. Mean follow-up was 28.25 months (range: 5-72 months). Conclusions: a suitable imaging technique, preferably CT, is important for the diagnosis of intussusception. Surgery is usually necessary but we favor conservative treatment in selected cases.<hr/>Objetivos: analizar las opciones terapéuticas en función de la clínica, localización y lesión asociada a la intususcepción, así como, su seguimiento y complicaciones. Pacientes y métodos: pacientes ingresados en el HGU Morales Meseguer (Murcia) desde enero de 1995 hasta enero 2009, con diagnóstico de invaginación intestinal. Se recogieron datos demográficos, clínicos, exploraciones complementarias, diagnóstico presuntivo, tratamiento, seguimiento y complicaciones. Resultados: 14 pacientes (edad media 41,9 años, rango: 17-77), 7 varones y 7 mujeres, que debutaron principalmente con dolor abdominal. La exploración más fiable en el diagnóstico fue la tomografía computerizada, TC (8 diagnósticos, de 10 exploraciones). El diagnóstico preoperatorio se obtuvo en 12 casos, encontrando, invaginaciones ileocólicas en 8 casos (las más frecuentes), entéricas en 5 casos y colocólicas en 2, teniendo en cuenta que son 14 los pacientes y 15 las lesiones debido a la coexistencia de 2 invaginaciones en un mismo sujeto. La etiología de las intususcepciones es idiopática o secundaria a una lesión que hace de cabeza de invaginación. Según la naturaleza de dichas lesiones la causa de intususcepciones entéricas fue benigna en 3 casos y maligna en 2. De las ileocólicas, se repartieron equitativamente (4 benignas y 4 malignas); y de las colocólicas, sus lesiones fueron benignas (2 casos). Se realizó tratamiento conservador en 4 pacientes y quirúrgico en 10 (7 urgente). Con 5 hemicolectomías derechas, 3 resecciones de intestino delgado, 2 hemicolectomías izquierdas y una resección ileocecal. Las complicaciones quirúrgicas: 3 menores y 1 mayor (de etiología maligna y consecuente exitus). En los pacientes con manejo conservador desapareció la lesión entre 3 días y 6 semanas. Se siguieron durante 28,25 meses de media (rango 5-72 meses). Conclusiones: para diagnosticar las intususcepciones es importante una adecuada técnica de imagen, recomendablemente TC. Abogamos por un tratamiento conservador en aquellos casos donde no se encuentre etiología de invaginación, según el tipo de intususcepción y clínica, siempre asociado a seguimiento. <![CDATA[<B><I>H. pylori</I> y alteraciones mitocondriales en células epiteliales</B>: <B>Relación con estrés oxidativo</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100006&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Cuerpo extraño en esófago</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100007&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Pólipo rectal como forma de presentación de colitis quística profunda</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100008&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Enfermedad de Wilson</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100009&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Transposición gástrica tras fracaso de esófago-coloplastia por necrosis del injerto en el tratamiento de atresia esofágica tipo I de brecha larga</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100110&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Hemorragia severa por enfermedad de Crohn complicada, tratada con infliximab</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100111&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>"Groove pancreatitis" o pancreatitis del surco con estenosis duodenal</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100112&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Otro caso de anisakiasis gástrica múltiple</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100113&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Bacteriemia por <I>Pantoea agglomerans</I> en paciente trasplantado hepático</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100114&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Sarcoma sinovial bifásico en tercera porción duodenal</B>: <B>caso clínico y revisión de la literatura</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100115&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Quiste linfoepitelial de páncreas</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100116&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Pseudoaneurisma de la arteria hepática tras colecistectomía</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100117&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Flebitis enterocólica linfocítica granulomatosa idiopática</B>: <B>presentación de un caso y revisión de la literatura</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100118&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Leiomiosarcoma primario de vesícula biliar</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100119&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Pseudoaneurisma esplénico fistulizado a yeyuno secundario a pancreatitis aguda grave</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100220&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection. <![CDATA[<B>Síncope en paciente con antecedente de pancreatitis aguda</B>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010001100221&lng=es&nrm=iso&tlng=es Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection.