Scielo RSS <![CDATA[Revista Española de Enfermedades Digestivas]]> http://scielo.isciii.es/rss.php?pid=1130-010820130007&lang=es vol. 105 num. 7 lang. es <![CDATA[SciELO Logo]]> http://scielo.isciii.es/img/en/fbpelogp.gif http://scielo.isciii.es <![CDATA[<b>Polimorfismos</b>: <b>variaciones genéticas asociadas al síndrome del intestino irritable</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700001&lng=es&nrm=iso&tlng=es <![CDATA[<b>Administración de propofol mediante bolus intermitente frente a infusión continua con bomba controlada por el endoscopista en la colonoscopia</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700002&lng=es&nrm=iso&tlng=es Background: non-anesthesiologist administration of propofol (NAAP) using continuous infusion systems may achieve a more sustained sedative action. Aim: to compare intermittent boluses (IB) with pump continuous infusion (PCI) for NAAP, targeted to moderate sedation, for colonoscopy. Methods: 192 consecutive outpatients were randomized to receive IB (20 mg propofol boluses on demand) or PCI (3 mg/kg/h plus 20 mg boluses on demand). Sedation could be stopped at cecal intubation at the discretion of the endoscopist. Satisfaction rates of the patient, nurses and endoscopist, propofol doses, depth of sedation (at the beginning, at cecal intubation and at the end), recovery times, complications and were collected. Results: there were no differences between groups regarding patient, nurse or endoscopist satisfaction rates with procedural sedation. Propofol doses (mg) were significantly higher during the induction phase (86 [30-172] vs. 78 [30-160], p 0.03) and overall (185 [72-400] vs. 157 [60-460], p = 0.003) for PCI group. 81 % of assessments of the depth of sedation were moderate. The level of sedation (O/AAS scale) was borderline significantly deeper at cecal intubation (2.38 vs. 2.72; p = 0.056) and at the end of the procedure (4.13 vs. 4.45; p = 0.05) for PCI group, prolonging thus early recovery time (6.3 vs. 5.1 minutes, p = 0.008), but not discharge time. Complications, all of them in minors, were non-significantly more frequent in the PCI group (9 vs. 7 %, p = 0.07). Conclusions: NAAP for colonoscopy was safely administered with comparable satisfaction and complication rates with either IB or PCI. <![CDATA[<b>Satisfacción de los pacientes con enfermedad inflamatoria intestinal de los servicios sanitarios recibidos</b>: <b>percepciones de médicos y enfermeras</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700003&lng=es&nrm=iso&tlng=es Background: patient satisfaction with healthcare services provided for inflammatory bowel diseases (IBD) is essential due to high resources use. Objectives: the study aimed to describe patient satisfaction with healthcare services using the CACHE questionnaire and to assess gastroenterologist and nurse perception on patients' satisfaction. Methods: observational multicentric prospective study in 35 Spanish hospitals. Patients included had Crohn's disease or ulcerative colitis. The study was approved by the Hospital Universitari Vall d'Hebron Ethics Committee. Scheduled study visits: baseline (patient sociodemographics and clinical data were collected), 2-4 and 6-months. Patient satisfaction with healthcare was assessed by CACHE questionnaire at each visit; it scores from 0-least satisfaction to 100-highest satisfaction. Gastroenterologists and nurses answered once an adapted questionnaire. Results: participating 290 patients (54.2 % males, 41.3 years old), 62 gastroenterologists and 47 nurses. At baseline mean (SD) CACHE score was 81.7 (10.9); satisfaction with clinician care was the highest, patient information the lowest. Scores did not change across study. Gastroenterologist global score was 72.5 (9.8); Staff Care satisfaction was the highest, patient information the lowest. All scores were significantly lower than patients'. Nurses' global score was 82.2 (8.5), clinician care satisfaction was the highest, centre facilities the lowest. Scores on satisfaction with clinician care, centre facilities, and patient information scored statistically lower than patients'. No relationship was found between patients' satisfaction and patients characteristics. Conclusions: IBD patients are satisfied with healthcare services provided, even though the information may be improved. Nurses' perception is similar to that of patients, physicians have a lower perception. <![CDATA[<b>Polimorfismos de IL-10 y TNF-α en sujetos con síndrome de intestino irritable en México</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700004&lng=es&nrm=iso&tlng=es Background: there has been recent evidence of an alteration in irritable bowel syndrome (IBS) immune regulation, as well as variations in cytokine polymorphisms. Aims: to determine the frequency of the IL-10 (-1082G/A) and TNF-α (-308G/A) polymorphisms in subjects with IBS in Mexico. Methods: volunteers answered the Rome II Questionnaire and were classified as IBS (n = 45) and controls (n = 92). The IBS subjects were then categorized as IBS-D: 22.2 %, IBS-C: 28.9 %, and IBS-A/M: 48.9 %. The polymorphism frequency among groups was compared. Results: there were no differences between IBS vs. controls in the frequency of the high (8.9 vs. 18.5 %), intermediate (60.0 vs. 57.6 %), or low (23.9 vs. 38.9 %) producer IL-10 genotypes, p = 0.315. Neither were there differences in the high (0 vs. 1.1 %), intermediate (55.4 vs. 43.2 %), or Low (43.5 vs. 56.8 %) producer TNF-α genotypes, p = 0.296. However the low producer of IL-10 was more frequent in IBS-D vs. IBS-C vs. IBS-A/M (63.6 vs. 7.1 vs. 33,3 %) p = 0.023. Conclusions: in this group of volunteers in Mexico, the frequency of the IL-10 (-1082G/A) and TNF-α (-308G/A) genotypes was similar in IBS and controls. However, there was a greater frequency of the low producer of IL-10 in those subjects with IBS-D, suggesting a genetic predisposition to abnormal immune regulation due to a lower anti-inflammatory component in this subgroup.<hr/>Antecedentes: evidencias recientes han mostrado una alteración en la regulación inmune en el síndrome de intestino irritable (SII) así como variaciones en los polimorfismos de citocinas. Objetivos: determinar la frecuencia de polimorfismos IL-10 (-1082G/A) y TNF-α (-308G/A) en sujetos con SII en México. Métodos: sujetos voluntarios contestaron el Cuestionario de Roma II y fueron clasificados como SII (n = 45) y controles (n = 92). Aquellos con SII fueron a su vez clasificados en SII-D: 22,2 %, SII-E: 28,9 % y SII-A/M: 48,9 %. Se comparó la frecuencia de los polimorfismos entre los grupos. Resultados: no hubo diferencias entre SII vs. controles en la frecuencia del genotipo alto (8,9 vs. 18,5 %), intermedio (60,0 vs. 57,6 %) y bajo productor (23,9 vs. 38,9 %) de IL-10, p = 0,315. Tampoco en alto (0 vs. 1,1 %), intermedio (55,4 vs. 43,2 %) o bajo productor (43,5 vs. 56,8 %) de TNF-α, p = 0,296. Sin embargo, el bajo productor de IL-10 fue más frecuente en SII-D vs. SII-E vs. SII-A/M (63,6 vs. 7,1 vs. 33,3 %) p = 0,023. Conclusiones: en este grupo de voluntarios en México la frecuencia de genotipos de IL-10 (-1082G/A) y TNF-α (-308G/A) fue similar en SII y controles, pero aquellos con SII-D presentaron mayor frecuencia del bajo productor de IL-10 sugiriendo una predisposición genética a una regulación inmune anormal dada por un menor componente antiinflamatorio en este subgrupo. <![CDATA[<b>Valoración de la calidad de la colonoscopia en un programa de cribado masivo poblacional basado en la prueba de sangre oculta en heces</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700005&lng=es&nrm=iso&tlng=es Background and aim: the success of colorectal cancer (CRC) screening programmes largely depends on the quality of the events, processes and outcomes and therefore, quality assurance of endoscopy is an essential component. The quality indicators for colonoscopy in a screening programme setting are different from those performed in symptomatic people. The objective of this study was to report the main quality indicators of colonoscopies performed after a positive faecal occult blood test (FOBT) in a CRC screening programme in Catalonia. Methods: the period of study includes three rounds of the CRC screening programme from June 2006 to July 2013. Two types of FOBT were used: a qualitative biochemical guaiac-based test (gFOBT) and a quantitative immunochemical test (FIT). Quality indicators analysed in this study were compared to recommended colonoscopy standards from the published guidelines. Results: during the study period, 1,806 colonoscopies were performed in 1,691 individuals with a positive FOBT. All indicators were within the standard except waiting time to colonoscopy. Caecal intubation rate was 95.6 % and adequate bowel cleansing 93.6 %. Adenoma detection rate was better using FIT than gFOBT, 30.7 and 3.8 per 1,000 screenees, respectively. Cancer detection rate was also greater using FIT. Nearly 62 % of cancers were diagnosed at an early stage. The overall complication rate was 10.7 ‰. Conclusion: although the majority of results reached the recommended standards, some areas have been identified for quality enhancement. Continuous monitoring of quality indicators is essential for improving the current effectiveness of CRC screening programmes. <![CDATA[<b>Etiopatogenia, diagnóstico y tratamiento de la enfermedad del hígado graso no alcohólica</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700006&lng=es&nrm=iso&tlng=es Non-alcoholic fatty liver disease (NAFLD) includes a broad spectrum of alterations that go from simple steatosis to steatohepatitis and cirrhosis. Type 2 diabetes mellitus (DM-2) and obesity are the principle factors associated to NAFLD. A 20-30 % prevalence in general population has been described. The survival of this type of patient is lower than the general population's, showing a higher incidence of hepatic and cardiovascular complications. The aetiopathogenesis is still unclear, but we know the intervention of different factors that produce fatty-acid accumulation in hepatic parenchyma, causing oxidative stress, oxygen-free radicals and the synthesis of an inflammatory cascade, that determine the progression of this disease from steatosis up to advanced fibrosis. The diagnostic gold-standard is still the liver biopsy, even though the development of newer non-invasive techniques, like serological and imaging (radiology), have opened a new field for research that allows bloodless testing of these patients and better study of the natural history of this disease. Nowadays, there is still no specific treatment for NAFLD. The development of healthy life habits and moderate exercise continue to be the pillars of treatment. Different pharmacological approaches have been studied and applied, such as the control of insulin resistance, lowering cholesterol levels, antioxidants, and other alternatives in experimental trials.<hr/>La enfermedad por hígado graso no alcohólica (EHGNA) comprende un amplio abanico de alteraciones que va desde la esteatosis simple hasta la esteatohepatitis y la cirrosis. La diabetes mellitus tipo 2 y la obesidad son los principales factores asociados a la EHGNA. Se ha descrito una prevalencia en la población general de entre el 20-30 %. La supervivencia de estos enfermos es menor que la población general, presentando una mayor incidencia de complicaciones hepáticas y cardiovasculares. La etiopatogenia es desconocida en parte pero se conoce la intervención de diferentes factores que provocan la acumulación de ácidos grasos en el parénquima hepático, produciendo una situación de estrés oxidativo, la formación de radicales libres de oxígeno y la síntesis de una cascada inflamatoria de citocinas que determinan la progresión de la enfermedad desde esteatosis hasta fibrosis avanzada. La prueba diagnóstica de elección continúa siendo la biopsia hepática, si bien el desarrollo de diferentes técnicas no invasivas, tanto serológicas como de imagen, ha abierto un nuevo campo de investigación que permite una evaluación incruenta de estos pacientes y un mejor estudio de la historia natural de la enfermedad. En la actualidad no existe un tratamiento específico. El desarrollo de hábitos de vida saludables y el ejercicio físico moderado continúan siendo los pilares básicos. Se han investigado y aplicado diferentes aproximaciones farmacológicas incluyendo el control de la resistencia a la insulina, hipolipemiantes, antioxidantes y otras alternativas en vía experimental. <![CDATA[<b>Tumor neurogénico retroperitoneal diagnosticado por ultrasonografía endoscópica</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700007&lng=es&nrm=iso&tlng=es Non-alcoholic fatty liver disease (NAFLD) includes a broad spectrum of alterations that go from simple steatosis to steatohepatitis and cirrhosis. Type 2 diabetes mellitus (DM-2) and obesity are the principle factors associated to NAFLD. A 20-30 % prevalence in general population has been described. The survival of this type of patient is lower than the general population's, showing a higher incidence of hepatic and cardiovascular complications. The aetiopathogenesis is still unclear, but we know the intervention of different factors that produce fatty-acid accumulation in hepatic parenchyma, causing oxidative stress, oxygen-free radicals and the synthesis of an inflammatory cascade, that determine the progression of this disease from steatosis up to advanced fibrosis. The diagnostic gold-standard is still the liver biopsy, even though the development of newer non-invasive techniques, like serological and imaging (radiology), have opened a new field for research that allows bloodless testing of these patients and better study of the natural history of this disease. Nowadays, there is still no specific treatment for NAFLD. The development of healthy life habits and moderate exercise continue to be the pillars of treatment. Different pharmacological approaches have been studied and applied, such as the control of insulin resistance, lowering cholesterol levels, antioxidants, and other alternatives in experimental trials.<hr/>La enfermedad por hígado graso no alcohólica (EHGNA) comprende un amplio abanico de alteraciones que va desde la esteatosis simple hasta la esteatohepatitis y la cirrosis. La diabetes mellitus tipo 2 y la obesidad son los principales factores asociados a la EHGNA. Se ha descrito una prevalencia en la población general de entre el 20-30 %. La supervivencia de estos enfermos es menor que la población general, presentando una mayor incidencia de complicaciones hepáticas y cardiovasculares. La etiopatogenia es desconocida en parte pero se conoce la intervención de diferentes factores que provocan la acumulación de ácidos grasos en el parénquima hepático, produciendo una situación de estrés oxidativo, la formación de radicales libres de oxígeno y la síntesis de una cascada inflamatoria de citocinas que determinan la progresión de la enfermedad desde esteatosis hasta fibrosis avanzada. La prueba diagnóstica de elección continúa siendo la biopsia hepática, si bien el desarrollo de diferentes técnicas no invasivas, tanto serológicas como de imagen, ha abierto un nuevo campo de investigación que permite una evaluación incruenta de estos pacientes y un mejor estudio de la historia natural de la enfermedad. En la actualidad no existe un tratamiento específico. El desarrollo de hábitos de vida saludables y el ejercicio físico moderado continúan siendo los pilares básicos. Se han investigado y aplicado diferentes aproximaciones farmacológicas incluyendo el control de la resistencia a la insulina, hipolipemiantes, antioxidantes y otras alternativas en vía experimental. <![CDATA[<b>Rotura duodenal aislada en un niño tras una coz de un caballo</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700008&lng=es&nrm=iso&tlng=es Non-alcoholic fatty liver disease (NAFLD) includes a broad spectrum of alterations that go from simple steatosis to steatohepatitis and cirrhosis. Type 2 diabetes mellitus (DM-2) and obesity are the principle factors associated to NAFLD. A 20-30 % prevalence in general population has been described. The survival of this type of patient is lower than the general population's, showing a higher incidence of hepatic and cardiovascular complications. The aetiopathogenesis is still unclear, but we know the intervention of different factors that produce fatty-acid accumulation in hepatic parenchyma, causing oxidative stress, oxygen-free radicals and the synthesis of an inflammatory cascade, that determine the progression of this disease from steatosis up to advanced fibrosis. The diagnostic gold-standard is still the liver biopsy, even though the development of newer non-invasive techniques, like serological and imaging (radiology), have opened a new field for research that allows bloodless testing of these patients and better study of the natural history of this disease. Nowadays, there is still no specific treatment for NAFLD. The development of healthy life habits and moderate exercise continue to be the pillars of treatment. Different pharmacological approaches have been studied and applied, such as the control of insulin resistance, lowering cholesterol levels, antioxidants, and other alternatives in experimental trials.<hr/>La enfermedad por hígado graso no alcohólica (EHGNA) comprende un amplio abanico de alteraciones que va desde la esteatosis simple hasta la esteatohepatitis y la cirrosis. La diabetes mellitus tipo 2 y la obesidad son los principales factores asociados a la EHGNA. Se ha descrito una prevalencia en la población general de entre el 20-30 %. La supervivencia de estos enfermos es menor que la población general, presentando una mayor incidencia de complicaciones hepáticas y cardiovasculares. La etiopatogenia es desconocida en parte pero se conoce la intervención de diferentes factores que provocan la acumulación de ácidos grasos en el parénquima hepático, produciendo una situación de estrés oxidativo, la formación de radicales libres de oxígeno y la síntesis de una cascada inflamatoria de citocinas que determinan la progresión de la enfermedad desde esteatosis hasta fibrosis avanzada. La prueba diagnóstica de elección continúa siendo la biopsia hepática, si bien el desarrollo de diferentes técnicas no invasivas, tanto serológicas como de imagen, ha abierto un nuevo campo de investigación que permite una evaluación incruenta de estos pacientes y un mejor estudio de la historia natural de la enfermedad. En la actualidad no existe un tratamiento específico. El desarrollo de hábitos de vida saludables y el ejercicio físico moderado continúan siendo los pilares básicos. Se han investigado y aplicado diferentes aproximaciones farmacológicas incluyendo el control de la resistencia a la insulina, hipolipemiantes, antioxidantes y otras alternativas en vía experimental. <![CDATA[<b>Hipercalcemia asociada a carcinoma adenoescamoso de páncreas</b>: <b>razones para iniciar tratamiento paliativo</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700009&lng=es&nrm=iso&tlng=es Background: hypercalcemia in patients with diagnosed carcinoma has predominantly a humoral basis mediated by parathyroid hormone-related protein (PTH-rP). Among the reported cases, hypercalcemia associated with the majority of abdominal malignancies indicates an advanced stage of disease. Case report: we present a case of a 78-year-old patient with an adenosquamous pancreatic carcinoma associated with humoral hypercalcemia mediated by PTH-rP. Conclusion: in this case, demonstration of unexpectantly rapid increase in calcium serum correlated with aggressive tumor growth led us to raise the hypothesis that PTH-rP could be a mediator of invasion and dissemination secreted by some tumors, and probably indicates the appropriate time to initiate palliative treatment. <![CDATA[<b>Grandes pliegues gástricos en síndromes de poliposis</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700010&lng=es&nrm=iso&tlng=es Large gastric folds (LGF) can be caused by benign conditions as well as malignancies. Unfortunately, endoscopic features and biopsy results are often equivocal, making the diagnosis and management of large gastric folds difficult. Polyposis syndromes encompass a group of conditions in which multiple gastrointestinal polyps occur in the lumen of the gut. Large gastric folds are extremely rare in these syndromes. We present the case of a patient with polyposis who was found to have large gastric folds in the entire gastric fundus and body, mimicking malignancy. The patient's medical history and endoscopic ultrasonography (EUS) with mucosal resection confirmed the diagnosis of a pre-malignant disease. The lesion was monitored by serial endoscopic ultrasonography and biopsy, abdominal computed tomography (CT), and positron emission and computed tomography (PET-CT) for 6 years. The lesion remained stable, with the exception of abnormal fluorodeoxyglucose uptake on PET-CT in the gastric folds, which was determined to be a false-positive sign. To date, the patient remains healthy. We further discuss the mechanisms underlying the formation of large gastric folds caused by polyposis syndromes. Helicobacter pylori (H. pylori) or cytomegalovirus (CMV) is unnecessary for this progression. Immunohistochemistry (IHC) staining suggested that overexpression of transforming growth factor alpha (TGF-α) and down-regulation of myocyte enhancer-binding factor 2 (MEF2) may be involved in this case. <![CDATA[<b>Hepatotoxicidad por productos de herboristería</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700011&lng=es&nrm=iso&tlng=es Large gastric folds (LGF) can be caused by benign conditions as well as malignancies. Unfortunately, endoscopic features and biopsy results are often equivocal, making the diagnosis and management of large gastric folds difficult. Polyposis syndromes encompass a group of conditions in which multiple gastrointestinal polyps occur in the lumen of the gut. Large gastric folds are extremely rare in these syndromes. We present the case of a patient with polyposis who was found to have large gastric folds in the entire gastric fundus and body, mimicking malignancy. The patient's medical history and endoscopic ultrasonography (EUS) with mucosal resection confirmed the diagnosis of a pre-malignant disease. The lesion was monitored by serial endoscopic ultrasonography and biopsy, abdominal computed tomography (CT), and positron emission and computed tomography (PET-CT) for 6 years. The lesion remained stable, with the exception of abnormal fluorodeoxyglucose uptake on PET-CT in the gastric folds, which was determined to be a false-positive sign. To date, the patient remains healthy. We further discuss the mechanisms underlying the formation of large gastric folds caused by polyposis syndromes. Helicobacter pylori (H. pylori) or cytomegalovirus (CMV) is unnecessary for this progression. Immunohistochemistry (IHC) staining suggested that overexpression of transforming growth factor alpha (TGF-α) and down-regulation of myocyte enhancer-binding factor 2 (MEF2) may be involved in this case. <![CDATA[<b><i>Aloe vera</i></b>: <b>no siempre tan beneficioso en pacientes con hepatopatía crónica</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700012&lng=es&nrm=iso&tlng=es Large gastric folds (LGF) can be caused by benign conditions as well as malignancies. Unfortunately, endoscopic features and biopsy results are often equivocal, making the diagnosis and management of large gastric folds difficult. Polyposis syndromes encompass a group of conditions in which multiple gastrointestinal polyps occur in the lumen of the gut. Large gastric folds are extremely rare in these syndromes. We present the case of a patient with polyposis who was found to have large gastric folds in the entire gastric fundus and body, mimicking malignancy. The patient's medical history and endoscopic ultrasonography (EUS) with mucosal resection confirmed the diagnosis of a pre-malignant disease. The lesion was monitored by serial endoscopic ultrasonography and biopsy, abdominal computed tomography (CT), and positron emission and computed tomography (PET-CT) for 6 years. The lesion remained stable, with the exception of abnormal fluorodeoxyglucose uptake on PET-CT in the gastric folds, which was determined to be a false-positive sign. To date, the patient remains healthy. We further discuss the mechanisms underlying the formation of large gastric folds caused by polyposis syndromes. Helicobacter pylori (H. pylori) or cytomegalovirus (CMV) is unnecessary for this progression. Immunohistochemistry (IHC) staining suggested that overexpression of transforming growth factor alpha (TGF-α) and down-regulation of myocyte enhancer-binding factor 2 (MEF2) may be involved in this case. <![CDATA[<b>Esplenosis perihepática simulando una lesión focal hepática en un paciente con hepatitis crónica C</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700013&lng=es&nrm=iso&tlng=es Large gastric folds (LGF) can be caused by benign conditions as well as malignancies. Unfortunately, endoscopic features and biopsy results are often equivocal, making the diagnosis and management of large gastric folds difficult. Polyposis syndromes encompass a group of conditions in which multiple gastrointestinal polyps occur in the lumen of the gut. Large gastric folds are extremely rare in these syndromes. We present the case of a patient with polyposis who was found to have large gastric folds in the entire gastric fundus and body, mimicking malignancy. The patient's medical history and endoscopic ultrasonography (EUS) with mucosal resection confirmed the diagnosis of a pre-malignant disease. The lesion was monitored by serial endoscopic ultrasonography and biopsy, abdominal computed tomography (CT), and positron emission and computed tomography (PET-CT) for 6 years. The lesion remained stable, with the exception of abnormal fluorodeoxyglucose uptake on PET-CT in the gastric folds, which was determined to be a false-positive sign. To date, the patient remains healthy. We further discuss the mechanisms underlying the formation of large gastric folds caused by polyposis syndromes. Helicobacter pylori (H. pylori) or cytomegalovirus (CMV) is unnecessary for this progression. Immunohistochemistry (IHC) staining suggested that overexpression of transforming growth factor alpha (TGF-α) and down-regulation of myocyte enhancer-binding factor 2 (MEF2) may be involved in this case. <![CDATA[<b>Pancreatitis aguda como manifestación atípica de infección por virus de Epstein-Barr</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700014&lng=es&nrm=iso&tlng=es Large gastric folds (LGF) can be caused by benign conditions as well as malignancies. Unfortunately, endoscopic features and biopsy results are often equivocal, making the diagnosis and management of large gastric folds difficult. Polyposis syndromes encompass a group of conditions in which multiple gastrointestinal polyps occur in the lumen of the gut. Large gastric folds are extremely rare in these syndromes. We present the case of a patient with polyposis who was found to have large gastric folds in the entire gastric fundus and body, mimicking malignancy. The patient's medical history and endoscopic ultrasonography (EUS) with mucosal resection confirmed the diagnosis of a pre-malignant disease. The lesion was monitored by serial endoscopic ultrasonography and biopsy, abdominal computed tomography (CT), and positron emission and computed tomography (PET-CT) for 6 years. The lesion remained stable, with the exception of abnormal fluorodeoxyglucose uptake on PET-CT in the gastric folds, which was determined to be a false-positive sign. To date, the patient remains healthy. We further discuss the mechanisms underlying the formation of large gastric folds caused by polyposis syndromes. Helicobacter pylori (H. pylori) or cytomegalovirus (CMV) is unnecessary for this progression. Immunohistochemistry (IHC) staining suggested that overexpression of transforming growth factor alpha (TGF-α) and down-regulation of myocyte enhancer-binding factor 2 (MEF2) may be involved in this case. <![CDATA[<b>Aspiración de cápsula endoscópica</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700015&lng=es&nrm=iso&tlng=es Large gastric folds (LGF) can be caused by benign conditions as well as malignancies. Unfortunately, endoscopic features and biopsy results are often equivocal, making the diagnosis and management of large gastric folds difficult. Polyposis syndromes encompass a group of conditions in which multiple gastrointestinal polyps occur in the lumen of the gut. Large gastric folds are extremely rare in these syndromes. We present the case of a patient with polyposis who was found to have large gastric folds in the entire gastric fundus and body, mimicking malignancy. The patient's medical history and endoscopic ultrasonography (EUS) with mucosal resection confirmed the diagnosis of a pre-malignant disease. The lesion was monitored by serial endoscopic ultrasonography and biopsy, abdominal computed tomography (CT), and positron emission and computed tomography (PET-CT) for 6 years. The lesion remained stable, with the exception of abnormal fluorodeoxyglucose uptake on PET-CT in the gastric folds, which was determined to be a false-positive sign. To date, the patient remains healthy. We further discuss the mechanisms underlying the formation of large gastric folds caused by polyposis syndromes. Helicobacter pylori (H. pylori) or cytomegalovirus (CMV) is unnecessary for this progression. Immunohistochemistry (IHC) staining suggested that overexpression of transforming growth factor alpha (TGF-α) and down-regulation of myocyte enhancer-binding factor 2 (MEF2) may be involved in this case. <![CDATA[<b>Pancreatitis aguda inducida por cuerpo extraño</b>: <b>diagnóstico ecográfico</b>]]> http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082013000700016&lng=es&nrm=iso&tlng=es Large gastric folds (LGF) can be caused by benign conditions as well as malignancies. Unfortunately, endoscopic features and biopsy results are often equivocal, making the diagnosis and management of large gastric folds difficult. Polyposis syndromes encompass a group of conditions in which multiple gastrointestinal polyps occur in the lumen of the gut. Large gastric folds are extremely rare in these syndromes. We present the case of a patient with polyposis who was found to have large gastric folds in the entire gastric fundus and body, mimicking malignancy. The patient's medical history and endoscopic ultrasonography (EUS) with mucosal resection confirmed the diagnosis of a pre-malignant disease. The lesion was monitored by serial endoscopic ultrasonography and biopsy, abdominal computed tomography (CT), and positron emission and computed tomography (PET-CT) for 6 years. The lesion remained stable, with the exception of abnormal fluorodeoxyglucose uptake on PET-CT in the gastric folds, which was determined to be a false-positive sign. To date, the patient remains healthy. We further discuss the mechanisms underlying the formation of large gastric folds caused by polyposis syndromes. Helicobacter pylori (H. pylori) or cytomegalovirus (CMV) is unnecessary for this progression. Immunohistochemistry (IHC) staining suggested that overexpression of transforming growth factor alpha (TGF-α) and down-regulation of myocyte enhancer-binding factor 2 (MEF2) may be involved in this case.