Blue rubber bleb nevus syndrome.

Gastrointestinal bleeding of obscure origin accounts for less than 5% of gastrointestinal hemorrhages. It is typically difficult to diagnose due to limited accessibility through standard endoscopic techniques and generally requires a significant number of procedures to reach a diagnosis. The "blue rubber bleb nevus syndrome" is a rare condition, of a probably hereditary origin, characterized by the presence of multiple hemangiomatous lesions, which can manifest as gastrointestinal bleeding of obscure origin. These lesions are generally nodular, rubbery to the touch, and have a submucosal appearance, primarily affecting the skin and gastrointestinal tract. We present the case of a 72-year-old male who was investigated for iron deficiency anemia with upper and lower gastrointestinal endoscopies conducted on two occasions, without revealing any findings that could explain the condition. Subsequently, a study with video-capsule endoscopy was performed, which revealed multiple submucosal and vascular lesions, measuring between 3-5 mm, located in the distal duodenum and jejunum, consistent with "Blue rubber bleb nevus syndrome".

Detection of Neuroendocrine Tumours by Enteroscopy: A Case Report.

We present the case of a 62-year-old patient who developed melenas and in whom conventional endoscopic tests could not detect any bleeding lesion. In our case, capsule endoscopy and enteroscopy were the pivotal elements in establishing the diagnosis of a neuroendocrine tumour with an atypical location. As a result, it was possible to surgically remove the lesions at an early stage of the malignancy without metastatic disease and without the need for adjuvant therapy. Our case demonstrates the need for these new techniques in tumours of atypical location and aggressive course. Otherwise, this malignancy may be underdiagnosed until an advanced stage.

Immune checkpoint inhibitor-mediated colitis in a patient with epidermoid metastatic lung cancer: new and emerging toxicities.

In recent years, the development of immunotherapy has been stablished with monoclonals antibodies against control immune molecules in T lymphocytes, tumor cells and other cells, which block lymphocyte activation and suppress immune response. These molecules are Cytotoxic T-Lymphocyte Antigen 4 (CTLA-4) and Programmed Death-ligand 1 (PD-1). Despite clinical benefits, these therapies are not exempt from side effects known as immune-related adverse events (irAEs). We report the case of a 68-year-old female with stage IIIB epidermoid lung cancer diagnosed in 2017.

Neurological manifestations of celiac disease. Importance of searching and understanding the spectrum. Potential novel markers for the diagnosis.

currently Celiac Disease corresponds to an entity mainly managed by expert gastroenterologists on the topic but which must be faced on many occasions by primary care physicians or general gastroenterologists. It is important for a good diagnosis to look closely at all the factors that lead to a correct diagnosis (manifestations, antibodies, biopsy). In the spectrum of manifestations we find the classic ones, where the patient suffers from gastrointestinal symptoms typical of a classic Celiac Disease. At the same time, it is important to know that some of these patients do not have these classic symptoms and sometimes their only expression is neurological.

Uncommon etiology of Cullen´s sign and Grey Turner sign.

Cullen´s sign and Grey Turner sign are, respectively, the cutaneous ecchymoses located in periumbilical region and tissues flanks along the lower portion of the abdomen. Both have been observed in <1% of individuals with acute pancreatitis, suggesting poor prognosis in terms of gravity and mortality. However, these signs are not exclusive for acute pancreatitis, as they can appear in other identities such as: ruptured ectopic pregnancy, aortic aneurysm, rectus abdominis muscle hematoma, perforated duodenal ulcer, common bile duct rupture and biliary peritonitis, idiopathic perirenal hemorrhage, infectious mononucleosis with splenic rupture, metastatic esophageal and thyroid cancer, non-Hodgkin lymphoma, amoebic liver abscess, portal hypertension, and liver tumor disease. Based on the review of the literature, it is patent that Cullen´s sign and Grey Turner sign are neither sensitive nor specific for acute pancreatitis, therefore it may be best to relate these findings in the physical examination to conditions associated with abdominal pathology and retroperitoneal hemorrhage. We report the case of a 60-year-old Spanish female, with previous history of squamous small cell neuroendocrine lung carcinoma with hepatic extension in follow-up by palliative care services. Due to disease progression after two palliative chemotherapy sessions, the patient came to the emergency room with jaundice and abdominal pain in superior regions. On physical examination, notable findings included ecchymoses in the right flank and periumbilical region. Laboratory findings showed elevated bilirubin and transaminase levels, as well as a small increase in the serum amylase and lipase levels. Cholangioresonance was performed to discard acute biliary pancreatitis. The imaging revealed no enlargement of the pancreas, dilatation of the common bile duct without visible stone, and a liver full of new cancerous liver implants. These findings were consistent with diffuse distribution metastases lesions, concluding the progression of liver disease.

An uncommon cause of digestive neoplasm: duodenal melanoma.

We present and discuss the case of one patient that presented to the emergency room with abdominal pain in the right hypochondrium radiated to epigastrium and low-grade fever with blood test that shows dissociated colesthasis therefore admitted in the gastroenterology service with choledocholithiasis suspicion. cholangioresonance performed with a sudden stenosis of the bile duct in its intrapancreatic portion due a tumor in the pancreatic head. CT without lessions in other parts of the body. Upper endoscopy shows an ulcerated growth in the papillary area whose biopsies found neoplastic proliferation with S100, SOX10, MelanA and HMB45 positivity.

Primitive neuroectodermal tumor of the esophagus with metastasis in the pineal gland.

Primitive neuroectodermal tumors (PNET) are very rare tumors that belong to a family of malignant neoplasms of tiny round cells which are derived from the neural crest. This report discusses a rare case of an adult woman with esophageal PNET, confirmed by immunohistochemistry, that presented with metastasis to the pineal gland. To our knowledge, this is the first case report of a PNET with these features. Despite surgery and chemotherapeutic treatment, our case has shown disease progression.

Depósito de lantano en la mucosa gástrica de paciente con enfermedad renal crónica / Deposits of lanthanum in the gastric mucosa of a patient with chronic kidney disease

El carbonato de lantano es un quelante de fósforo no cálcico utilizado en el tratamiento de la hiperfosfatemia asociada a la enfermedad renal crónica. Los depósitos de lantano en la pared gastrointestinal han sido descritos desde 2015. Su significado clínico es incierto. Describimos un caso de paciente varón de 62 años con enfermedad renal crónica en tratamiento con carbonato de lantano durante 3 años, quien presentó depósitos en la mucosa gástrica biopsiada por dispepsia. Los depósitos se observaban como material acelular, con formas irregulares, rodeados de macrófagos y con reacción gigantocelular. Se confirmó la presencia de lantano en los depósitos mediante estudio de espectroscopia de rayos X. En su diagnóstico diferencial con otros depósitos, la clave para hacer su correcta identificación es la realización de una detallada historia clínica que incluya medicamentos administrados y el conocimiento de su aspecto microscópico

Lanthanum carbonate is a non-calcium phosphorus chelator used in the treatment of hyperphosphatemia associated with chronic renal disease. Deposits of lanthanum in the gastrointestinal wall have been recently described but its clinical significance is uncertain. We present a case of a 62-year-old male with chronic renal disease treated with lanthanum carbonate for 3 years, with deposits in his gastric mucosa, found on biopsy for dyspepsia. The deposits were acellular and of irregular shape, surrounded by macrophages and foreign body giant cells. The presence of lanthanum in the deposits was confirmed by X-ray spectroscopy. Diagnosis is reached with knowledge of its microscopic appearance and a thorough clinical history

[Deposits of lanthanum in the gastric mucosa of a patient with chronic kidney disease]. / Depósito de lantano en la mucosa gástrica de paciente con enfermedad renal crónica.

Lanthanum carbonate is a non-calcium phosphorus chelator used in the treatment of hyperphosphatemia associated with chronic renal disease. Deposits of lanthanum in the gastrointestinal wall have been recently described but its clinical significance is uncertain. We present a case of a 62-year-old male with chronic renal disease treated with lanthanum carbonate for 3 years, with deposits in his gastric mucosa, found on biopsy for dyspepsia. The deposits were acellular and of irregular shape, surrounded by macrophages and foreign body giant cells. The presence of lanthanum in the deposits was confirmed by X-ray spectroscopy. Diagnosis is reached with knowledge of its microscopic appearance and a thorough clinical history.

Disminución de las infecciones frente al ascenso de la alergia, autoinmunidad e inmunoinflamación / Reduction of infections versus the increase of allergy, auto-immunity and inflammation

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Esofagitis eosinofílica: algoritmo secuencial de opciones terapéuticas / Esofagitis eosinofílica: sequential algorithm of therapeutic options

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[Multifactorial etiology and pathogenic factors in inflammatory bowel disease]. / Etiología multifactorial y parcelas patogénicas de la enfermedad inflamatoria intestinal.

All the currently available evidence suggests that the two types of inflammatory bowel disease (IBD), Crohn's disease (CD) and ulcerative colitis (UC), involve a conflict between the immune system of the intestinal mucosa and intraluminal antigens, mainly the intestinal microflora, which are normally tolerated by the immune system. This conflict is modulated by numerous environmental factors and a clear polygenetic predisposition. The present article reviews the behavior of all the etiologic circumstances (microbial, genetic and environmental) and subsequently analyzes the possible pathogenic factors in which the etiologies can be found, namely: dysfunction of the intestinal epithelium, innate immune system alterations, and distortion of the cellular and humoral arms of the acquired immune system. The role of tissue ischemia in CD and expression of "extraintestinal inflammatory metastases", both in CD and UC, are briefly discussed. Finally, the view that IBD may be a spectrum of pathological processes provoked by distinct etiopathogenic factors and the possible biological significance of the growing incidence of this disease in the western world, coinciding with the decline in infectious diseases in this geographical area, are discussed.

[Gastric mucosa as a target of persistent proinflammatory aggression: pathogenic models of chronic gastritis]. / La mucosa gástrica como estructura diana de agresiones proinflamatorias persistentes: modelos patogénicos de gastritis crónica.

There are several causes of damage and regeneration of the gastric epithelium (erosive gastropathy) and/or histological inflammation of the gastric mucosa (acute or chronic gastritis). After outlining the usual morphology of chronic gastritis, the authors attempt to identify the biological profile of the main pathogenic models. The first, and by far the most frequent, is the model associated with Helicobacter pylori, which, without crossing the mucosal epithelium, provokes an immune reaction. Although incapable of eradicating this bacterium, this immune reaction contributes to the inflammatory lesion provoked by H. pylori in the mucosa. The second -and much less frequent- model is that causing progressive atrophic gastritis through a humoral and cellular autoimmune mechanism. In third place are a group of models defined by a peculiar cytohistologic pattern of inflammation (granulomatous, lymphocytic or eosinophilic gastritis), suggesting similar pathogenic mechanisms for each of these rare morphological forms of gastritis. Lastly, there is a model barely fitting within the scope of this review, which is that provoking chemical gastropathies (bile reflux, NSAIDs, etc.) with minimal cellular inflammation, i.e., minimal gastritis. To aid understanding of the article, the authors provide a brief outline of the functional histology of the gastric wall and the mechanisms defending its integrity in physiological conditions.

La mucosa gástrica como estructura diana de agresiones proinflamatorias persistentes: modelos patogénicos de gastritis crónica / Gastric mucosa as a target of persistent proinflammatory aggression: pathogenic models of chronic gastritis

Son numerosas las circunstancias etiológicas capaces de producir daño y regeneración del epitelio gástrico (gastropatías erosivas) y/o inflamación histológica de su mucosa (gastritis aguda o crónica). Después de recordar la morfología habitual de las llamadas gastritis crónicas, los autores han intentado identificar el perfil biológico de los principales modelos patogénicos de dichas gastritis. El primero, y con mucho el más frecuente, está asociado a la infección por Heliocobacter pylori, germen que, sin atravesar el epitelio mucoso, provoca una reacción inmune que, aunque es incapaz de eliminarlo, contribuye a la lesión inflamatoria que aquél provoca en la mucosa. El segundo modelo, mucho menos frecuente, es el responsable de una gastritis progresivamente atrófica, a través de un mecanismo autoinmune humoral y celular. En tercer lugar podemos citar un conjunto de modelos definidos por el peculiar perfil citohistológico de la inflamación (gastritis granulomatosa, linfocítica o eosinofílica), hecho que sugiere vías patogénicas similares para cada una de estas raras formas morfológicas de gastritis. Por último, hay un modelo que está situado en la frontera del tema de esta revisión, que es el que provoca algunas gastropatías químicas (reflujo biliar, toma de antiinflamatorios no esteroideos, etc.), con mínima expresión inflamatoria celular, es decir, con gastritis mínima. Para comprender mejor el contenido de este trabajo, se recuerda brevemente la histología funcional de la pared gástrica y los mecanismos defensivos de su integridad, en condiciones fisiológicas (AU)

There are several causes of damage and regeneration of the gastric epithelium (erosive gastropathy) and/or histological inflammation of the gastric mucosa (acute or chronic gastritis). After outlining the usual morphology of chronic gastritis, the authors attempt to identify the biological profile of the main pathogenic models. The first, and by far the most frequent, is the model associated with Helicobacter pylori, which, without crossing the mucosal epithelium, provokes an immune reaction. Although incapable of eradicating this bacterium, this immune reaction contributes to the inflammatory lesion provoked by H. pylori in the mucosa. The second —and much less frequent— model is that causing progressive atrophic gastritis through a humoral and cellular autoimmune mechanism. In third place are a group of models defined by a peculiar cytohistologic pattern of inflammation (granulomatous, lymphocytic or eosinophilic gastritis), suggesting similar pathogenic mechanisms for each of these rare morphological forms of gastritis. Lastly, there is a model barely fitting within the scope of this review, which is that provoking chemical gastropathies (bile reflux, NSAIDs, etc.) with minimal cellular inflammation, i.e., minimal gastritis. To aid understanding of the article, the authors provide a brief outline of the functional histology of the gastric wall and the mechanisms defending its integrity in physiological conditions (AU)

Etiología multifactorial y parcelas patogénicas de la enfermedad inflamatoria intestinal / Multifactorial etiology and pathogenic factors in inflammatory bowel disease

Actualmente todo inclina a pensar que la enfermedad inflamatoria intestinal (EII) en sus 2 variantes, la enfermedad de Crohn (EC) y la colitis ulcerosa (CU), traduce un conflicto entre el sistema inmunitario de la mucosa intestinal y los antígenos intraluminales, fundamentalmente de la microflora intestinal, a los que normalmente toleraba. Todo eso modulado por numerosos factores ambientales y una evidente predisposición de carácter poligénico.Sobre este argumento se revisa el comportamiento del conjunto de circunstancias etiológicas (microbianas, genéticas y ambientales) para analizar, a continuación, las posibles parcelas patogénicas en donde se expresan aquellos factores etiológicos, como la disfunción del epitelio intestinal, las alteraciones del sistema inmunitario innato y la distorsión de los brazos celular y humoral del sistema inmunitario adquirido. Se comenta brevemente el papel de la isquemia tisular en la EC y la expresión de las “metástasis inflamatorias extraintestinales”, tanto en la EC como en la CU.Finalmente, se especula sobre la probable consideración de la EII como un espectro de procesos patológicos provocados desde ángulos etiopatogénicos diferentes y el posible significado biológico de su creciente incidencia en el mundo occidental, en coincidencia con el declive de las enfermedades infecciosas en éste(AU)

All the currently available evidence suggests that the two types of inflammatory bowel disease(IBD), Crohn’s disease(CD) and ulcerative colitis(UC), involve a conflict between the immune system of the intestinal mucosa and intraluminal antigens, mainly the intestinal microflora, which are normally tolerated by the immune system. This conflict is modulated by numerous environmental factors and a clear polygenetic predisposition. The present article reviews the be havi or of all the etiologic circumstances(microbial, genetic and environmental)and subsequently analyzes the possible pathogenic factors in which the etiologies can be found, namely: dysfunction of the intestinal epithelium, innate immune system alterations, and distortion of the cellular and humoral arms of the acquired immune system. The role of tissue is chemiain CD and expression of‘‘ extraintestinal inflammatory metastases’’, bothin CD and UC, are briefly discussed. Finally, the view that IBD may be aspectrum of pathological processes provoked by distinct etiopathogenic factor sand the possible biological significance of the growing incidence of this disease in the western world, coinciding with the decline in infectious diseases in this geographical area, are discussed(AU)