Beyond Tumors: Gastric Syphilis Emulating a Gastric Neoplasia.

We present the case of a 35-year-old male with a first-degree family history of gastric cancer (his father was diagnosed at the age of 45), who was presumed to have gastric cancer himself when evaluating the features of his upper endoscopy performed after hematemesis. Surprisingly, no cancer cells were found in the biopsies. Thanks to a different diagnostic suspicion subsequent to performing a full clinical history, a more favorable diagnosis was reached: gastric syphilis.

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.

[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.

[Genetic abnormalities of digestive tract adenocarcinomas and correlation with the histologic sequence of their development]. / Alteraciones genéticas de los adenocarcinomas del aparato digestivo y su correlación con la secuencia de su gestación.

Over 90% of digestive tract malignancies are adenocarcinomas (ADC) and almost 95% of them have gastric (G), colorectal (CR) or pancreatic (P) localizations. The objectives of this work are to review the genetic abnormalities of ADC in these locations and their potential coincidences, along with the histogenetic correlation of their emergence. Genetic abnormalities affecting over 50% of cases include: in G-ADC, inactivation of suppressor genes of p53, APC and DCC tumor in its intestinal variant, hypoexpression of of caderine E in the diffuse variant and hyperexpression of cyclooxygenase-2 and cyclyn D in the intestinal form; in in CR-ADC, inactivation of of genes p53, APC and DCC together with mutational activation of k-ras oncogen, and in P-ADC, the inactivation of suppressor genes p53, p16 and DPC4 along with mutational activation of k-ras oncogen. P-ADC is the one showing a more characteristic and exclusive genetic mark, followed by CR-ADC. Finally, the histogenetic correlation in the tumorigenic sequence is more evident in CR-ADC, followed by P-ADC. The complex biologic reality of G-ADC makes it more difficult to draw its genetic profile and its histogenetic correlation. In order to understand better the arguments of this work, the authors comment on the genetic-molecular basis governing the life and death of normal somatic cells and the biologic profile of the groups of genes mainly involved in tumorigenesis.

[Gastrointestinal carcinoid tumors: cellular biology, molecular expression and physiopathological consequences of an enigmatic neoplasia]. / Tumores carcinoides gastrointestinales. Biología celular, expresión molecular y consecuencias fisiopatológicas de una neoplasia enigmática.

Gastrointestinal carcinoid tumors arise from cells of the diffuse neuroendocrine system localized in the digestive trace and represent more than 70% of all carcinoid tumors in humans. The present article reviews the following topics: 1) The biological profile of these tumors (histopathology, cytokine markers, metabolic alterations, storage of neuroamines and hormonal proteins, cytodynamic behavior, and biological behavior according to embryological origin). 2) The etiological circumstances (exceptional hereditary factors, association of gastric carcinoid tumors with autoimmune gastritis, little-known exogenous factors). 3) Pathogenic aspects (persistent mitogenesis of endocrine cells associated with hypergastrinemia, inactivation of some putative tumor suppressor genes, the doubtful participation of oncogenes, autocrine action of some cellular growth-stimulating proteins). 4) The repercussions of certain physiopathological events (peritumoral desmoplastic reaction causing the "mass effect" on the digestive tube, the "kidnapping" of dietary tryptophan by tumoral cells toward an abnormal metabolic pathway; the easy metastatic dissemination coexisting with low tumoral aggressivity, and the release into the bloodstream of stored secretory products leading to "carcinoid syndrome" and some endocrine hyperfunction syndromes. Finally, it should be remembered that gastrointestinal carcinoid tumors represent only a proportion of the neoplasms classified as neuroendocrine tumors.

[Genetic profile and molecular bases of pancreatic carcinogenesis]. / Perfil genético y bases moleculares de la carcinogénesis pancreática.

The possibility that carcinogenesis is a multiphasic process has been well demonstrated in colorectal cancer, at least in cancers arising from a benign adenomatous polyp. However, because of the difficulty of performing histopathological studies of the pancreas, the multiphasic nature of carcinogenesis is proving more difficult to demonstrate in pancreatic ductal adenocarcinoma (d-ADC), although a series of findings, reviewed in the present article, strongly support this characteristic. Firstly, d-ADC shows a fairly exclusive genetic-molecular profile, found in 70% of cases; this profile consists of the association of the K-ras oncogene and inactivation of the tumor suppressor genes p16, p53 and DPC4. Secondly, a series of lesions in the ductal epithelium, in healthy pancreatic tissue close to a d-ADC, have been identified, which seem to represent precancerous histopathological stages. Lastly, there is the suspicion that the mutations defining this genetic-molecular profile appear gradually, in a certain sequence, throughout the stages of progression. Most probably, rather than the order of appearance, the accumulation of these genetic-molecular events are what prompt quiescent ductal epithelium to progress to mitogenic cellular hyperplasia, leading to irreversible mutagenic cellular dysplasia.

[Eosinophilic granulocytes: from common residents in normal gastrointestinal mucosa to aggressive agents of eosinophilic gastroenteritis]. / Los granulocitos eosinófilos: de residentes habituales de la mucosa gastrointestinal normal a protagonistas agresivos de la gastroenteritis eosinofílica.

Because of their biological affinity for normal gastrointestinal (GI) mucosa, eosinophilic granulocytes are "normal residents" in the mucosa. This physiological GI eosinophilia translates into a state of "permanent normal inflammation", which means that the mucosa's local immune system is constantly confronted by dietary proteins and indigenous microorganisms. This eosinophilic infiltration of the GI mucosa is increased, reactively, in the course of local inflammatory processes, collagenosis, infections (especially helminthic infections), vasculitis, neoplasms and IgE-dependent allergic reactions to food. Lastly, GI eosinophilia that is clearly aggressive, both because of its intensity and its persistence, is what characterizes eosinophilic gastroenteritis. In the present article, we summarize the ethiopathogenic and clinico-epidemiological features of this process, as well as its position within the field of immunopathologic food intolerance.