[Inflammatory pancreatic disease due to enzyme autodigestion: an exceptional model of glandular crinophagy]. / Enfermedad inflamatoria del páncreas por autoagresión enzimática: un modelo excepcional de crinofagia glandular.

The exocrine pancreas is a functionally dangerous structure since it is exposed to digestion by its most aggressive enzymes (proteases, etc) despite self-protective measures such as the synthesis of some of these enzymes in the form of inactive zymogens (trypsinogen, etc.). We review inflammatory pancreatic disease by separately analyzing its classical forms of onset: acute and chronic pancreatitis (AP and CP). There is general consensus that the initial pathogenic event in AP is intraacinar activation of trypsinogen into trypsin, followed by that of the remaining proenzymes, giving rise to an unusual model of autophagic inflammation. In contrast, consensus is lacking on the initial pathogenic event in CP (toxic-metabolic lesion, oxidative stress, ductal hypertension, etc.?), although in some cases a <> sequence due to recurrent episodes of AP seems evident. The pathogenic features shared by both forms of the disease and which justify some recent attempts to formulate an overall explanation of the pathogenesis of pancreatitis are discussed. Such an explanation would place both forms of pancreatitis within the conceptual framework of an <>.

[Eosinophilic esophagogastroenteritis within the spectrum of food allergies]. / Las esofagogastroenteritis eosinofílicas dentro del espectro de las alergias alimentarias.

Under normal conditions, the digestive tube immune system is capable of establishing an effective plan of tolerance to food that is eaten daily by the human beings. However, this tolerance plan sometimes fails and in the final steps of this immunological dysreaction, other cellular elements, usual residents of the digestive mucous, such as eosinophil granulocytes, generally participate, together with the main cells of this system. This is the case, among others, of the so-called EGE-Eos. The authors summarize the spectrum of pathogenic options of these immunological food intolerances that range from those in which "all" depend on a specific IgE (GI food anaphylaxis) and those others in which "nothing" depends on this reagin (celiac sprue). An intermediate position would be occupied by the EGE-Eos in which there seems to be overlapping of immune reactions of cellular character together with a certain role of the IgE. These pathogenic pathways frequently cross a tangle of cellular and molecular events that cannot be untangled with either an image or one thousand words.

Las esofagogastroenteritis eosinofílicas dentro del espectro de las alergias alimentarias / Eosinophilic esophagogastroenteritis within the spectrum of food allergies

En condiciones normales el sistema inmune del tubo digestivo es capaz de montar un plan de tolerancia eficaz frente a los alimentos que diariamente ingieren los seres humanos. Sin embargo, a veces fracasa este plan de tolerancia y en los escalones finales de esta disreacción inmunológica suelen participar, junto a las células protagonistas de dicho sistema, otros elementos celulares, residentes habituales de la mucosa digestiva, como son los granulocitos eosinófilos. Éste es el caso, entre otras, de las llamadas gastroenteritis eosinofílicas (EGE-Eos). Los autores resumen el espectro de opciones patogénicas de estas intolerancias alimentarias inmunológicas que oscila entre aquellas en que «todo» depende de una IgE específica (anafilaxias alimentarias GI) y aquellas otras en que «nada» depende de esta reagina (esprue celíaco). Una posición intermedia ocuparían las EGE-Eos en las que parecen solaparse reacciones inmunes de carácter celular, junto a un cierto papel de la IgE. Estos caminos patogénicos se cruzan con frecuencia en una maraña de acontecimientos celulares y moleculares que «ni una imagen ni tampoco mil palabras» logran desenredar (AU)

Under normal conditions, the digestive tube immune system is capable of establishing an effective plan of tolerance to food that is eaten daily by the human beings. However, this tolerance plan sometimes fails and in the final steps of this immunological dysreaction, other cellular elements, usual residents of the digestive mucous, such as eosinophil granulocytes, generally participate, together with the main cells of this system. This is the case, among others, of the so-called EGE-Eos. The authors summarize the spectrum of pathogenic options of these immunological food intolerances that range from those in which «all» depend on a specific IgE (GI food anaphylaxis) and those others in which «nothing» depends on this reagin (celiac sprue). An intermediate position would be occupied by the EGE-Eos in which there seems to be overlapping of immune reactions of cellular character together with a certain role of the IgE. These pathogenic pathways frequently cross a tangle of cellular and molecular events that cannot be untangled with either an image or one thousand words (AU)

Enfermedad inflamatoria intestinal: parcelas etiopatogénicas a hilvanar / Inflammatory bowel disease: pathogenic pieces of ground to be sewn

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Vigilancia evolutiva y opciones terapéuticas del esófago de Barrett / Evolutive surveillance and therapeutical options in the Barrett's esophagus

No disponible

Cáncer colorrectal: circunstancias inductoras (etiología) y caminos de realización (patogenia) / Colorectal carcinoma: inductor circumstances (etilogy) and pathogenic ways (pathogenesis)

No disponible

[Immunoproliferative small intestinal disease (IPSID): IPSID-like lymphomas, IPSID equivalents?, in 12 Spanish patients]. / Enfermedad inmunoproliferativa del intestino delgado (EIPID): linfomas "EIPID-símiles"--EIPID-equivalentes?--en doce pacientes españoles.

BACKGROUND: Immunoproliferative small intestine disease (IPSID) encompasses a primary intestinal lymphoma of underpriviliged populations of North Africa, Middle East, etc. This epidemiological feature strongly implicates environmental and host (genetic) factors in its pathogenesis. IPSID can be distinguished on clinicopathological grounds from "Western-type" intestinal lymphomas. "IPSID-like" lymphomas had been sporadically identified, i.e., patients with original clinico-analytical data of IPSID (chronic diarrhoea, malabsortion, clubbing of fingers, diffuse intestinal involvement, etc.) without its conventional histopathologic (lymphoplasmocytic or plasmocytic infiltration) and immunological (alpha-heavy-chain paraprotein) background. PURPOSE: The aim of this study has been: 1) to identify, in a series of small intestine lymphomas, a group of patients with a long-lasting history of chronic diarrhoea and a clinico-biologic pattern of "IPSID-like" lymphoma; 2) to analyze its clinicopathological profile; 3) to search for differences with the pattern of the remaining cases ("Western-type" lymphomas) and 4) To suggest a possible epidemiological significance. PATIENTS AND METHODS: Patients considered were 12 Spanish caucasians with primary intestinal lymphoma and a long-lasting history of chronic diarrhoea vs 31 cases of "Western-type" intestinal lymphomas admitted in our Hospital over a 33-year period. Statistical significance of differences in clinico-biological features (symptoms/signs, analytical data, patterns of involvement, histopathology, immunophenotype and tumor staging) between these two groups was evaluated using X2 test. RESULTS: The results of this retrospective study allow us to delineate a relatively homogeneous "IPSID-like" group (12 cases) among 43 cases of primary small intestine lymphoma diagnosed between 1960 and 1993. The clinico-pathological behavior of these patients was significantly different from that exhibited by the 31 cases of so-called "Western-type" lymphomas. CONCLUSIONS: It is suggested that they may represent a group of patients suffering an evanescent "IPSID-equivalent" disorder (last case diagnosed in 1975), that probably has evolved in similar but not identical epidemiological circumstances to those present in the "Third World" countries of our Mediterranean area.