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.

Entecavir has high efficacy and safety in white patients with chronic hepatitis B and comorbidities.

OBJECTIVES: The aim of this study was to evaluate the efficacy and safety of entecavir monotherapy in nucleos(t)ide-naive chronic hepatitis B patients and to analyse the influence of the comorbidity burden on therapy outcome. METHODS: We retrospectively analysed data from 237 nucleos(t)ide-naive chronic hepatitis B white patients treated with entecavir (0.5 mg/day) at 23 Spanish centres. For the efficacy and safety analyses, patients were grouped according to their baseline comorbidities. RESULTS: The mean age of the cohort was 43 years (range: 19-82 years); 73% were male, 83% were white, and 33% were hepatitis B e antigen (HBeAg) positive. At baseline, the median hepatitis B virus DNA level was 6.20 log10 IU/ml. Of the patients, 18% had cirrhosis, 9.7% had diabetes, 16.3% had hypertension, and 15.7% had obesity; 13.4% of patients had more than one comorbid condition. Virological and biochemical responses at month 36 were obtained independently of the patients' baseline comorbid condition. Of 10 HBeAg-positive patients who discontinued treatment after HBeAg seroconversion, those who had not also cleared HBsAg (six) experienced virological recurrence in a median 5.6 months. There were no treatment discontinuations due to adverse events. Three patients were diagnosed with hepatocellular carcinoma at months 12, 30 and 54, and six experienced hepatic decompensation during follow-up. The median serum creatinine levels did not increase after 36 months of treatment, even in patients with comorbidities. CONCLUSION: Entecavir is safe, well tolerated, and highly effective, even in patients with comorbid condition(s). Discontinuation of treatment in patients who have not been cleared of HBsAg may lead to virological recurrence.

[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.

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

Los tumores carcinoides gastrointestinales (TCa-GI) surgen desde células del sistema neuroendocrino difuso localizadas en el tracto digestivo y representan más del 70% de todos los TCa de los seres humanos. En este trabajo se revisan los siguientes argumentos: 1) El perfil biológico de los TCa-GI (dibujo histopatológico, marcadores citoquímicos, alteraciones metabólicas, almacenamiento de neuroaminas y proteínas hormonales, comportamiento citodinámico y características biológicas en función del origen embriológico). 2) Las circunstancias etiológicas (factores hereditarios excepcionales, asociación de TCa gástricos con gastritis autoinmune, factores exógenos poco conocidos). 3) Aspectos patogénicos (mitogénesis persistente de células endocrinas asociada a hipergastrinemia, inactivación de algunos presuntos genes supresores de tumor, dudosa participación de oncogenes, acción autocrina de algunas proteínas estimuladoras de crecimiento celular). 4) Las repercusiones de ciertos episodios fisiopatológicos (reacción desmoplástica peritumoral responsable del «efecto masa» sobre el tubo digestivo, el «rapto» del triptófano alimentario por parte de las células tumorales hacia una vía metabólica anormal, la fácil diseminación metastásica coexistente con una escasa agresividad tumoral, la liberación al torrente sanguíneo de productos secretores almacenados responsables del «síndrome carcinoide» y de algunos cuadros de hiperfunción endocrina). Conviene recordar que los TCa-GI representan sólo un segmento de los llamados tumores neuroendocrinos y, como tales, deben considerarse

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

[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 <>.

[Gastric adenocarcinoma: approach to a complex biological reality]. / Adenocarcinoma gástrico: intento de aproximación a una realidad biológica compleja.

The authors review the complex biological reality of gastric adenocarcinoma from several viewpoints. It is a neoplasm histologically expressed as a dual process (intestinal and diffuse types) with a broad cytological diversity. From an epidemiological point of view, it behaves as an entity with a deep geographical asymmetry and a changing incidence, currently decreasing. There is a multifactorial etiology with a combination of genetic, infectious (H. pylori), nutritional and environmental factors. It might have a multiphasic gestation from precancerous lesions, though not always following a lineal sequence. We only know fragmentary portions of its pathogenesis whose common denominator is a potentially mutagenic mitogenic activation of the epithelial cells implicated. A good knowledge of this complex biological reality will allow the identification of better markers for an early diagnosis as well as vulnerable etiopathogenetic points for a useful prevention and therapy.

Adenocarcinoma gástrico: intento de aproximación a una realidad biológica compleja / Gastric adenocarcinoma: approach to a complex biological reality

En el presente artículo se revisa la compleja realidad biológica del adenocarcinoma gástrico desde varios puntos de vista. Se trata de una neoplasia que se expresa histopatológicamente como un proceso dual (tipos intestinal y difuso) con una amplia diversidad citológica. Epidemiológicamente se comporta como una entidad con una profunda asimetría geográfica y un perfil de incidencia cambiante, en declive. Presenta una etiología multifactorial, en la que se combinan factores genéticos, infecciosos (Helicobacter pylori), alimentarios y ambientales. Podría tener una gestación multifásica desde lesiones precancerosas, aunque no siempre sigue una secuencia lineal. Sólo conocemos parcelas fragmentarias de su patogenia, cuyo común denominador es una activación mitógena potencialmente mutágena de las células epiteliales implicadas. Conocer bien esta compleja realidad biológica nos permitirá identificar mejores marcadores para un diagnóstico precoz y puntos etiopatogénicos vulnerables para una prevención y un tratamiento más eficaces

The authors review the complex biological reality of gastric adenocarcinoma from several viewpoints. It is a neoplasm histologically expressed as a dual process (intestinal and diffuse types) with a broad cytological diversity.From an epidemiological point of view, it behaves as an entity with a deep geographical asymmetry and a changing incidence, currently decreasing. There is a multifactorial etiology with a combination of genetic, infectious (H. pylori), nutritional and environmental factors. It might have a multiphasic gestation from precancerous lesions, though not always following a lineal sequence. We only know fragmentary portions of its pathogenesis whose common denominator is a potentially mutagenic mitogenic activation of the epithelial cells implicated. A good knowledge of this complex biological reality will allow the identification of better markers for an early diagnosis as well as vulnerable etiopathogenetic points for a useful prevention and therapy

[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.

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

La afinidad biológica que muestran los granulocitos eosinófilos por la mucosa gastrointestinal (GI) normal los convierte en «residentes habituales». Esta eosinofilia GI fisiológica indica el estado de «inflamación normal permanente» que somete a esta mucosa a la confrontación continua del sistema inmunitario local con las proteínas alimentarias y los microorganismos autóctonos. Esta infiltración de eosinófilos de la mucosa GI se incrementa, con carácter reactivo, en el curso de procesos inflamatorios locales, colagenosis, infecciones (sobre todo helmínticas), vasculitis, neoplasias y reacciones alérgicas alimentarias «IgE-dependientes». Por último, una eosinofilia GI claramente agresiva, tanto por su intensidad como por su persistencia, es la que define a la entidad anatomoclínica conocida como gastroenteritis eosinofílica. Los autores resumen los aspectos etiopatogénicos y clínico-epidemiológicos de este proceso, así como su posición patogénica dentro del campo oscuro de las intolerancias alimentarias inmunopáticas

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