RESUMO
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.
Assuntos
Neoplasias Gástricas , Sífilis , Humanos , Masculino , Adulto , Sífilis/diagnóstico , Sífilis/complicações , Diagnóstico Diferencial , Gastropatias/diagnósticoRESUMO
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.
Assuntos
Antivirais/uso terapêutico , Guanina/análogos & derivados , Hepatite B Crônica/complicações , Hepatite B Crônica/tratamento farmacológico , Adulto , Idoso , Idoso de 80 Anos ou mais , Alanina Transaminase/sangue , Antivirais/efeitos adversos , Creatinina/sangue , DNA Viral/sangue , Diabetes Mellitus , Feminino , Seguimentos , Guanina/efeitos adversos , Guanina/uso terapêutico , Anticorpos Anti-Hepatite B/sangue , Antígenos de Superfície da Hepatite B/imunologia , Antígenos E da Hepatite B/imunologia , Vírus da Hepatite B/genética , Hepatite B Crônica/sangue , Humanos , Hipertensão/complicações , Cirrose Hepática/complicações , Masculino , Pessoa de Meia-Idade , Obesidade/complicações , Recidiva , Estudos Retrospectivos , População Branca , Adulto JovemRESUMO
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.
Assuntos
Tumor Carcinoide , Neoplasias Gastrointestinais , Tumor Carcinoide/etiologia , Tumor Carcinoide/metabolismo , Tumor Carcinoide/patologia , Tumor Carcinoide/fisiopatologia , Neoplasias Gastrointestinais/etiologia , Neoplasias Gastrointestinais/metabolismo , Neoplasias Gastrointestinais/patologia , Neoplasias Gastrointestinais/fisiopatologia , HumanosRESUMO
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 <
Assuntos
Pancreatite/etiologia , Doença Aguda , Fibrose , Humanos , Pâncreas/patologia , Pancreatite/enzimologia , Pancreatite/patologia , Pancreatite Crônica/enzimologia , Pancreatite Crônica/etiologia , Pancreatite Crônica/patologiaRESUMO
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.
Assuntos
Adenocarcinoma , Neoplasias Gástricas , Acloridria/complicações , Adenocarcinoma/diagnóstico , Adenocarcinoma/epidemiologia , Adenocarcinoma/etiologia , Adenocarcinoma/genética , Adenocarcinoma/patologia , Idoso , Dieta/efeitos adversos , Diagnóstico Precoce , Células Epiteliais/citologia , Células Epiteliais/patologia , Feminino , Mucosa Gástrica/patologia , Gastrite Atrófica/complicações , Infecções por Helicobacter/complicações , Helicobacter pylori , Humanos , Incidência , Masculino , Metaplasia , Pessoa de Meia-Idade , Mitose , Lesões Pré-Cancerosas/induzido quimicamente , Lesões Pré-Cancerosas/patologia , Fatores de Risco , Estômago/patologia , Neoplasias Gástricas/diagnóstico , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/etiologia , Neoplasias Gástricas/genética , Neoplasias Gástricas/patologiaRESUMO
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.