RESUMO
BACKGROUND: Though a few studies in animal models suggest that intestinal helminths (IH) favorably affect evolution of gastritis associated with Helicobacter pylori (H. pylori) the studies supporting this concept in humans are only a few and are based on serological data. METHODS: To evaluate the possible influence of IH on the human gastric mucosa, three groups of Venezuelan adults with gastropathy (endoscopically diagnosed) were studied: H. pylori-/IH- (n = 17), H. pylori+/IH- (n = 18), and H. pylori+/IH+ (n = 11). Histological analysis (hematoxylin-eosin) and immunohistochemical staining (peroxidase) for cytokines interleukin-1beta (IL-1ß), tumor necrosis factor alpha (TNF-α), gamma interferon (IFN-γ), and interleukin 4 (IL-4) were undertaken in gastric antral biopsies. RESULTS: Expression of the four cytokines was detected in all individuals in varying degrees, but proinflammatory cytokines were expressed in a higher degree in the H. pylori+/IH- group, mainly IL-1ß (Th1-dominant immune response), associated with a higher degree of both histological inflammation and gastric cancer risk index (GCRI), as compared to the H. pylori-/IH- group. In contrast, an increased expression of IL-4 and a reduced expression of proinflammatory cytokines (Th2-dominant response), plus the tendency to a lower degree of mononuclear infiltration, mucosal atrophy in gastric corpus, and GCRI, were evidenced in the coinfected group. CONCLUSIONS: The findings of the present study is perhaps the first histological evidence of a possible modulatory effect of IH on the gastric mucosal inflammatory response due to H. pylori infection in humans.
Assuntos
Coinfecção/metabolismo , Coinfecção/patologia , Citocinas/metabolismo , Mucosa Gástrica/metabolismo , Mucosa Gástrica/patologia , Gastrite/microbiologia , Gastrite/patologia , Infecções por Helicobacter , Helicobacter pylori , Mediadores da Inflamação/metabolismo , Enteropatias Parasitárias/metabolismo , Enteropatias Parasitárias/patologia , Adolescente , Adulto , Atrofia , Coinfecção/imunologia , Feminino , Mucosa Gástrica/imunologia , Gastrite/imunologia , Gastrite/metabolismo , Humanos , Imuno-Histoquímica , Enteropatias Parasitárias/imunologia , Leucócitos Mononucleares/patologia , Masculino , Pessoa de Meia-Idade , Adulto JovemRESUMO
Herbs and other botanicals have been used in different cultures with medicinal and dietary purposes for centuries. Contrary to the belief of being natural and safe products, their hepatotoxic potential is recognized in several studies worldwide, and represent a health problem that deserves greater attention. The reported prevalence of hepatotoxicity associated with botanicals is variable and depends on various factors such as population, period and design of the study. There have been reports of a total of 60 products with herbal medicinal and dietary purposes, which may cause liver damage; however, the pathophysiological mechanisms involved are not fully elucidated. Their clinical and histological features, not unlike liver injury associated with drugs in most patients, have a pattern of hepatocellular injury. Diagnosis is by exclusion, and represents a clinical challenge. It is essential the clinical suspicion and the differential diagnosis with other acute and chronic conditions. Hence, future researches are aimed at improving existing diagnostic methods and introducing new toxicological, genetic and immunological technologies. Treatment is complex and presents a challenge for the specialist, as there are no antidotes. Management based on the discontinued use of the product and in the symptomatic treatment, decreases the progression to an acute fulminant hepatic failure.
Assuntos
Doença Hepática Induzida por Substâncias e Drogas/etiologia , Preparações de Plantas/efeitos adversos , Plantas Medicinais/efeitos adversos , Doença Hepática Induzida por Substâncias e Drogas/diagnóstico , Doença Hepática Induzida por Substâncias e Drogas/epidemiologia , Suplementos Nutricionais/efeitos adversos , Humanos , Medicina Tradicional/efeitos adversos , Fitoterapia/efeitos adversos , Plantas Medicinais/química , PrevalênciaRESUMO
Las hierbas y otros productos de origen botánico, han sido utilizados por siglos en diversas culturas con fines medicinales y dietéticos. Contrario a la creencia de ser productos naturales y seguros, su potencial hepatotóxico es reconocido en diversos estudios a nivel mundial, lo que constituye un problema de salud que amerita mayor atención. La prevalencia reportada de hepatotoxicidad asociada a productos botánicos es variable y depende de diversos factores como población estudiada, período y diseño del estudio. Se han reportado un total de 60 productos a base de hierbas con fines medicinales y dietéticos, que pueden causar lesión hepática; sin embargo, el mecanismo fisiopatológico no está completamente dilucidado. Su cuadro clínico y características histológicas, no difieren de la lesión hepática asociada a medicamentos y la mayoría de los pacientes tienen un patrón de lesión hepatocelular. El diagnóstico se hace por exclusión, representando un desafío clínico importante, por lo que resulta fundamental la sospecha clínica y el diagnóstico diferencial de otras patologías agudas y crónicas. De allí que las investigaciones futuras están orientadas a mejorar los métodos diagnóstico existentes e introducir nuevas tecnologías toxicológicas, genéticas e inmunológicas. El manejo es complejo y representa un reto para el especialista puesto que no existe antídoto; el manejo se basa en suspender el uso del producto y en el tratamiento sintomático que disminuya la progresión a la falla hepática aguda fulminante.
Herbs and other botanicals have been used in different cultures with medicinal and dietary purposes for centuries. Contrary to the belief of being natural and safe products, their hepatotoxic potential is recognized in several studies worldwide, and represent a health problem that deserves greater attention. The reported prevalence of hepatotoxicity associated with botanicals is variable and depends on various factors such as population, period and design of the study. There have been reports of a total of 60 products with herbal medicinal and dietary purposes, which may cause liver damage; however, the pathophysiological mechanisms involved are not fully elucidated. Their clinical and histological features, not unlike liver injury associated with drugs in most patients, have a pattern of hepatocellular injury. Diagnosis is by exclusion, and represents a clinical challenge. It is essential the clinical suspicion and the differential diagnosis with other acute and chronic conditions. Hence, future researches are aimed at improving existing diagnostic methods and introducing new toxicological, genetic and immunological technologies. Treatment is complex and presents a challenge for the specialist, as there are no antidotes. Management based on the discontinued use of the product and in the symptomatic treatment, decreases the progression to an acute fulminant hepatic failure.
Assuntos
Humanos , Plantas Medicinais/efeitos adversos , Preparações de Plantas/efeitos adversos , Doença Hepática Induzida por Substâncias e Drogas/etiologia , Plantas Medicinais/química , Prevalência , Suplementos Nutricionais/efeitos adversos , Doença Hepática Induzida por Substâncias e Drogas/diagnóstico , Doença Hepática Induzida por Substâncias e Drogas/epidemiologia , Fitoterapia/efeitos adversos , Medicina Tradicional/efeitos adversosRESUMO
Changes in the Ca(2+) homeostasis have been implicated in cell injury and death. However, Ca(2+) participation in ethanol-induced chronic gastric mucosal injury has not been elucidated. We have developed a model of ethanol-induced chronic gastric injury in rats, characterized by marked alterations in plasma membranes from gastric mucosa and a compensatory cell proliferation, which follows ethanol withdrawal. Therefore, the present study explored the possible role of intracellular Ca(2+) in the oxidative metabolism and in acid secretion in this experimental model. Glucose oxidation was greatly enhanced in the injured mucosa, as evaluated by CO(2) production by isolated mucosal preparations incubated with (14)C-radiolabeled glucose in different carbons. Oxygen consumption and acid secretion (aminopyrine accumulation) were also stimulated. A predominating secretory status was morphologically identified by electron microscopy in oxyntic cells of gastric mucosa from ethanol-treated rats. A coupling between secretory and metabolic effects induced by ethanol (demonstrated by an inhibitory effect of omeprazole in both parameters) was found. These ethanol-induced effects were also inhibited by addition of Ca(2+) chelators to isolated gastric mucosa samples. Lanthanum, a Ca(2+) channel blocker, inhibited ethanol-promoted increase of oxidative metabolism. In addition, a stimulated Ca(2+) uptake by mucosal minces and increased in vivo Ca(2+) levels in cytosolic and mitochondrial fractions, were also noticed. Enhanced glucose and oxygen consumptions were associated with higher ATP and NADP+ availability, whereas cytosolic NAD/NADH ratio (assessed by mucosal levels of lactate and pyruvate) was not significantly modified by the chronic ethanol administration. In conclusion, changes in Ca(2+) homeostasis, probably mainly due to increased extracellular Ca(2+) uptake, could mediate secretory and metabolic alterations found in the gastric mucosa from rats chronically treated with ethanol.