Journal of Gastroenterology and Hepatology
About: Journal of Gastroenterology and Hepatology is an academic journal. The journal publishes majorly in the area(s): Cirrhosis & Hepatocellular carcinoma. It has an ISSN identifier of 0815-9319. Over the lifetime, 10641 publication(s) have been published receiving 249395 citation(s).
Papers published on a yearly basis
Ashley B. Price1•Institutions (1)
TL;DR: It is appropriate to review the existing classifications and to produce a system that, in the light of new knowledge, will find widespread acceptance, was the remit given to a small multidisciplinary Working Party by the Scientific Committee of the 9th World Congresses in Gastroenterology.
Abstract: Gastritis, inflammation of the gastric mucosa, represents the stomach’s response to injury. A continuing dilemma has been the very large size of the population with gastritis in contrast to the lack of knowledge about specific causes. The discovery of Helicobacter pylori as the major cause of inflammation of the gastric antrum has helped resolve this As a result, accurate and uniform documentation of gastritis from gastric endoscopic biopsies assumes prime importance for understanding the dynamics of gastritis and has a major contribution to make to the study of the natural history of peptic ulcer disease and also, perhaps, to the evolution of gastric cancer. Increasing numbers of papers are appearing in the literature documenting the pathology of gastritis, its relation to H. pylori and the response to therapeutic agents.+” At present, a variety of classifications and systems of grading are in use, making it difficult to compare the results.10*12-21 It is therefore appropriate to review the existing classifications and to produce a system that, in the light of new knowledge, will find widespread acceptance. This was the remit given to a small multidisciplinary Working Party by the Scientific Committee of the 9th World Congresses in Gastroenterology. The Working Party sought additional advice from an ad hoc Advisory Group of European pathologists sharing a special interest in gastric pathology. T o gain widespread acceptance, any proposed classification must be simple, easy to apply, flexible, correlate with existing classifications, be sensitive to monitoring therapy and appeal to generalists as well as dedicated gastroenterologists, and diagnosticians as well as research workers.
TL;DR: Non‐alcoholic fatty liver disease (NAFLD) is a chronic liver disease that affects a high proportion of the world’s population and has the potential to progress to steatohepatitis, fibrosis and even cirrhosis.
Abstract: Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease that affects a high proportion of the world's population. Insulin resistance and oxidative stress play a critical role in the pathogenesis of NAFLD. Clinical, biochemical and imaging studies are of value in the diagnostic evaluation of patients with NAFLD, but liver biopsy remains the most sensitive and specific means of providing important diagnostic and prognostic information. Simple steatosis has the best prognosis within the spectrum of NAFLD, but NAFLD has the potential to progress to steatohepatitis, fibrosis and even cirrhosis. No effective medical therapy is currently available for all patients with NAFLD. In patients with diabetes mellitus and hyperlipidemia, appropriate metabolic control is always recommended, but rarely effective in resolving the liver disease. Weight reduction, when achieved and sustained, may improve the liver disease, although the results with weight loss have been inconsistent. Pharmacological therapy aimed at the underlying liver disease holds promise. Several medications with different mechanisms of action and potential benefit are currently being evaluated in clinical trials. Liver transplantation is a life-extending therapeutic alternative for patients with end-stage NAFLD, but NAFLD may recur after liver transplantation.
TL;DR: The incidence, pathology and clinical features of antituberculosis drug‐induced hepatotoxicity, the metabolism and mechanisms of toxicity of isoniazid, rifampicin and pyrazinamide, and risk factors and management are reviewed.
Abstract: The cornerstone of tuberculosis management is a 6-month course of isoniazid, rifampicin, pyrazinamide and ethambutol. Compliance is crucial for curing tuberculosis. Adverse effects often negatively affect the compliance, because they frequently require a change of treatment, which may have negative consequences for treatment outcome. In this paper we review the incidence, pathology and clinical features of antituberculosis drug-induced hepatotoxicity, discuss the metabolism and mechanisms of toxicity of isoniazid, rifampicin and pyrazinamide, and describe risk factors and management of antituberculosis drug-induced hepatotoxicity. The reported incidence of antituberculosis drug-induced hepatotoxicity, the most serious and potentially fatal adverse reaction, varies between 2% and 28%. Risk factors are advanced age, female sex, slow acetylator status, malnutrition, HIV and pre-existent liver disease. Still, it is difficult to predict what patient will develop hepatotoxicity during tuberculosis treatment. The exact mechanism of antituberculosis drug-induced hepatotoxicity is unknown, but toxic metabolites are suggested to play a crucial role in the development, at least in the case of isoniazid. Priorities for future studies include basic studies to elucidate the mechanism of antituberculosis drug-induced hepatotoxicity, genetic risk factor studies and the development of shorter and safer tuberculosis drug regimens.
TL;DR: It was recommended that H. pylori infection should be tested for and eradicated prior to long‐term aspirin or non‐steroidal anti‐inflammatory drug therapy in patients at high risk for ulcers and ulcer‐related complications and in communities with high incidence of gastric cancer prevention.
Abstract: The Asia-Pacific Consensus Conference was convened to review and synthesize the most current information on Helicobacter pylori management so as to update the previously published regional guidelines. The group recognized that in addition to long-established indications, such as peptic ulcer disease, early mucosa-associated lymphoid tissue (MALT) type lymphoma and family history of gastric cancer, H. pylori eradication was also indicated for H. pylori infected patients with functional dyspepsia, in those receiving long-term maintenance proton pump inhibitor (PPI) for gastroesophageal reflux disease, and in cases of unexplained iron deficiency anemia or idiopathic thrombocytopenic purpura. In addition, a population 'test and treat' strategy for H. pylori infection in communities with high incidence of gastric cancer was considered to be an effective strategy for gastric cancer prevention. It was recommended that H. pylori infection should be tested for and eradicated prior to long-term aspirin or non-steroidal anti-inflammatory drug therapy in patients at high risk for ulcers and ulcer-related complications. In Asia, the currently recommended first-line therapy for H. pylori infection is PPI-based triple therapy with amoxicillin/metronidazole and clarithromycin for 7 days, while bismuth-based quadruple therapy is an effective alternative. There appears to be an increasing rate of resistance to clarithromycin and metronidazole in parts of Asia, leading to reduced efficacy of PPI-based triple therapy. There are insufficient data to recommend sequential therapy as an alternative first-line therapy in Asia. Salvage therapies that can be used include: (i) standard triple therapy that has not been previously used; (ii) bismuth-based quadruple therapy; (iii) levofloxacin-based triple therapy; and (iv) rifabutin-based triple therapy. Both CYP2C19 genetic polymorphisms and cigarette smoking can influence future H. pylori eradication rates.
TL;DR: The evidence base for restricting rapidly fermentable, short‐chain carbohydrates (FODMAPs) in controlling functional gastrointestinal symptoms is described.
Abstract: Background and Aim: Functional gastrointestinal symptoms are common and their management is often a difficult clinical problem. The link between food intake and symptom induction is recognized. This review aims to describe the evidence base for restricting rapidly fermentable, short-chain carbohydrates (FODMAPs) in controlling such symptoms. Methods: The nature of FODMAPs, their mode of action in symptom induction, results of clinical trials and the implementation of the diet are described. Results: FODMAPs are widespread in the diet and comprise a monosaccharide (fructose), a disaccharide (lactose), oligosaccharides (fructans and galactans), and polyols. Their ingestion increases delivery of readily fermentable substrate and water to the distal small intestine and proximal colon, which are likely to induce luminal distension and induction of functional gut symptoms. The restriction of their intake globally (as opposed to individually) reduces functional gut symptoms, an effect that is durable and can be reversed by their reintroduction into the diet (as shown by a randomized placebo-controlled trial). The diet has a high compliance rate. However it requires expert delivery by a dietitian trained in the diet. Breath hydrogen tests are useful to identify individuals who can completely absorb a load of fructose and lactose so that dietary restriction can be less stringent. Conclusions: The low FODMAP diet provides an effective approach to the management of patients with functional gut symptoms. The evidence base is now sufficiently strong to recommend its widespread application.