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NAFLD prevalence in most regions of Asia is increasing. This Review presents emerging data on genetic polymorphisms that predispose Asian people to NAFLD, NASH and cirrhosis, and discusses the clinical and pathological outcomes of these diseases.
The gut is innervated by many types of extrinsic sensory neurons, and little consensus exists about the different classes that these afferents might belong to. In this Review, Simon Brookes and colleagues suggest that five different morphological types of endings can be distinguished by their structure, and that this scheme is compatible with physiologically based classifications.
Shigellainfection continues to have a high disease burden worldwide, especially in young children in developing countries. Here, the latest progress inShigella vaccine research is reviewed—including the identification of new vaccine antigens and technological advances in vaccine design and manufacture—as well as the barriers that impede the development of a successful Shigellavaccine.
Surgery is a key feature of IBD management. Here, the authors present an overview of IBD surgical management, focusing on the potential benefits and drawbacks of laparoscopy compared with open surgery.
Patients with IBD are at risk of the same vaccine-preventable illnesses as the general population. However, the characteristics of IBD and the immunosuppressive agents prescribed to treat it can lead to low response rates to vaccinations in these patients. Gisbert and Chaparro provide practical advice on vaccination strategies for clinicians who diagnose and treat patients with IBD.
Worldwide, ∼170 million people are thought to be chronically infected with HCV. These patients can develop serious long-term complications. Therapy for hepatitis C has progressed rapidly in the past few years; here, Donald Jensen and Noura Dabbouseh discuss the latest advances.
The Rome III consensus has divided functional dyspepsia into two subgroups; postprandial distress syndrome, characterized by postprandial fullness and early satiation, and epigastric pain syndrome, characterized by epigastric pain or burning. This Review describes the symptoms of functional dyspepsia and discusses the evidence to support the two subgroups.
Functional gastrointestinal disorders span a wide spectrum of clinical phenotypes. This Review discusses advances in the diagnosis and management of achalasia, gastroparesis, intestinal pseudo-obstruction and chronic constipation that result from enteric neuropathies, including both primary (idiopathic) and secondary forms.
Functional dyspepsia treatment remains unsatisfactory for too many patients. Here, the authors provide an overview of current management strategies, covering both lifestyle modifications for patients with mild or intermittent symptoms and drug therapy for patients with severe symptoms or non-responders.
After 1 year of nucleos(t)ide analogue therapy for chronic hepatitis B, hepatic inflammation decreases in 50–70% of patients; fibrosis, however, frequently remains unchanged. A study has now revealed that 5-year treatment with the nucleotide analogue tenofovir disoproxil fumarate leads to regression of hepatic fibrosis and cirrhosis in 50% of patients.
Helicobacter pyloriinfection is one likely cause of functional dyspepsia. Here, the authors discuss the clinical evidence in relation toH. pylorieradication in patients with functional dyspepsia if they test positive for this bacterium.
In this Review, Van Oudenhove and Aziz provide an overview of epidemiological studies that demonstrate an association between functional dyspepsia and psychological traits, states or psychiatric disorders. They also describe pathophysiological evidence on how psychosocial factors and psychiatric disorders might exert their role in functional dyspepsia.
The phenotype and behaviour of primary tumours in the liver is widely believed to reflect their cell of origin. A new study in mice shows that this relationship is not always the case—the cells of origin of intrahepatic cholangiocarcinomas might be hepatocytes rather than the expected cholangiocytes or bipotential hepatic progenitor cells.
Functional dyspepsia is thought to be a heterogeneous disorder, with a wide variety of pathophysiological mechanisms underlying the varied symptoms observed in patients. Here, Vanheel and Farré provide an overview of the pathogenesis of functional dyspepsia, adding insight on the diverse functional and structural changes in the gastrointestinal tract in this condition.
In 2012, important advances were made in understanding the pathogenesis of IBD—the Immunochip project increased the number of known IBD loci to 163, and underscored the common susceptibility to infectious diseases. With regard to management of IBD, novel non-anti-TNF agents have shown efficacy in phase II and III trials.
Knowledge of colorectal cancer (CRC) risks has been rebalanced in 2012. The 'serrated pathway' to CRC, exemplified by serrated polyposis syndrome, emphasizes the importance of serrated lesions. The dogma that patients with IBD are at high risk of CRC, however, might be overstated; optimizing CRC prevention needs to focus on patients at increased risk.
With the first HCV protease inhibitors approved in 2011, we are currently in a transition phase towards a shift in treatment paradigm. Within the next 3 years, the vast majority of patients with hepatitis C will probably be treated with completely different drugs in most Western countries.
Liver cancer remains an evolving indication for liver transplantation in the year 2012 as advances are made in patient selection, neoadjuvant treatment and living-donor liver transplantation. Patient survival is improving and, as patient selection and treatment advances, more transplantations can be conducted on patients with liver cancer.
New techniques have introduced unprecedented sensitivity to the investigation of the gut microbiota, enabling insights into the discrete contributions of select bacterial species and advancing our mechanistic appreciation of the roles of diet and host immunity in limiting or enabling metabolic and inflammatory disease.
Efforts to understand fatty liver disease have focused on the gut microbiome's stimulation of hepatic injury and fibrosis through specialized signalling complexes at the cell surface and in the cytosol of liver cells. Combined with increased hedgehog activity and progenitor cell expansion, new clues are emerging to elucidate the pathogenesis of fibrosis.