Peutz-Jeghers syndrome (PJS, MIM175200) is an autosomal dominant condition defined by the development of characteristic polyps throughout the gastrointestinal tract and mucocutaneous pigmentation. The majority of patients that meet the clinical diagnostic criteria have a causative mutation in the STK11 gene, which is located at 19p13.3. The cancer risks in this condition are substantial, particularly for breast and gastrointestinal cancer, although ascertainment and publication bias may have led to overestimates in some publications. Current surveillance protocols are controversial and not evidence-based, due to the relative rarity of the condition. Initially, endoscopies are more likely to be done to detect polyps that may be a risk for future intussusception or obstruction rather than cancers, but surveillance for the various cancers for which these patients are susceptible is an important part of their later management. This review assesses the current literature on the clinical features and management of the condition, genotype-phenotype studies, and suggested guidelines for surveillance and management of individuals with PJS. The proposed guidelines contained in this article have been produced as a consensus statement on behalf of a group of European experts who met in Mallorca in 2007 and who have produced guidelines on the clinical management of Lynch syndrome and familial adenomatous polyposis.

Guidelines on histopathological techniques and reporting for adult and paediatric gastrointestinal neuromuscular pathology have been produced recently by an international working group (IWG). These addressed the important but relatively neglected areas of histopathological practice of the general pathologist, including suction rectal biopsy and full-thickness intestinal tissue. Recommendations were presented for the indications, safe acquisition of tissue, histological techniques, reporting and referral of such histological material.

Targeted treatments have generated a lot of hope and hype in the treatment of gastrointestinal tumours. Indeed, the introduction of targeted treatments particularly for colorectal cancer has resulted in substantial improvements in tumour response and progression-free survival of patients. However, it is not fully understood how these agents act in patients, and the preclinical models are not appropriate to predict clinical efficacy. Here the current state of targeted treatments in colorectal cancer is reviewed, focusing on antiepidermal growth factor receptor (EGFR) and antiangiogenic strategies, describing how these agents fit into the therapeutic algorithm of this disease and discussing current understanding of the mechanism of action, biomarkers as well as future therapeutic strategies targeting multiple signalling pathways in colorectal cancer.

With few exceptions, the most commonly recommended triple Helicobacter pylori regimen (proton pump inhibitor (PPI), amoxicillin and clarithromycin) now provides unacceptably low treatment success. A review of worldwide results suggests that successful eradication using a triple regimen is not consistently observed in any population. Clinicians should use 'only use what works locally' and ignore consensus statements and society guidelines if they are not consistent with local results. Clinical trials should be result based, with the goal of identifying regimens with >90-95% success. New treatments should be only be compared with the currently locally effective treatment (>90%) or a historical untreated control (which has been shown to reliably yield 0% eradication); trials using placebos or treatments known to be inferior are with rare exceptions unethical. If a highly effective regimen is not available locally, we recommend trying a 14 day concomitant quadruple treatment regimen containing a PPI, amoxicillin, clarithromycin and a nitroimidazole; 10 day sequential treatment (PPI plus amoxicillin for 5 days followed by a PPI, clarithromycin and a nitroimidazole for 5 days); or 14 day bismuth-containing quadruple treatments. Treatments needing further evaluation include those containing furazolidone or nitazoxanide, hybrids of sequential-concomitant therapies and amoxicillin-PPI dual therapy with PPI doses such that they maintain intragastric pH >6.

Chronic hepatitis B is one of the most common infectious diseases worldwide. In patients with an impaired immune system the prevalence of HBsAg is even higher and the course of hepatitis B infection is often aggravated. In HIV/HBV co-infected patients, liver related morbidity and mortality can be reduced by implementing highly active antiretroviral treatment (HAART) that contains substances active against HBV. Reactivation of HBV during chemotherapy may occur in HBsAg positive patients but can even occur in serologically recovered anti-HBc positive, HBsAg negative patients resulting in high mortality from liver disease. HBsAg positive patients irrespective of HBV DNA levels should receive preemptive treatment with HBV polymerase inhibitors which should be continued for 12 months after cessation of chemo- and or immunosuppressive therapy. The combination prophylaxis of passive immunisations with hepatitis B immunoglobulins (HBIG) and nucleos(t)ide analogues (NUC) is able to reduce HBV recurrence rates after transplantation to 0-10%. This review will summarise the current knowledge on pathogenesis, frequency and treatment options of HBV reactivations in patients with impaired immunity.

The purpose of this article is to review recent developments in the role of CT colonography with an emphasis on colorectal cancer screening. An introduction to the concept and method of CT colonography is given as well as a summary of the data on performance of CT colonography. Furthermore, details on side effects, efficacy and cost-effectiveness and the possible role of extracolonic findings are provided. The impact CTC could have on colonoscopy and other possible indications of the method are also mentioned.

The British Society of Gastroenterology (BSG) and the Association of Coloproctology for Great Britain and Ireland (ACPGBI) commissioned this update of the 2002 guidance. The aim, as before, is to provide guidance on the appropriateness, method and frequency of screening for people at moderate and high risk from colorectal cancer. This guidance provides some new recommendations for those with inflammatory bowel disease and for those at moderate risk resulting from a family history of colorectal cancer. In other areas guidance is relatively unchanged, but the recent literature was reviewed and is included where appropriate.

Refractory coeliac disease (RCD) is defined by persistent or recurrent malabsorptive symptoms and villous atrophy despite strict adherence to a gluten-free diet (GFD) for at least 6-12 months in the absence of other causes of non-responsive treated coeliac disease and overt malignancy. Symptoms are often severe and require additional therapeutic intervention besides a GFD. RCD can be classified as type 1 (normal intraepithelial lymphocyte phenotype), or type 2 (defined by the presence of abnormal (clonal) intraepithelial lymphocyte phenotype). Patients with RCD may never have responded to a GFD or may have relapsed despite adherence and initial response to the GFD. RCD type 1 usually improves after treatment with a combination of aggressive nutritional support, adherence to a GFD, and alternative pharmacological therapies. By contrast, clinical response to alternative therapies in RCD type 2 is less certain and the prognosis is poor. Severe complications such as ulcerative jejunitis and enteropathy-associated T cell lymphoma may occur in a subgroup of patients with RCD. The aims of this article are to (1) review recent advances in the diagnosis and management of patients with RCD, and (2) describe current and novel methods for classification of patients with RCD into categories that are useful to predict outcome and direct treatment.

In the recent 1-2 decades, we have seen a considerable development in colorectal cancer (CRC) screening modalities and programme implementation, but major challenges remain. While CRC is still the second leading cause of cancer death in both the USA and Europe, there are limited data on the efficacy and effectiveness of all screening modalities except for the faecal occult blood test (FOBT). Newer screening tests, such as faecal immunochemical tests, molecular markers and CT colonography are being introduced and variably adopted, though overall rates of screening are suboptimal. Professional societies and governmental bodies have endorsed screening, though recommended approaches are quite variable, which may help to explain the great variation in screening practices. Unfortunately, quality assurance programmes are underutilised. Comparing the USA and Europe there may be more variation in CRC screening recommendation and practice within each continent than between them, but there seems to be a stronger emphasis on programmatic screening in Europe, facilitating quality assurance. The much debated need for randomised trials as new screening modalities emerge could be more easily handled if running screening programmes are regarded as natural platforms for testing out and evaluating presumed improvements in the service--including new emerging screening modalities.

Liver failure is associated with high morbidity and mortality without transplantation. There are two types of device for temporary support: artificial and bioartificial livers. Artificial livers essentially use non-living components to remove the toxins accumulated during liver failure. Bioartificial livers have bioreactors containing hepatocytes to provide both biotransformation and synthetic liver functions. We review here the operating principles, chemical effects, clinical effects and complications of both types, with specific attention paid to bioartificial systems. Several artificial support systems have FDA marketing authorisation or are CE labelled, but the improvement they provide in terms of patient clinical outcome has not yet been fully demonstrated. At present, different bioartifical systems are being investigated clinically on the basis of their promises and capacity to provide and replace most liver functions. However, important issues such as cost, cell availability, maintenance of cell viability and functionality throughout treatment, and regulatory issues, as well as difficult challenges, including implementing cell-housing devices at the patient's bedside on an emergency basis, have delayed their appearance in intensive care units and on the market. Bioreactors are, nevertheless, when combined with artificial components, a pragmatic approach for future treatment of liver failure.

Postoperative ileus (POI) is a common clinical condition arising after almost every abdominal surgical procedure, leading to increased patient morbidity and prolonged hospitalisation. Recent advances in insight into the underlying pathophysiology have identified intestinal inflammation triggered by handling of the intestine as the main mechanism. Not only does the local inflammatory process compromise the contractile activity of the handled intestine, but it also activates inhibitory neural pathways and possibly triggers inflammation at distant untouched areas, leading to a generalised impairment of gastrointestinal motility. Macrophages residing in the muscularis externa and mast cells are the key players in this inflammatory cascade. Pharmacological interventions preventing the activation of these immune cells reduce the influx of leucocytes into the intestine, an effect associated with a reduction of the duration of POI. New potential therapeutic strategies to shorten POI based on these new insights will undoubtedly enter the clinical arena soon.