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AIM In intestinal failure, delineation of both structure and function are key to both controlling symptoms and planning further intervention. We have developed a template for developing an "anatomy at a glance" patient-specific map to aid decision making and counselling. METHOD A core data set was developed and used to create an editable template to demonstrate the gastrointestinal tract, its relationship to the genitourinary tract, and specific anterior abdominal wall features. This was then used to create an anatomical template, specific to each patient, and stored in the electronic patient record and imaging archive. RESULTS We have developed a technique for integration of multi-modal information into one diagram, easily referenced by the multidisciplinary team. Radiology, endoscopy and previous operation notes can be used to fill out a core data set, which is then transposed into a standardised template. A worked example is shown in the main article. CONCLUSION The mapping template has been successfully integrated into practice, and aided decision making at all stages of the patient's therapeutic journey. It has been found helpful in planning routes of nutrition, pre-operative optimisation, surgical planning, interpreting post-operative imaging and managing patient expectations.

Intestinal failure (IF) is a condition characterized by the inability to maintain a state of adequate nutrition, or fluid and electrolyte balance due to an anatomical or a physiological disorder of the gastrointestinal system. IF can be an extremely debilitating condition, significantly affecting the quality of life of those affected. The surgical management of patients with acute and chronic IF requires a specialist team who has the expertise in terms of technical challenges and decision-making. A dedicated IF unit will have the expertise in patient selection for surgery, investigative workup and planning, operative risk assessment with relevant anesthetic expertise, and a multidisciplinary team with support such as nutritional expertise and interventional radiology. This article covers the details of IF management, including the classification of IF, etiology, prevention of IF, and initial management of IF, focusing on sepsis treatment and nutritional support. It also covers the surgical aspects of IF such as intestinal reconstruction, abdominal wall reconstruction, and intestinal transplantation.

Coeliac disease affects approximately 1% of Northern American and European populations. It is caused by an inappropriate immune response to dietary gluten. Gluten comprises of two major protein fractions: gliadins and glutenins. Glutenins have recently been found to be toxic to coeliac individuals. Proliferation assays suggest in some but not all paediatric coeliac individuals there may be immunological stimulation with high molecular weight (HMW) glutenins. Less evidence pertains to low molecular weight (LMW) glutenins. The aim is to assess adaptive, T-cell driven, and innate immune response in adult coeliac individuals towards HMW glutenin peptide, glut04, and LMW glutenin peptide, glt156.Coeliac patients were recruited attending endoscopy for routine monitoring. Adaptive immune response towards glut04 and glt156 was measured by proliferation assays and measurement of interferon-γ secretion in 28 T-cell lines. The innate immune response was assessed by measurement of enterocyte cell height (ECH) in coeliac small intestinal biopsies following overnight incubation in organ culture chambers in a further nine individuals.There were 3/28 and 2/28 positive proliferation results using gluten-sensitive T-cells with glut04 and glt156, respectively. All coeliac biopsies tested in organ culture chambers demonstrated clear reduction in ECH with peptic-tryptic digest of whole industrial gluten, glut04 and glt156 when compared to negative control ovalbumin (p 0.005). Three individuals had both T-cell and organ culture study data. Their proliferation assays showed no stimulation of the T-cells.This study demonstrates glutenin epitopes glut04 and glt156, while minor T-cell epitopes, are important in their ability to trigger the innate immune response.

Celiac disease is an enteropathy triggered by dietary gluten found in wheat, rye, and barley. Treatment involves a strict gluten-free diet (GFD). Quinoa is a highly nutritive plant from the Andes that has been recommended as part of a GFD. However, in-vitro data suggested that quinoa prolamins can stimulate innate and adaptive immune responses in celiac patients. Therefore, we aimed to evaluate the in-vivo effects of eating quinoa in adult celiac patients.Nineteen treated celiac patients consumed 50 g of quinoa every day for 6 weeks as part of their usual GFD. We evaluated diet, serology, and gastrointestinal parameters. Furthermore, we carried out detail histological assessment of 10 patients before and after eating quinoa.Gastrointestinal parameters were normal. The ratio of villus height to crypt depth improved from slightly below normal values (2.8:1) to normal levels (3:1), surface-enterocyte cell height improved from 28.76 to 29.77 μm and the number of intra-epithelial lymphocytes per 100 enterocytes decreased from 30.3 to 29.7. Median values for all the blood tests remained within normal ranges, although total cholesterol (n=19) decreased from 4.6 to 4.3 mmol/l, low-density lipoprotein decreased from 2.46 to 2.45 mmol/l, high-density lipoprotein decreased from 1.8 to 1.68 mmol/l and triglycerides decreased from 0.80 to 0.79 mmol/l.Addition of quinoa to the GFD of celiac patients was well tolerated and did not exacerbate the condition. There was a positive trend toward improved histological and serological parameters, particularly a mild hypocholesterolemic effect. Overall, this is the first clinical data suggesting that daily 50 g of quinoa for 6 weeks can be safely tolerated by celiac patients. However, further studies are needed to determine the long-term effects of quinoa consumption.

Coeliac disease is a common disease that affects approximately 1% of Northern European and American populations. Evidence suggests it is caused by an inappropriate immune response in genetically susceptible patients to dietary gluten found in wheat, rye, barley and, in a small minority of patients, oats. Treatment involves a lifelong gluten-free diet. This diet limits nutritional variety and is costly and difficult to maintain.This review covers the current treatment options available and discusses novel emerging therapies for coeliac disease.Novel therapies are still in early stages of development and therefore, at present, a gluten-free diet remains the treatment of choice in coeliac disease due to its low side-effect profile. A replacement for a gluten-free diet would be superior to an adjunct; in this case dietary modification of gluten may well have the least side effects, be tolerated by a wider group of coeliac patients and therefore be accepted. Search terms used: Pubmed, Medline and clinicaltrials.gov were searched with 'celiac disease' and 'therapy' as MESH terms. Patent database was searched using the term 'celiac disease'. Conference attendance at DDW Chicago 2011 and Columbia 2010 was also used to gain further information from conference abstracts.

AIM: To investigate all patients referred to our center with non-responsive celiac disease (NRCD), to establish a cause for their continued symptoms. METHODS: We assessed all patients referred to our center with non-responsive celiac disease over an 18-mo period. These individuals were investigated to establish the eitiology of their continued symptoms. The patients were first seen in clinic where a thorough history and examination were performed with routine blood work including tissue transglutaminase antibody measurement. They were also referred to a specialist gastroenterology dietician to try to identift any lapses in the diet and sources of hidden gluten ingestion. A repeat small intestinal biopsy was also performed and compared to biopsies from the referring hospital where possible. Colonoscopy, lactulose hydrogen breath testing, pancreolauryl testing and computed tomography scan of the abdomen were undertaken if the symptoms persisted. Their clinical progress was followed over a minimum of 2 years. RESULTS: One hundred and twelve consecutive patients were referred with NRCD. Twelve were found not to have celiac disease (CD). Of the remaining 100 patients, 45% were not adequately adhering to a strict gluten-free diet, with 24 (53%) found to be inadvertently ingesting gluten, and 21 (47%) admitting non-compliance. Microscopic colitis was diagnosed in 12% and small bowel bacterial overgrowth in 9%. Refractory CD was diagnosed in 9%. Three of these were diagnosed with intestinal lymphoma. After 2 years, 78 patients remained well, eight had continuing symptoms, and four had died. CONCLUSION: In individuals with NRCD, a remediable cause can be found in 90%: with continued gluten ingestion as the leading cause. We propose an algorithm for investigation.

Introduction The aim of this study is to describe the clinical outcomes of those patients in UK tertiary referral centre referred with a diagnosis of refractory coeliac disease (RCD). This is compared to the grim multicentre survival data12 in current literature- 5-year survival RCD type 1 96% and type 2 44%. Methods Patients were entered into a database from clinic letters. Notes were reviewed for patient demographics, past medical history with dates, drug history and dietetic input and clinical course. The hospital electronic computer system was trawled for clinical parameters at time of diagnosis and during subsequent follow-up. Results Review of 32 of the 44 patient notes was able to be done and 12 patients were found to have true RCD. 4 patients had RCD type 1 and 8 patients had RCD type 2. The follow-up range (mths) was as follows type 1 3–56, type 2 3–96 and the age range (years) type 1 28–74, type 2 44–79. There is one primary enteropathy associated T-Cell lymphoma in the type 2 group who has undergone resection and CHOP chemotherapy in 1997. The HLA type II status is known for 9 of the 12 RCD patients. Type1 RCD have 1 DQ2 and 1 heterogeneous DQ2/DQ8 whereas type 2 RCD have 4 DQ2 and 3 DQ8. All RCD patients had normal albumen and haemoglobin at time of presentation. Four of the RCD type 2 patients changed to type 1 with steroids and azathioprine, however none of the type 1 RCD improved histologically. All RCD patients are alive to date. 20 non-responsive coeliac disease patients were found to have the following diagnoses: normal treated coeliac disease 4, not on gluten free diet (GFD) 6, small bowel bacterial overgrowth 10, lactose intolerance 2, Crohn9s disease 1. Conclusion Compared to the current literature available with grim prognosis for type 2 RCD, our patient data would not support this. Part of the discrepancy is perhaps to do with the use of T-cell receptor in the diagnosis of RCD which was not used in reference 2. Interestingly there is a high DQ8 penetrance which may implicate a different mechanism driving RCD. More numbers are required to be analysed however our evidence supports treatment with steroids and azathioprine.