Related Enteropathy Research Articles

Severe Olmesartan related enteropathy - a case report and literature review

Severe Olmesartan related enteropathy - a case report and literature review

RETRACTED: Protective effect of naringin on small intestine injury in NSAIDs related enteropathy by regulating ghrelin/GHS-R signaling pathway

To investigate the mechanism of Ghrelin/GHS-R signaling pathway in small intestine injury induced by NSAIDs related enteropathy. To clarify the mechanism network of intestinal mucosal repair with naringin as a new therapeutic method. Naringin was used as the intervention method, observed the damage of small intestinal mucosa and detected the expression of ghrelin, GHS-R, leptin and TNF-α by electron microscopy, HE staining and immunohistochemistry. Compared with the control group, the weight of rats in the model group decreased, the thickness of intestinal mucosa became thinner, the structure of intestinal mucosa changed, the expression of ghrelin, GHS-R and leptin decreased, the expression of TNF-α increased. Compared with the model group, the intestinal mucosa of the treatment group was repaired, the expression of ghrelin, GHS-R and leptin was increased, and the expression TNF-α was decreased. The mechanism of intestinal mucosal damage in patients with NSAIDs related enteropathy may be related to the decreased expression of ghrelin, GHS-R and leptin, and promotion of TNF-α secretion. Naringin can effectively promote the secretion of ghrelin and leptin, the expression of GSH-R, and inhibit the release of TNF-α, so as to repair intestinal mucosa naringin will become a new method to treat and prevent NSAIDs related intestinal diseases.

NSAIDs and the small bowel.

The review describes the effects of NSAID gastrointestinal toxicity on the small bowel, wherein injury is as prevalent as in the gastroduodenum. This is well documented by capsule endoscopy, which also provides an endoscopic endpoint for novel treatment strategies. Appreciation of the prevalence of NSAID enteropathy has grown with capsule endoscopy and the use of composite end points that include obscure haemoglobin decreases in clinical studies. Along with dual cyclo-oxygenase isoform inhibition, gram-negative antigen presentation plays a role in the pathogenesis of NSAID enteropathy. The concomitant use of proton pump inhibitor (PPI) agents with both selective and nonselective NSAIDs in gastroduodenal protection exacerbates endoscopic enteropathy, which is thought to be due to intestinal dysbiosis. Strategies for small bowel mucosal protection include prostaglandin repletion and augmenting the intestinal flora. NSAID- related enteropathy is common and often presents subclinically. The most common presentation is anaemia, which may be less common in those on cyclo-oxygenase (COX)-2 inhibitors than nonselective NSAIDs. PPI use worsens NSAID enteropathy with more occult bleeding and ulceration and has been linked to gram-negative intestinal dysbiosis. If NSAID cessation is not possible, COX-2 inhibition without PPI therapy should be considered in patients with upper gastrointestinal risk factors. Mucoprotective agents such as misoprostol and rebamipide show promise and probiotics may have a future role.

An Unexpected IgG4-Related Enteropathy Masquerading as a Stricturing Malignancy

IgG related enteropathy is a rare entity with a characteristic histologic picture and elevated IgG plasma cells that may mimic malignancy on clinical presentation This report describes a year old female that developed abdominal pain nausea and vomiting refractory to medical management A CT scan showed a centimeter segment of thickened and strictured right colon Biopsies of the mucosa showed ulceration granulation tissue and mucosal injury Due to concern for malignancy a right hemicolectomy was performed with the final pathology displaying multifocal lymphoplasmacytic infiltrates and IgG positive plasma cells within fibrotic regions of the submucosa This case highlights the unique and challenging presentation of IgG enteropathy with an emphasis on early detection and preventing unnecessary surgical morbidity as this disease process is highly responsive to steroids

PTU-058 Colon Capsule Endoscopy: A Useful Tool in the Diagnosis and Management of Inflammatory Bowel Disease: Abstract PTU-058 Table 1

Introduction Colon capsule endoscopy (CCE) is a novel non-invasive means of directly imaging the colonic mucosal surface. Limited data is available regarding the utility of CCE in the diagnosis and re-assessment of inflammatory bowel disease (IBD), but it is attractive to patients due to its non-invasive nature and ability to obtain small bowel and pan-colonic images. We present a large series of patients with known or suspected IBD undergoing CCE. Methods Retrospective, single-centre, including 193 patients with known or suspected IBD attending for CCE using PillCam Colon (Given Imaging, Israel). All patients known to have IBD successfully passed a PillCam Patency device prior. Demographical and procedural data was collated together with final diagnosis and management outcome. Results Mean age 38.8 years (range 17–82), 129 female, median follow-up 43 months (range 3–99). 71 chose CCE over colonoscopy, 66 refused colonoscopy, 49 had an incomplete colonoscopy, and 7 were unfit for colonoscopy. Indication for the procedure: known IBD (n = 66, 5 with ulcerative colitis, 61 with Crohn’s disease) of which 30 patients were undergoing CCE for disease re-assessment after 12 months of anti-TNF therapy and 36 due to a relapse in symptoms. The remaining 127 had suspected IBD. Procedure completion rate 75.5%, bowel preparation was good or adequate in 64.3%. There were no adverse events. In the known IBD group, 45 patients were diagnosed with active disease based on the CCE findings. This lead to changes in management in 44 patients (67%); mainly in the form of medication alteration (40 patients), but also by further investigation (4 patients). In the suspected IBD group, CCE diagnostic yield for IBD was 6%, 5 patients were diagnosed with Crohn’s disease and 2 patients were diagnosed with ulcerative colitis. In the group with small bowel inflammation 1 patient was diagnosed with NSAID related enteropathy and 1 had non-specific histology and is undergoing further investigation. Other clinically relevant alternative findings are outlined in Table 1 . Overall CCE made 37 clinically significant diagnoses in the small bowel rather than the colon; 27 in the known IBD group and 10 in the suspected IBD group. Abbreviations: IBD=inflammatory bowel disease Conclusion CCE is a useful patient friendly alternative for the diagnosis and re-assessment of patients with known or suspected IBD and impacts management. The distal small bowel is visualised with excellent clarity making CCE particularly useful for those with suspected or known ileocolonic disease. Disclosure of Interest None Declared

Foodborne, food related illness and role of the healthcare professionals.

Foodborne infection is a major health issue and its impact on global social and economic development remains unknown (1). A paper published in the journal Nature estimates 30% of all infections over the last 60 years were Foodborne (2). The Centre for Disease Control in the United States estimates that 76 million people per year are affected by Foodborne illness, with 300,000 requiring hospital treatment and 5000 fatalities (3). Specific foods are associated with specific Foodborne infections and food poisoning (3). Examples include unpasteurised milk (Campylobacter); shellfish (noroviruses); unpasteurized apple cider (Escherichia coli O157:H7), raw and undercooked eggs (Salmonella); fish (ciguatera poisoning); raspberries (Cyclospora); strawberries (hepatitis A virus); and ready-to-eat meats (Listeria). In clinical practice, healthcare professionals, including physicians, have to interpret clinical symptoms; enabling correct diagnosis and the differentiation of Foodborne illness from food allergy and intolerance, celiac disease, the irritable bowel syndrome, inflammatory bowel disease, viral infection and malignancy (4). An up to date understanding of diagnostic testing is fundamental to the identification of a food related illnesses. Obasanjo published a review in Medscape (5) that summarises the key aspects of the primer published in 2001 by the Foodborne Illness Primer Work Group (FIPWG) and its subsequent updates published in Morbidity and Mortality Weekly Reports (MMWR) (6). The article highlights that in routine clinical practice it is important to maintain good communication between physicians, local testing laboratories and public health authorities. The review reports that most laboratories limit stool culture to screening for species such as Salmonella, Shigella, Campylobacter jejuni or E. coli. Laboratories require advanced notification if Yersinia, Vibrio, E Coli 0157:H7 or other Campylobacter species are suspected, because additional media and incubation conditions are required. Special laboratory procedures are also required to identify infection due to parasites such as Cryptosporidium and Cyclospora cayetanensis. In practice, this means physicians need to communicate with their local laboratories to ensure that arrangements for specialist testing are in place prior to the sending of samples. Furthermore public health authorities need a close relationship with local laboratories to provide advice regarding local antibiotic sensitivities and to initiate community investigation of outbreak sources. Electronic request, information technology, eLearning, etc., have become synonyms or replacements for new and different types of communication. Although new models of communication have added a litany of words to our vocabulary and created novel ways to highlight tasks and develop plans, the way we communicate has become more complicated and potentially more confusing. Maintaining good communication is a necessity within each clinical setting and across clinical speciliaties. The paper by Obasanjo serves as a reminder that knowledge about rarer conditions can aid differential diagnosis. Specific considerations are required when investigating Foodborne infections in severely ill patients, immunocompromised patients, those with a significant travel history or in those who fail to respond to empiricial treatment. Identifying the underlying Foodborne infection may necessitate repeating stool cultures, reviewing histology results and serology. Obasanjo reminds us that physicians need be aware of unusual symptoms and signs such as rashes, myalgia, arthralgia and focal neurological weakness (5). Neurological signs such as meningism or orofacial weakness may indicate life-threatening diagnoses such as Botulism, seafood contamination, mushroom poisoning or chemical poisoning (e.g. organophosphates). The review also highlights that treatment of Foodborne microbial infections with antibiotics needs to be considered carefully and should be based upon evidence of appropriateness of treatment, antimicrobial susceptibility tests as well as interpretation of signs, symptoms and results of stool microscopy/culture. Antibiotics have no effect upon viral infections such as the common head cold and only about 5-10% of bronchitis cases are caused by a bacterial infection. Misuse and overuse of antibiotics has serious effects on public health. Antibiotic resistant bacteria are a growing threat and becoming increasingly common. Unfortunately, the low threshold of using antibiotics, in certain countries in the Middle East, might create multi-antibiotic resistant life threatening infections or "super bugs" (7). Antibiotic abuse also places the patient at unnecessary risk of adverse effects of antibiotics. Judicial use of antibiotics is therefore recommended. In conclusion, healthcare professionals play a key role in the identification and treatment of Foodborne illness. Awareness of algorithms for the correct diagnosis of food related enteropathies, good communication with testing laboratories and prompt case reporting to public health authorities are essential. Awareness on the limited benefits of antibiotics therapy should also be a priority to prevent the development of antibiotic resistant “superbugs.”

PTU-030 Obesity: a risk factor for Crohn's disease or a distinct obesity-related enteropathy?

<h3>Introduction</h3> Obesity is a rapidly increasing problem with an increasing number of adverse health consequences being discovered. It is associated with a pro-inflammatory state.1 In epidemiological studies obesity has been associated with diarrhoeal symptoms,2 and increased levels of a marker of inflammation, calprotectin, in the faeces.3 The objective was to determine whether obesity at diagnosis is a risk factor for Crohn9s disease vs ulcerative colitis and also vs community controls. <h3>Methods</h3> 524 consecutive patients attending gastroenterology clinics at Mayday University Hospital and St George9s Medical School were administered a questionnaire enquiring about weight at diagnosis if not available from the notes and height as well as other risk factors for inflammatory bowel disease. 480 community controls aged 50–70 were randomly selected from the registers of 4 local general practices as part of another study. Outcome measures: odds ratio of association of obesity at diagnosis with Crohn9s disease vs ulcerative colitis at all ages and Crohn9s disease vs community controls in the 50–70-year age group as a secondary analysis. <h3>Results</h3> Obesity at diagnosis was more common in subjects with Crohn9s disease vs ulcerative colitis odds ratio 2.017 (1.18–3.43) p=0.01 and also Crohn9s disease vs community controls in the 50–70-year age group odds ratio 3.22 (1.59–6.52) p=0.001 after controlling for age at diagnosis, sex and smoking at the time of diagnosis. The strength of association for CD vs UC was increased further after adjustment for weight and height at diagnosis to odds ratio 3.84 (1.83–8.15) p=0.0003 as was the case when BMI and BMI squared were modelled as the explanatory variables. This reflects a U shaped relationship between BMI at diagnosis and risk of Crohn9s vs ulcerative colitis. <h3>Conclusion</h3> Obesity may play a role in the pathogenesis of Crohn9s disease and it maybe that an obesity related enteropathy is a distinct entity.

Microscopic enteritis: Novel prospect in coeliac disease clinical and immuno-histogenesis. Evolution in diagnostic and treatment strategies

The diagnosis of coeliac disease has traditionally depended on symptoms and intestinal biopsies; nowadays, the diagnosis has been expanded to include an array of serological markers and subtle microscopic lesions. The most important advance in classifying mucosal lesions in coeliac disease was forwarded by Marsh (1992), who provided the biological explanation of how the small bowel reacts to a variety of environmental antigenic challenges including gluten. In the modified version of this classification (Arnhem 1998-1999) autoantibodies have integrated into Marsh's histopathological scheme. As a large part of the coeliac 'iceberg' remains unrecognised, the difficulties in diagnosis continue to challenge clinicians and researchers. Advances in immuno-histochemistry and discovery of the other sensitive markers have acquainted us with so-called Microscopic enteritis, the distinctive subtle abnormalities behind the atypical gluten sensitivity symptoms that often remain unrecognised. Current diagnostic pathways do not always include facilities for looking for this common histological feature in atypical cases. This is essential since improving of the detection rate has been shown to be directly proportional to recognition of cases with milder or minimal mucosal abnormalities. In this revision, we will define and characterise microscopic enteritis as the entity behind a wide range of unexplained gastrointestinal symptoms. Screening for this subtle and distinctive presentation in small bowel pathology will open a new prospect in recognising the most common but unrecognised atypical forms of symptomatic gluten related enteropathies.

Toxicity mechanisms of wheat and other cereals in celiac disease and related enteropathies.

This paper is a critical appraisal of current theories on the mechanisms of toxicity of wheat and other cereals in celiac disease and some related enteropathies. The "peptidase deficiency," "primary immune defect," and "gluten-lectin" theories on celiac disease are examined and critically discussed on the basis of the relevant data available in 88 references. Special attention has been paid in this review to the nature of the cereal components triggering the appearance of toxic symptoms and signs in celiac disease as well as to underlying action mechanisms. The gluten-lectin theory is the one best able to explain, in addition to celiac disease, some secondary intolerances that may occur in temporarily predisposed individuals as a consequence of several causes, including viral hepatitis and intestinal infections, as well as the occurrence of intestinal lesions in healthy subjects administered very high amounts of gluten.

Toxicity Mechanisms of Wheat and Other Cereals in Celiac Disease and Related Enteropathies

This paper is a critical appraisal of current theories on the mechanisms of toxicity of wheat and other cereals in celiac disease and some related enteropathies. The “peptidase deficiency,” “primary immune defect,” and “gluten‐lectin” theories on celiac disease are examined and critically discussed on the basis of the relevant data available in 88 references. Special attention has been paid in this review to the nature of the cereal components triggering the appearance of toxic symptoms and signs in celiac disease as well as to underlying action mechanisms. The gluten‐lectin theory is the one best able to explain, in addition to celiac discase, some secondary intolerances that may occur in temporarily predisposed individuals as a consequence of several causes, including viral hepatitis and intestinal infections, as well as the occurrence of intestinal lesions in healthy subjects administered very high amounts of gluten.