Academic literature on the topic 'NSAID-induced enteropathy'

BACKGROUNDThe diagnosis of non-steroidal anti-inflammatory drug (NSAID) induced enteropathy is difficult, requiring enteroscopy or the use of four day faecal excretion of 111In labelled white cells.AIMSTo assess faecal calprotectin (a non-degraded neutrophil cytosolic protein) as a method for diagnosing NSAID enteropathy.METHODSSingle stool faecal calprotectin concentrations were compared with the four day faecal excretion of 111In labelled white cells in 47 patients taking NSAIDs. The prevalence and severity of NSAID enteropathy was assessed using this method in 312 patients (192 with rheumatoid arthritis, 65 with osteoarthritis, 55 with other conditions) taking 18 different NSAIDs.RESULTSThe four day faecal excretion of 111In white cells correlated significantly with faecal calprotectin concentrations. In the group of 312 patients on NSAIDs faecal calprotectin concentrations were significantly higher than in controls, the prevalence of NSAID enteropathy being 44%. The prevalence and severity of NSAID enteropathy was independent of the particular type or dose of NSAID being taken or other patient variables.CONCLUSIONSAssay of faecal calprotectin provides a simple practical method for diagnosing NSAID enteropathy in man. Forty four per cent of patients receiving these drugs had NSAID induced enteropathy when assessed by this technique; 20% of these had comparable levels of inflammation to that previously reported in patients with inflammatory bowel disease.

The review analyzes the main etiological and pathogenetic mechanisms of the development of NSAID-enteropathy. Particular attention is paid to the role of intestinal microbiota in the manifestation and progression of NSAID-enteropathy. The special role of probiotics in the prevention and treatment of NSAIDs enteropathy is considered.

Background. The purpose of study was to evaluate the diagnostic yield of capsule endoscopy for NSAID-induced enteropathy and clinical, laboratory, and endoscopic characteristics of disease in patients with rheumatoid arthritis.Methods. 37 rheumatoid arthritis patients (30 women; mean age 55) treated with NSAIDs (>1 month), presented with anaemia and/or positive faecal occult blood testing, entered the study and underwent capsule endoscopy (EndoCapsule; Olympus), laboratory tests, and filled in questionnaires.Results. The prevalence of NSAID-induced enteropathy diagnosed by capsule endoscopy was 68% (25/37), classified as mild (red spots or erosions) in 18 (49%), moderate (10–20 erosions) in 4 (11%), and severe enteropathy (>20 erosions or ulcers) in 3 (8%) patients. We did not find statistically significant relationship between the enteropathy and gender, age, haemoglobin, leukocytes, albumin and CRP, or dyspepsia. The difference between subgroups of NSAIDs according to the COX specificity was not statistically significant.Conclusions. Capsule endoscopy is a highly accurate noninvasive method for evaluation of NSAID-induced enteropathy. It was revealed in a substantial section of the patients with rheumatoid arthritis and occult gastrointestinal bleeding, mostly classified as mild damage. No simple clinical or laboratory markers of the presence or severity of NSAID-induced enteropathy were recognised. This trial is registered withDRKS00004940.

The use of nonsteroidal anti-inflammatory drugs (NSAID), even if short-term, may be associated to small intestinal complications, such as erosions, ulcers and chronic mucosal inflammation. Video capsule endoscopy allows for identification of such lesions in 20 to 55% of the patients who have taken nonselective NSAID for 2 to 4 weeks. The pathophysiology of NSAID-induced enteropathy is related to a reduced reparative potential of the mucosa and abnormalities of the microbial balance in the small intestine. In real world practice, NSAID enteropathy is commonly asymptomatic, and its manifestations, such as bleeding, perforation and ileus, are quite rare (about 0.3 episodes per 100 patient-years). The main manifestation of NSAID enteropathy is chronic iron deficient anemia. The use of rebamipide, sulfasalazine, mesalazine, and rifaximin has been discussed in the treatment of NSAID enteropathy, whereas its prevention implies preferential administration of coxibs, the use of rebamipide and probiotics.

Nonsteroidal anti-inflammatory drug (NSAID)-induced small bowel injuries (NSAID enteropathies) become clinically important. Videocapsule endoscopy shows that the small bowel is involved in NSAID-related gastrointestinal tract (GIT) injury in almost two-thirds of all cases. Due to a large number of patients who receive NSAIDs, combined antiplatelet therapy, or long use anticoagulants, GIT injury prevention becomes an actual problem. Treatment for NSAID enteropathy is different from that for NSAID gastropathy. In NSAID enteropathy, it is advisable to use drugs that are able to increase the production of prostaglandins and mucus, to restore intestinal epithelial permeability, and to exert anti-inflammatory and antioxidant effects. Rebamipide that produces many pleiotropic effects and also has cytoprotective properties may become the drug of choice for treating patients with NSAID enteropathy. In addition, rebamipide has no effects on various cytochrome P-450 enzyme systems, by reducing the risk of drug interactions.

AbstractNonsteroidal anti-inflammatory drug (NSAID)-induced enteropathy is an increasingly recognized entity. Patients of older age and those suffering from conditions such as arthritis requiring long term NSAIDs are thought to be at greater risk. Introduction of enteroscopic techniques has greatly improved understanding of NSAID-related small intestinal injury. Complementary high-resolution cross-sectional imaging techniques aid in initial evaluation and for exclusion of alternative etiology. Erosions, superficial ulcerations, and short segment strictures are the most commonly described findings. The diagnosis of the condition lies in obtaining relevant history in addition to a high degree of suspicion during investigation of anemia, obscure gastrointestinal bleeding, small bowel obstruction, and protein losing enteropathy. Herein, the authors present a review of pathogenesis and imaging findings of NSAID enteropathy with particular emphasis on distinction from Crohn’s enteropathy.

Objective of the Review: to discuss the most common adverse events from the use of non-steroidal anti-inflammatory drugs (NSAID) for GIT: NSAID-induced esophago-, gastroduodeno- and enteropathy, possible management and the use of various therapies in order to minimize the risks of this pathology. Key Points. NSAIDs are efficient analgetics and anti-inflammatory products widely used in clinical setting. NSAIDs are prescribed mostly to patients with chronic joint and spine conditions. As a lot of patients who take NSAIDs are comorbid, they have frequent adverse reactions to drugs, including NSAIDs, and need stricter control if this is a therapy of choice. Selective NSAIDs (nimesulide) are characterised by good bioavailability; they are efficient pain killers, possess marked anti-inflammatory properties and are relatively safe, thus making it possible to minimise the rate of adverse reactions for GIT. Conclusion. It should be emphasised that the issue of NSAID-induced GIT disorders is still challenging and can be aggravated in comorbid patients. Of prime importance are timely prevention and diagnosis of NSAID-induced GIT disorders and sustainable and individuated NSAID prescription. Keywords: non-steroidal anti-inflammatory drugs, comorbidity, NSAID-induced gastroduodenopathy, NSAID-induced enteropathy, nimesulide, Nise

Nonsteroidal anti-inflammatory drug (NSAID)-induced enteropathy is considered a serious and increasing clinical problem without available treatment. Glycomacropeptide (GMP) is a 64-amino acid peptide derived from milk κ-casein with numerous biological activities. The aim of this study was to investigate the protective effect of GMP on NSAID enteropathy in rats. Enteropathy was induced by seven days oral indomethacin administration. Rats were orally GMP treated from seven days previous and during the establishment of the enteropathy model. Changes in metabolism, hematological and biochemical blood alterations, intestinal inflammation and oxidative damage were analyzed. Integrity barrier markers, macroscopic intestinal damage and survival rate were also evaluated. GMP treatment prevented anorexia and weight loss in animals. Furthermore, prophylaxis with GMP ameliorated the decline in hemoglobin, hematocrit, albumin and total protein levels. The treatment had no therapeutic efficacy on the decrease of occludin and mucin (MUC)-2 expression in intestinal tissue. However, GMP markedly decreased neutrophil infiltration, and CXCL1, interleukin-1β and inducible nitric oxide synthase expression. Nitric oxide production and lipid hydroperoxide level in the small intestine were also diminished. These beneficial effects were mirrored by preventing ulcer development and increasing animal survival. These results suggest that GMP may protect against NSAID enteropathy through anti-inflammatory and antioxidant properties.

Non-steroidal anti-inflammatory drug (NSAIDs) induced enteropathy represents an important complication of one of the most commonly used drugs worldwide. Due to previous diagnostics difficulties the real prevalence of this disease was underestimated for a long time. The pathogenesis of NSAID-enteropathy is more multifactorial and complex than formerly assumed but has still not been fully uncovered. A combination of the local and systemic effect plays an important role in pathogenesis. Thanks to novel enteroscopy methods (wireless capsule endoscopy, double balloon enteroscopy), small bowel lesions are described in a substantial section of NSAID users although most are clinically asymptomatic. The other non-invasive tests (small bowel permeability, faecal calprotectin, scintigraphy using faecal excretion of 111-indium-labelled leukocytes etc.) proposed for diagnostics are not generally used in clinical practice, mainly because of their non-specificity. Despite intensive research into possible treatment, the main measure for patients with NSAID-enteropathy is still withdrawal of NSAIDs. Double balloon enteroscopy plays an important role in the treatment of complications (bleeding, strictures).

Several disorders of the gastrointestinal (GI) tract including ulcerative colitis, chemotherapy-induced mucositis and non-steroidal anti-inflammatory drug (NSAID)- induced enteropathy, are characterised by inflammation, ulceration, mucosal damage and malabsorption. Treatment options are variably effective, highlighting the need to broaden therapeutic approaches, including adjunctive strategies. Emu Oil, derived from subcutaneous and retroperitoneal Emu adipose tissue, is a rich source of fatty acids (FA). Despite limited rigorous scientific studies, topically applied Emu Oil has demonstrated potent anti-inflammatory properties in vivo. Previously, orally administered Emu Oil improved intestinal architecture in a rat model of mucositis, with early indications of enhanced intestinal repair. Accordingly, this thesis investigated the effects of orally administered Emu Oil in rat models of colitis (colonic damage), NSAID-enteropathy (small intestinal [SI] damage) and on the time course of SI repair in chemotherapy-induced mucositis. In the current study, Emu Oil improved colonic tissue damage associated with dextran sulphate sodium-induced colitis in Sprague Dawley rats and facilitated the repair process (Chapter 2). Improvements were indicated histologically by reduced intestinal damage severity scores and enhanced crypt compensatory elongation in the colon. These findings suggested the potential for Emu Oil to augment conventional treatment approaches for colitis. The effectiveness of Emu Oil in the colon provided impetus to further investigate Emu Oil action proximally, in the SI. In a rat model of chemotherapy (5-Fluorouracil; 5- FU)-induced mucositis, Emu Oil maintained SI villus height and crypt depth during the phase of maximal damage (Chapter 3). This was followed by an enhanced compensatory mucosal thickening, suggesting an acceleration of the repair process. Furthermore, Emu Oil significantly decreased myeloperoxidase (MPO) activity, indicative of acute inflammation, in the jejunum and ileum of 5-FU-injected rats. Potent anti-inflammatory properties of Emu Oil were reaffirmed in NSAID (Indomethacin)-induced enteropathy, whereby MPO activity in the jejunum and ileum of Indomethacin-treated rats was markedly decreased following Emu Oil administration (Chapter 4). Treatments for diseases such as coronary artery disease and GI disorders seek to minimise oxidative damage by free radicals through the use of antioxidants. Oils derived from ratites (flightless birds) predominantly comprise FA varying in composition between ratite species. The influence of farm location, rendering method, duration and storage mode was investigated for free radical scavenging activity (RSA) against 2,2-diphenyl-1-picryl hydracyl and primary oxidation status of Ratite Oils (Chapter 5). Emu Oil conferred the greatest RSA compared to Ostrich and Rhea Oil, potentially attributed to its high unsaturated FA: saturated FA ratio and non-triglyceride fraction minor constituents. Rendering and storage variables impacted on Emu Oil RSA and primary oxidation. This thesis identified Emu Oil as a safe, renewable and economical means to augment pharmaceutical options for GI disorders. A new mechanism of action for Emu Oil could represent a promotion of repair from injury together with decreased SI inflammation. This suggests potential for Emu Oil as an adjunct to conventional treatment approaches for colitis, cancer management and long-term NSAID usage.
Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2013

Over 700 drugs have been implicated as cause of chronic diarrhea and potential enteral damage. Pathophysiologic mechanisms include intrinsic malabsorption as their main mode of action (i.e., acarbose or orlistat), increased risk of microscopic colitis/enteritis (proton-pump inhibitors (PPI), non-steroidal anti-inflammatory drugs (NSAID), selective serotonin reuptake inhibitors (SSRI)), dysbiosis (antibiotics, metformin, PPI), and microscopic or overt enteropathy (angiotensin inhibitors, antineoplastic agents, targeted therapy and check-point inhibitors). According to type, diarrhea can be malabsorptive, inflammatory or mixed, and may affect different portions of small intestine, colon, or both. Drug-induced enteropathy ranges from asymptomatic histological changes to macroscopic damage similar to that seen in inflammatory bowel disease. Treatment may include discontinuation of drug, correction of dysbiosis, and in severe cases, directed therapy towards intestinal wall inflammatory states, in similar mode as in other inflammatory bowel diseases.