Journal articles: 'NSAID-induced enteropathy'

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Tibble, J. A., G. Sigthorsson, R. Foster, D. Scott, M. K. Fagerhol, A. Roseth, and I. Bjarnason. "High prevalence of NSAID enteropathy as shown by a simple faecal test." Gut 45, no. 3 (September 1, 1999): 362–66. http://dx.doi.org/10.1136/gut.45.3.362.

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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.

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Svistunov, A. A., M. A. Osadchuk, N. V. Kireeva, A. A. Hudarova, and E. E. Achkasov. "NSAID-induced enteropathy: the current state of the problem." Terapevticheskii arkhiv 90, no. 8 (August 15, 2018): 95–100. http://dx.doi.org/10.26442/terarkh201890895-100.

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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.

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Tachecí, Ilja, Petr Bradna, Tomáš Douda, Drahomíra Baštecká, Marcela Kopáčová, Stanislav Rejchrt, and Jan Bureš. "NSAID-Induced Enteropathy in Rheumatoid Arthritis Patients with Chronic Occult Gastrointestinal Bleeding: A Prospective Capsule Endoscopy Study." Gastroenterology Research and Practice 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/268382.

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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.

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Elfeky, Omar, Parker Ellison, and Daniel Raines. "S2942 Management of NSAID-Induced Enteropathy." American Journal of Gastroenterology 116, no. 1 (October 2021): S1218—S1219. http://dx.doi.org/10.14309/01.ajg.0000785300.55206.77.

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Karateev, A. E., E. V. Moroz, and E. V. Kryukov. "Small intestinal damage associated with the use of nonsteroidal anti-inflammatory drugs." Almanac of Clinical Medicine 47, no. 6 (December 22, 2019): 559–67. http://dx.doi.org/10.18786/2072-0505-2019-47-048.

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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.

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Drapkina, O. M., and O. N. Korneeva. "Small bowel injuries due to nonsteroidal anti-inflammatory drugs and antiplatelet therapy. Approaches to prevention and treatment." Terapevticheskii arkhiv 88, no. 12 (December 15, 2016): 133–39. http://dx.doi.org/10.17116/terarkh20168812133-139.

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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.

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Raju, Smita Esther, Rajvinder Singh, and Mahima Raju. "NSAID Enteropathy: A Review of the Disease Entity and Its Distinction from Crohn’s Enteropathy." Journal of Gastrointestinal and Abdominal Radiology 02, no. 02 (July 17, 2019): 078–86. http://dx.doi.org/10.1055/s-0039-1691846.

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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.

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Pakhomova, I. G., and G. Yu Knorring. "Details of the Use of Non-steroidal Anti-inflammatory Drugs in Comorbid Patients. Ways to Minimise the Risks of NSAID-induced GIT Complications." Doctor.Ru 19, no. 7 (2020): 68–75. http://dx.doi.org/10.31550/1727-2378-2020-19-7-68-75.

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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

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Cervantes-García, Daniel, Armida I. Bahena-Delgado, Mariela Jiménez, Laura E. Córdova-Dávalos, Vanessa Ruiz-Esparza Palacios, Esperanza Sánchez-Alemán, María C. Martínez-Saldaña, and Eva Salinas. "Glycomacropeptide Ameliorates Indomethacin-Induced Enteropathy in Rats by Modifying Intestinal Inflammation and Oxidative Stress." Molecules 25, no. 10 (May 18, 2020): 2351. http://dx.doi.org/10.3390/molecules25102351.

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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.

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Tachecí, Ilja, Marcela Kopáčová, Stanislav Rejchrt, and Jan Bureš. "Non-steroidal Anti-inflammatory Drug Induced Injury to the Small Intestine." Acta Medica (Hradec Kralove, Czech Republic) 53, no. 1 (2010): 3–11. http://dx.doi.org/10.14712/18059694.2016.56.

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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).

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Lim, Yun Jeong, and Hoon Jai Chun. "Recent Advances in NSAIDs-Induced Enteropathy Therapeutics: New Options, New Challenges." Gastroenterology Research and Practice 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/761060.

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The injurious effects of NSAIDs on the small intestine were not fully appreciated until the widespread use of capsule endoscopy. It is estimated that over two-thirds of regular NSAID users develop injury in the small intestinal injuries and that these injuries are more common than gastroduodenal mucosal injuries. Recently, chronic low-dose aspirin consumption was found to be associated with injury to the lower gut and to be a significant contributing factor in small bowel ulceration, hemorrhage, and strictures. The ability of aspirin and NSAIDs to inhibit the activities of cyclooxygenase (COX) contributes to the cytotoxicity of these drugs in the gastrointestinal tract. However, many studies found that, in the small intestine, COX-independent mechanisms are the main contributors to NSAID cytotoxicity. Bile and Gram-negative bacteria are important factors in the pathogenesis of NSAID enteropathy. Here, we focus on a promising strategy to prevent NSAID-induced small intestine injury. Selective COX-2 inhibitors, prostaglandin derivatives, mucoprotective drugs, phosphatidylcholine-NSAIDs, and probiotics have potential protective effects on NSAID enteropathy.

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Bjarnason, Ingvar, and Ken Takeuchi. "Intestinal permeability in the pathogenesis of NSAID-induced enteropathy." Journal of Gastroenterology 44, S19 (January 2009): 23–29. http://dx.doi.org/10.1007/s00535-008-2266-6.

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Lim, D. R., D. Farina, W. Huang, and J. Zhu. "A181 ENDOSCOPIC BALLOON DILATION IS EFFECTIVE AND SAFE IN THE MANAGEMENT OF NSAID-INDUCED NON-ULCERATIVE GASTRIC OUTLET OBSTRUCTION." Journal of the Canadian Association of Gastroenterology 3, Supplement_1 (February 2020): 48–50. http://dx.doi.org/10.1093/jcag/gwz047.180.

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Abstract Background We describe an unusual case of NSAID-induced gastric outlet obstruction (GOO) in the absence of malignancy or ulcers. This was successfully managed conservatively with drug withdrawal and serial endoscopic balloon dilation (EBD). Aims Case Report Methods Case Report and Literature Review Results A 58-year-old woman with 20-year history of daily Ketorolac use for osteoarthritis presented with iron deficiency anemia (IDA) of 58 g/L and post-prandial emesis for 2 months. There was no overt GI bleeding. Gastroscopy revealed severe erosive esophagitis and GOO with no ulcers. After a negative CT imaging ruled out extrinsic malignant compression, GOO was managed with EBD. Examination of the duodenum post-EBD revealed complete atrophy and scalloping. Focused biopsies reveal chronic gastritis, complete villous atrophy in the duodenum; ruled out H. Pylori, celiac disease, amyloidosis and dysplasia. EUS negative for infiltrative disease or regional adenopathy. Vitamin B12, anti-TTG I IgA, HLA DQ2/8 were normal. These findings made drug-induced enteropathy the top contender. PPI therapy was initiated and NSAID discontinued. Five serial EBD were performed over 4 months to 18mm. A pureed diet was tolerated after 2 dilations. Follow-up at 3 months showed partial recovery of enteropathy and pyloric stenosis. No adverse events were seen. The severe esophagitis was likely an erosive process secondary to reflux from GOO. Her IDA is likely multifactorial: Severe enteropathy and GOO may have led to chronic malabsorption; occult GI bleeding from erosions or ulcers that have healed may further contribute. Ketorolac could explain the enteropathy. COX-1 inhibition leads to decreased gastric cytoprotection. In rat models, COX-2 inhibition has been suggested to delay gastric healing and dysregulated immune response to food antigens in the small bowel [4–6]. NSAID-induced GOO almost always occur in the context of peptic ulcer disease [1,2]. A similar case [3] found pyloric stenosis in a 75-year old woman with esophagitis and ulcer-induced pyloric stenosis. They postulate that post ulcerative healing led to benign pyloric stenosis and explained the absence of ulcers. Historically, surgical intervention and stent placement have played a major role in the management of benign mechanical GOO. EBD has replaced surgical intervention as first line therapy [7] showing promising results beyond 3 months post EBD[8], sparing patients from surgery related morbidity. An algorithm has been suggested by us [Img 1] for the management of benign GOO. Conclusions We present an unusual case of NSAID-induced mechanical GOO and enteropathy. This case highlights these entities as rare but serious complications of chronic NSAID use. Management of benign mechanical GOO should be individualized. Prudence with prescribing NSAIDs to at risk populations is recommended. Funding Agencies None

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Yamawaki, Hidemoto, Hiroshi Mihara, Nobuhiro Suzuki, Hirofumi Nishizono, Kunitoshi Uchida, Shiro Watanabe, Makoto Tominaga, and Toshiro Sugiyama. "Role of transient receptor potential vanilloid 4 activation in indomethacin-induced intestinal damage." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 1 (July 1, 2014): G33—G40. http://dx.doi.org/10.1152/ajpgi.00105.2013.

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Gastrointestinal ulcers and bleeding are serious complications of nonsteroidal anti-inflammatory drug (NSAID) use. Although administration of antibiotics and Toll-like receptor 4 knockdown mitigate NSAID-induced enteropathy, the molecular mechanism of these effects is poorly understood. Intestinal hyperpermeability is speculated to trigger the initial damage due to NSAID use. Transient receptor potential vanilloid 4 (TRPV4) is a nonselective cation channel expressed throughout the gastrointestinal tract epithelium that is activated by temperature, extension, and chemicals such as 5,6-epoxyeicosatrienoic acid (5,6-EET). The aim of this study was to investigate the possible role of TRPV4 in NSAID-induced intestinal damage. TRPV4 mRNA and protein expression was confirmed by RT-PCR and immunochemistry, respectively, in mouse and human tissues while TRPV4 channel activity of the intestinal cell line IEC-6 was assessed by Ca2+-imaging analysis. TRPV4 activators or the NSAID indomethacin significantly decreased transepithelial resistance (TER) in IEC-6 cells, and indomethacin-induced TER decreases were inhibited by specific TRPV4 inhibitors or small-interfering RNA TRPV4 knockdown, as well as by the epoxygenase inhibitor N-(methylsulfonyl)-2-(2-propynyloxy)-benzenehexanamide, which decreased 5,6-EET levels. In TRPV4 knockout mice, indomethacin-induced intestinal damage was significantly reduced compared with WT mice. Taken together, these results show that TRPV4 activation in the intestinal epithelium caused epithelial hyperpermeability in response to NSAID-induced arachidonic acid metabolites and contributed to NSAID-induced intestinal damage. Thus, TRPV4 could be a promising new therapeutic target for the prevention of NSAID-induced intestinal damage.

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Nakamura, Shiro, Toshio Watanabe, Tetsuya Tanigawa, Sunao Shimada, Yuji Nadatani, Takako Miyazaki, Masaki Iimuro, and Yasuhiro Fujiwara. "Isoliquiritigenin Ameliorates Indomethacin-Induced Small Intestinal Damage by Inhibiting NOD-Like Receptor Family, Pyrin Domain-Containing 3 Inflammasome Activation." Pharmacology 101, no. 5-6 (2018): 236–45. http://dx.doi.org/10.1159/000486599.

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Activation of the NOD-Like Receptor Family, Pyrin Domain-Containing 3 (NLRP3) inflammasome, which consists of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and pro-caspase-1, triggers pro-caspase-1 cleavage promoting the processing of pro-interleukin (IL)-1β into mature IL-1β, which is critical for the development of non-steroidal anti-inflammatory drug (NSAID)-induced enteropathy. We investigated the effects of isoliquiritigenin, a flavonoid derived from the roots of Glycyrrhiza species, on NSAID-induced small intestinal damage and the inflammasome activation. To induce enteropathy, mice were administered indomethacin by gavage with or without isoliquiritigenin pretreatment. Some mice received an intraperitoneal injection of recombinant murine IL-1β in addition to isoliquiritigenin and indomethacin. Indomethacin induced small intestinal damage and increased protein levels of cleaved caspase-1 and mature IL-1β in the small intestine. Treatment with 7.5 and 75 mg/kg isoliquiritigenin inhibited indomethacin-induced small intestinal damage by 40 and 56%, respectively. Isoliquiritigenin also inhibited the indomethacin-induced increase in cleaved caspase-1 and mature IL-1β protein levels, whereas it did not affect the mRNA expression of NLRP3, ASC, caspase-1, and IL-1β. Protection against intestinal damage in isoliquiritigenin-treated mice was completely abolished with exogenous IL-1β. NLRP3–/– and caspase-1–/– mice exhibited resistance to intestinal damage, and isoliquiritigenin treatment failed to inhibit the damage in NLRP3–/– and caspase-1–/– mice. Isoliquiritigenin prevents NSAID-induced small intestinal damage by inhibiting NLRP3 inflammasome activation.

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Herz, Hussein, Yang Song, Yuanchao Ye, Liping Tian, Benjamin Linden, Marwa Abu El Haija, Yi Chu, Justin L. Grobe, Randall W. Lengeling, and Mohamad Mokadem. "NSAID-Induced Enteropathy Affects Regulation of Hepatic Glucose Production by Decreasing GLP-1 Secretion." Nutrients 14, no. 1 (December 28, 2021): 120. http://dx.doi.org/10.3390/nu14010120.

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Background/Aim: Given their widespread use and their notorious effects on the lining of gut cells, including the enteroendocrine cells, we explored if chronic exposure to non-steroidal anti-inflammatory drugs (NSAIDs) affects metabolic balance in a mouse model of NSAID-induced enteropathy. Method: We administered variable NSAIDs to C57Blk/6J mice through intragastric gavage and measured their energy balance, glucose hemostasis, and GLP-1 levels. We treated them with Exendin-9 and Exendin-4 and ran a euglycemic-hyperinsulinemic clamp. Results: Chronic administration of multiple NSAIDs to C57Blk/6J mice induces ileal ulcerations and weight loss in animals consuming a high-fat diet. Despite losing weight, NSAID-treated mice exhibit no improvement in their glucose tolerance. Furthermore, glucose-stimulated (glucagon-like peptide -1) GLP-1 is significantly attenuated in the NSAID-treated groups. In addition, Exendin-9—a GLP-1 receptor antagonist—worsens glucose tolerance in the control group but not in the NSAID-treated group. Finally, the hyper-insulinemic euglycemic clamp study shows that endogenous glucose production, total glucose disposal, and their associated insulin levels were similar among an ibuprofen-treated group and its control. Exendin-4, a GLP-1 receptor agonist, reduces insulin levels in the ibuprofen group compared to their controls for the same glucose exchange rates. Conclusions: Chronic NSAID use can induce small intestinal ulcerations, which can affect intestinal GLP-1 production, hepatic insulin sensitivity, and consequently, hepatic glucose production.

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Neag, Maria-Adriana, Carmen-Stanca Melincovici, Adrian Catinean, Dana-Maria Muntean, Raluca-Maria Pop, Ioana-Corina Bocsan, Andrei-Otto Mitre, Mihai-Bogdan Cardos, Andreea-Ioana Inceu, and Anca-Dana Buzoianu. "The Role of Probiotic Bacillus Spores and Amino Acids with Immunoglobulins on a Rat Enteropathy Model." Biomedicines 10, no. 10 (October 7, 2022): 2508. http://dx.doi.org/10.3390/biomedicines10102508.

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Non-steroidal anti-inflammatory drugs (NSAIDs) are some of the most widely used drugs due to their anti-inflammatory, analgesic and antipyretic pharmacological effects. Gastrointestinal side effects are some of the most severe and frequent side effects of NSAIDs. These depend on the balance of the gut microbiome, the abundance of Gram-negative bacteria, and the amount of lipopolysaccharide released. Therefore, restoring or improving gut bacteria balance with probiotic supplements could prove to be an adjuvant therapy against mild NSAID-induced enteropathy. Twenty-five Wistar albino male rats were divided into five groups. The negative control group was administered carboxymethylcellulose and the positive control group diclofenac (DIC), 8 mg/kg for 7 days, which represented the enteropathy model. Treatment groups consisted of a combination of pro-biotic spores (MSB), amino acids and immunoglobulins supplement (MM), which were also administered for 7 days. We analyzed hepatic injury markers (AST, ALT) and creatinine, and inflammatory markers, IL-6, TNF-α, PGE2, iNOS, as well as total antioxidant capacity. The results obtained in the present study suggest that the modulation of the intestinal microbiota by administration of probiotics (Bacillus spores), alone or in combination with immunoglobulins and amino acids, represents an attractive therapy for the prevention of NSAID-induced enteropathy.

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Amagase, Kikuko, Yuki Kimura, Akimitsu Wada, Tohru Yukishige, Toshiko Murakami, Eiji Nakamura, and Koji Takeuchi. "Prophylactic Effect of Monosodium Glutamate on NSAID-Induced Enteropathy in Rats." Current Pharmaceutical Design 20, no. 16 (May 31, 2014): 2783–90. http://dx.doi.org/10.2174/13816128113199990579.

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Macdonald, CE, DP Calnan, T. Podas, W. Johnson, and RJ Playford. "Clinical trial of, bovine colostrum for protection against NSAID-induced enteropathy." Gastroenterology 114 (April 1998): A209. http://dx.doi.org/10.1016/s0016-5085(98)80849-4.

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Auld, Michael C., Benjamin R. Dodd, Andrew P. Barbour, and Mark Smithers. "Two cases of NSAID-induced gastropathy and enteropathy of the ileum." ANZ Journal of Surgery 85, no. 7-8 (November 20, 2013): 584–85. http://dx.doi.org/10.1111/ans.12462.

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Abimosleh, Suzanne M., Cuong D. Tran, and Gordon S. Howarth. "Emu Oil Reduces Small Intestinal Inflammation in the Absence of Clinical Improvement in a Rat Model of Indomethacin-Induced Enteropathy." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/429706.

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Nonsteroidal-anti-inflammatory-drug (NSAID) enteropathy is characterized by small intestinal damage and ulceration. Emu Oil (EO) has previously been reported to reduce intestinal inflammation.Aim. We investigated EO for its potential to attenuate NSAID-enteropathy in rats.Methods. Male Sprague Dawley rats (n=10/group) were gavaged with Water, Olive Oil (OO), or EO (0.5 mL; days 0–12) and with 0.5 mL Water or the NSAID, Indomethacin (8 mg/kg; days 5–12) daily. Disease activity index (DAI), 13C-sucrose breath test (SBT), organ weights, intestinal damage severity (IDS), and myeloperoxidase (MPO) activity were assessed.P<0.05was considered significant.Results. In Indomethacin-treated rats, DAI was elevated (days 10–12) and SBT values (56%) and thymus weight (55%) were decreased, relative to normal controls. Indomethacin increased duodenum (68%), colon (24%), SI (48%), caecum (48%), liver (51%) and spleen (88%) weights, IDS scores, and MPO levels (jejunum: 195%, ileum: 104%) compared to normal controls. Jejunal MPO levels were decreased (64%) by both EO and OO, although only EO decreased ileal MPO (50%), compared to Indomethacin controls.Conclusions. EO reduced acute intestinal inflammation, whereas other parameters of Indomethacin-induced intestinal injury were not affected significantly. Increased EO dose and/or frequency of administration could potentially improve clinical efficacy.

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Balabantseva, A. P., and A. E. Karateev. "The frequency and clinical and endoscopic features of mixed NSAIDs-induced gastrointestinal injuries." Modern Rheumatology Journal 12, no. 4 (December 10, 2018): 95–100. http://dx.doi.org/10.14412/1996-7012-2018-4-95-100.

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Non-steroidal anti-inflammatory drugs (NSAIDs) can cause undesirable reactions in all parts of the gastrointestinal tract (GIT). However, the frequency of mixed injuries of various GIT parts due to the use of these drugs has not been investigated.Objective: to estimate the frequency of mixed NSAID-induced injuries of the upper GIT, small and large intestine.Patients and methods. A total of 112 patients (62.5% were women) (mean age, 56.2±14.6 years) with rheumatic diseases who had regularly taken NSAIDs were examined. All the patients underwent esophagogastroduodenoscopy and video colonoscopy. Video capsule endoscopy was performed in 35 patients with signs of NSAID-induced gastropathy.Results and discussion. The signs of NSAID-induced gastropathy (gastric and duodenal erosions and/or ulcers) were found in 43.8% of patients; those of NSAID-induced enteropathy (small bowel hemorrhages, erosions, and ulcers) were present in 68.6%; and those of NSAIDinduced colopathy (colonic hemorrhages, erosions, and ulcers) were in 14.3%. The concurrence of NSAID-induced gastro- and colonopathy was present in 28.6% of the patients (odds ratio 12.2; 95% confidence interval, 2.619–56.84); that of NSAID-induced gastro-, entero-, and colopathy was in 10 (20.4% of all the patients with NSAID-induced gastropathy). There was a significant association of the risk of mixed pathology in all GIT parts with the diagnosis of spondylarthritis, the presence of abdominal pain, the signs of dysbiosis and bacterial overgrowth syndrome, as well as with the carriage of CYP2C19 gene polymorphism (the CYP2C19*17*1/*17 allele).Conclusion. Mixed injury of various GIT parts due to the use of NSAIDs is a frequent and serious pathology that requires comprehensive diagnostic tests and combined use of preventive therapies with different mechanisms of action.

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Espenschied, Scott T., Mark R. Cronan, Molly A. Matty, Olaf Mueller, Matthew R. Redinbo, David M. Tobin, and John F. Rawls. "Epithelial delamination is protective during pharmaceutical-induced enteropathy." Proceedings of the National Academy of Sciences 116, no. 34 (August 7, 2019): 16961–70. http://dx.doi.org/10.1073/pnas.1902596116.

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Intestinal epithelial cell (IEC) shedding is a fundamental response to intestinal damage, yet underlying mechanisms and functions have been difficult to define. Here we model chronic intestinal damage in zebrafish larvae using the nonsteroidal antiinflammatory drug (NSAID) Glafenine. Glafenine induced the unfolded protein response (UPR) and inflammatory pathways in IECs, leading to delamination. Glafenine-induced inflammation was augmented by microbial colonization and associated with changes in intestinal and environmental microbiotas. IEC shedding was a UPR-dependent protective response to Glafenine that restricts inflammation and promotes animal survival. Other NSAIDs did not induce IEC delamination; however, Glafenine also displays off-target inhibition of multidrug resistance (MDR) efflux pumps. We found a subset of MDR inhibitors also induced IEC delamination, implicating MDR efflux pumps as cellular targets underlying Glafenine-induced enteropathy. These results implicate IEC delamination as a protective UPR-mediated response to chemical injury, and uncover an essential role for MDR efflux pumps in intestinal homeostasis.

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Tibble, JA, R. Foster, G. Sigthorsson, D. Scott, A. Roseth, and I. Bjarnason. "Faecal calprotectin: A simple method for the diagnosis of NSAID-induced enteropathy." Gastroenterology 114 (April 1998): A310. http://dx.doi.org/10.1016/s0016-5085(98)81259-6.

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Yanai, S., S. Nakamura, M. Hirahashi, T. Ueki, T. Matsumoto, and T. Kitazono. "Gastrointestinal: MALT lymphoma of the small bowel accompanied by NSAID-induced enteropathy." Journal of Gastroenterology and Hepatology 27, no. 6 (May 24, 2012): 1126. http://dx.doi.org/10.1111/j.1440-1746.2012.07138.x.

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Hotz-Behofsits, C. M., M. J. M. Walley, R. Simpson, and I. T. Bjarnason. "COX-1, COX-2 and the topical effect in NSAID-induced enteropathy." InflammoPharmacology 11, no. 4-6 (December 2003): 363–70. http://dx.doi.org/10.1163/156856003322699546.

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Higashimori, A., T. Watanabe, Y. Nadatani, S. Takeda, K. Otani, T. Tanigawa, H. Yamagami, et al. "Mechanisms of NLRP3 inflammasome activation and its role in NSAID-induced enteropathy." Mucosal Immunology 9, no. 3 (September 9, 2015): 659–68. http://dx.doi.org/10.1038/mi.2015.89.

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Hnepa, Yana Y., Ivan V. Chopey, Ksenia I. Chubirko, and Andriy M. Bratasyuk. "SHORT- AND LONG-TERM EFFECTS OF NSAIDS ON THE GASTROINTESTINAL MUCOSA: COMPLEX ANALYSIS OF BENEFITS AND COMPLICATIONS PREVENTION." Wiadomości Lekarskie 74, no. 4 (2021): 1011–18. http://dx.doi.org/10.36740/wlek202104138.

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The aim: To analyse data from recent studies, dedicated to the use of non-steroidal anti-inflammatory drugs (NSAIDs); to evaluate the best clinical practice in the use of NSAIDs in order to prevent side effects (SEs) in different clinical scenarios; to optimise treatment of patients at risk of NSAIDs-related SEs. Materials and methods: A comprehensive bibliographic search was performed using the keywords “NSAIDs”, “NSAID gastropathy”, “NSAID enteropathy”, “complications of NSAID therapy”, “cardiovascular disease”, “cardiovascular risk” in the PubMed, Web of Science, Cochrane Library, Google Academy databases. Conclusions: NSAID-induced gastrointestinal lesions are а relevant problem of internal medicine, this is due to the fact that the pathogenic mechanisms of this process are still unclear. All the gastrointestinal tract (GIT) related risk factors(RFs) for gastro- and enterocolonopathies associated with the use of NSAIDs should be taken into consideration by physicians of all specialties. The examination and diagnostic of the GIT should be performed regularly to prevent complications. Uncontrolled, long-lasting, unprescribed NSAID usage should draw the attention of doctors, especially in patients with comorbid states.

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Blackler, Rory W., Giada De Palma, Anna Manko, Gabriela J. Da Silva, Kyle L. Flannigan, Premysl Bercik, Michael G. Surette, Andre G. Buret, and John L. Wallace. "Deciphering the pathogenesis of NSAID enteropathy using proton pump inhibitors and a hydrogen sulfide-releasing NSAID." American Journal of Physiology-Gastrointestinal and Liver Physiology 308, no. 12 (June 15, 2015): G994—G1003. http://dx.doi.org/10.1152/ajpgi.00066.2015.

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The small intestine is a significant site of ulceration and bleeding induced by nonsteroidal anti-inflammatory drugs (NSAIDs). The pathogenesis is poorly understood. The present study explored the roles of bile, bacteria, and enterohepatic circulation to NSAID enteropathy, using both a conventional NSAID (naproxen) and a gastrointestinal-safe naproxen derivative (ATB-346), as well as proton pump inhibitors (PPIs). Rats were treated orally with naproxen or equimolar doses of ATB-346 over a 5-day period, with or without PPI administration, and intestinal damage was quantified. The cytotoxicity of bile from the rats was evaluated in vitro. Biliary excretion of naproxen and ATB-346 was determined. The impact of the NSAIDs and of PPIs on the composition of the intestinal microbiota was examined by deep sequencing of 16s rRNA. Naproxen caused significant intestinal damage and inflammation, whereas ATB-346 did not. Naproxen, but not ATB-346, dose dependently increased the cytotoxicity of bile, and it was further increased by PPI coadministration. Whereas biliary excretion of naproxen was significant in naproxen-treated rats, it was greatly reduced in rats treated with ATB-346. The enteric microbiota of naproxen-treated rats was distinct from that in vehicle- or ATB-346-treated rats, and PPI administration caused significant intestinal dysbiosis. The increase in cytotoxicity of bile induced by naproxen and PPIs may contribute significantly to intestinal ulceration and bleeding. Some of these effects may occur secondary to significant changes in the jejunal microbiota induced by both naproxen and PPIs.

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Davies, Neal M., and Fakhreddin Jamali. "Pharmacological protection of NSAID- induced intestinal permeability in the rat: effect of tempo and metronidazole as potential free radical scavengers." Human & Experimental Toxicology 16, no. 7 (July 1997): 345–49. http://dx.doi.org/10.1177/096032719701600701.

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Recently, NSAID-induced changes in both the structure and function of the distal intestine have been found to occur more frequently and with greater toxicological significance than previously thought. We have previously validated a suitable animal model to evaluate intestinal permeability changes using orally administered 51Cr- EDTA that correlates with intestinal ulceration. In this study we investigated the suitability of metronidazole and the nitroxide stable free radical scavenger (tempo) as protective agents against NSAID-induced intestinal per meability. Male Sprague-Dawley rats were dosed with two doses of metronidazole (50 mg/kg, 12 and 1 h pre-NSAID) or a single 100 mg/kg dose of tempo 1 h prior to NSAIDs. The urinary excretion of the orally administered marker 51Cr-EDTA was measured. Both tempo and metronidazole dramatically reduced indomethacin (20 mg/kg) and flur biprofen (10 mg/kg)-induced intestinal permeability. All the animals exposed to indomethacin alone died within 48-96 h and presented with histological evidence of drug- induced enteropathy, ulceration and frank peritonitis. Protection by tempo and metronidazole suggests that free radicals and/or bacteria may be important mediators in the pathogenesis of intestinal mucosal damage induced by NSAIDs. Nitric oxide donor compounds used concomi tantly with NSAIDs may protect gastrointestinal tract.

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Fornai, Matteo, Carolina Pellegrini, Laura Benvenuti, Erika Tirotta, Daniela Gentile, Gianfranco Natale, Larisa Ryskalin, et al. "Protective effects of the combination Bifidobacterium longum plus lactoferrin against NSAID-induced enteropathy." Nutrition 70 (February 2020): 110583. http://dx.doi.org/10.1016/j.nut.2019.110583.

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Ramirez-Alcantara, Veronica, Amanda LoGuidice, and Urs A. Boelsterli. "Protection from diclofenac-induced small intestinal injury by the JNK inhibitor SP600125 in a mouse model of NSAID-associated enteropathy." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 5 (November 2009): G990—G998. http://dx.doi.org/10.1152/ajpgi.00219.2009.

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Small intestinal ulceration, bleeding, and inflammation are major adverse effects associated with the use of diclofenac (DCF) or other nonsteroidal anti-inflammatory drugs (NSAIDs). The underlying mechanisms of DCF enteropathy are poorly understood, but there is increasing evidence that topical effects are involved. The aim of this study was to explore the role of c-Jun- N-terminal kinase (JNK) in DCF-induced enterocyte death because JNK not only regulates mitochondria-mediated apoptosis but also is a key node where many of the proximal stress signals converge. Male C57BL/6J mice were injected intraperitoneally with DCF or vehicle (Solutol HS-15), and the extent of small intestinal ulceration was determined. A single dose of DCF (60 mg/kg) produced numerous ulcers in the third and fourth quartiles of the jejunum and ileum, with maximal effects after 18 h and extensive recovery after 48 h. To study the molecular pathways leading to enterocyte injury, we isolated villi-enriched mucosal fractions from DCF-treated mice. Immunoblot studies with a phosphospecific JNK antibody revealed that JNK1/2 (p46) was activated at 6 h, leading to phosphorylation of the downstream target c-Jun. The levels of the JNK-regulated proapoptotic transcription factor C/EBP homologous protein (CHOP) were also increased after DCF. The selective JNK inhibitor SP600125 (30 mg/kg ip), given both 1 h before and 1 h after DCF, blocked JNK kinase activity and afforded significant protection against DCF enteropathy. In conclusion, these data demonstrate that the JNK pathway is critically involved in the pathogenesis of DCF-induced enteropathy and suggest a potential application of JNK inhibitors in the prevention of NSAID-induced enteropathy.

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Basina, Olesja, Jelena Derova, Aleksejs Derovs, and Sandra Lejniece. "Iron Deficiency Anaemia and Anaemia of Inflammation in Enteropathies Caused by Commonest Small Intestine Disorders: Current Evidence." Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 76, no. 5-6 (December 1, 2022): 561–68. http://dx.doi.org/10.2478/prolas-2022-0088.

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Abstract It is no mystery that iron deficiency is the most common anaemia and multiple studies have shown that anaemia is a main factor for decreased quality of life. The focus of our article is an up-to-date review of different enteropathies caused by specific disorders and the prevalence of iron deficiency anaemia (IDA), starting with the understanding of physiology of iron absorption and regulation in the intestine. The pathologies that we tried to cover were celiac disease, Crohn’s disease, nonsteroidal anti-inflammatory drugs (NSAID)-induced enteropathy and protein losing enteropathy. Unfortunately, not everything still understood and questions still remain. The main questions are associated with our understanding of iron regulation beyond the ferroportin-hepcidin axis and what mechanism is behind changes of epithelium in different conditions. Depending on the study and pathology of enteropathy, almost half of the studied patients had iron deficiency anaemia. However, in all enteropathies, IDA is more an additional finding or an additional symptom that needs further investigations. That is why many authors consider that IDA is caused by secondary mechanisms and not enteropathy per se and should be correlating with undernourishment, severe mucosal atrophy, malabsorption, and bleeding.

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Fornai, Matteo, Luca Antonioli, Rocchina Colucci, Carolina Pellegrini, Giulio Giustarini, Lara Testai, Alma Martelli, et al. "NSAID-Induced Enteropathy: Are the Currently Available Selective COX-2 Inhibitors All the Same?" Journal of Pharmacology and Experimental Therapeutics 348, no. 1 (October 17, 2013): 86–95. http://dx.doi.org/10.1124/jpet.113.207118.

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Teutsch, Brigitta, Eszter Boros, Szilárd Váncsa, Alex Váradi, Levente Frim, Szabolcs Kiss, Fanni Dembrovszky, et al. "Mucoprotective drugs can prevent and treat nonsteroidal anti-inflammatory drug-induced small bowel enteropathy: a systematic review and meta-analysis of randomized controlled trials." Therapeutic Advances in Gastroenterology 14 (January 2021): 175628482110387. http://dx.doi.org/10.1177/17562848211038772.

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Background: Small bowel enteropathy (SBE) is a complication of nonsteroidal anti-inflammatory drug (NSAID) therapy occurring in 71% of NSAID users. We aimed to analyse the efficacy and safety of medications to prevent and treat NSAID-induced SBE in randomized controlled trials (RCTs). Methods: This review was registered on PROSPERO (CRD42021223371). We systematically searched four databases until 20 October for comparing mucoprotective (MP), antibiotic and probiotic treatments to placebo, proton-pump inhibitors (PPIs) or histamine-2 (H2) receptor antagonists in NSAID-associated small intestinal injuries. The main outcomes were mucosal integrity, mucosal breaks after treatment, mucosal injury improvement and complete healing of mucosal breaks. Meta-analytical calculations for weighted mean differences (WMDs) and odds ratios (ORs) were performed with the random-effects model and interpreted with 95% confidence intervals (CIs). Results: A total of 18 RCTs were included in the quantitative synthesis. MP medications administered preventively reduced the number of mucosal erosions (WMD = −1.24, CI: −2.15 to −0.34) and lead to a significantly lower chance of developing mucosal breaks after treatment (OR = 0.38, CI: 0.16–0.93). MP therapy was associated with a higher rate of complete healing of mucosal breaks (OR = 5.39, CI: 2.79–10.42). In the qualitative synthesis, there were tendencies for a lower increase in the mean number of mucosal breaks and reddened lesions with prophylactic and a higher decrease in mucosal breaks with therapeutic MP drug administration. Conclusion: MP treatment administered with NSAIDs can prevent and reduce small intestinal mucosal lesions.

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Bielsa-Fernández, M. V., J. L. Tamayo-de la Cuesta, J. Lizárraga-López, J. M. Remes-Troche, R. Carmona-Sánchez, J. M. Aldana-Ledesma, J. M. Avendaño-Reyes, et al. "The Mexican consensus on the diagnosis, treatment, and prevention of NSAID-induced gastropathy and enteropathy." Revista de Gastroenterología de México (English Edition) 85, no. 2 (April 2020): 190–206. http://dx.doi.org/10.1016/j.rgmxen.2019.11.001.

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Battarbee, H. D., M. B. Grisham, G. G. Johnson, and J. H. Zavecz. "Superior mesenteric artery blood flow and indomethacin-induced intestinal injury and inflammation." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 4 (October 1, 1996): G605—G612. http://dx.doi.org/10.1152/ajpgi.1996.271.4.g605.

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Intestinal injury caused by nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with increased mucosal permeability, microvascular injury, focal intravascular thrombus formation, fibrin deposition, and neutrophil infiltration. Ulcerations and adhesions are also prominent feature of this injury. Although NSAID-induced inhibition of prostaglandin formation has been suggested to produce ischemic injury and inflammation, no studies have directly assessed intestinal blood flow in experimental NSAID-induced enteropathy. This study tested the hypothesis that indomethacin-induced small bowel injury and inflammation result from intestinal ischemia. With the use of pulsed Doppler flowmetry, superior mesenteric artery blood flow was continuously monitored in conscious rats after doses of indomethacin known to promote acute and then chronic small bowel inflammation (7.5 mg/kg, 2 sc doses spaced 24 h apart). After 72 h, rats were anesthetized and a section of small bowel was removed for histology and intestinal myeloperoxidase activity measurements. Mean arterial blood pressure was not affected until 32 h after indomethacin, when it decreased 20% (P < 0.05) to P < 0.01). Sustained blood flow changes first occurred at 20 h, when an increase of 15% (P < 0.01) was observed, whereas flow resistance decreased. Flow resistance continued to decrease for the remainder of the 72-h period, and there was an accompanying blood flow increase to +40% (P < 0.05 to P < 0.01). Intestinal ulcers developed in 86% of indomethacin-treated rats. Adhesions, dilation, and thickening of the distal jejunum and proximal ileum were observed in most indomethacin-treated rats. Histological grading of intestinal injury yielded scores of 7.1 +/- 1.2 and zero for indomethacin-treated and vehicle-injected rats, respectively (P < 0.01). Myeloperoxidase activity was greater in indomethacin-treated rats (6.7 +/- 1.9 vs. 1.8 +/- 0.3 U/cm, P < 0.05). These results suggest that indomethacin-induced enteropathy is associated with an increase, not a decrease, in superior mesenteric artery blood flow. Therefore, ischemia dose not appear to be a mechanism by which subcutaneous indomethacin administration produces small intestinal injury and inflammation.

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&NA;. "Patients with NSAID-induced enteropathy can be identified by a simple, non-invasive, single stool assay." Reactions Weekly &NA;, no. 772 (October 1999): 4. http://dx.doi.org/10.2165/00128415-199907720-00007.

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Syer, Stephanie D., Webb McKnight, Anne Aucouturier, Rebeca Martin, Philippe Langella, and John L. Wallace. "Su1724 Bifidobacteria Exert a Protective Effect Against NSAID-Induced Enteropathy That is Dependent on Lactate Production." Gastroenterology 142, no. 5 (May 2012): S—489. http://dx.doi.org/10.1016/s0016-5085(12)61867-8.

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Fujimori, Shunji, Koya Fukunaga, Atsushi Takahashi, Taisei Mushiroda, Michiaki Kubo, Ryuzo Hanada, Mari Hayashida, Toshiyuki Sakurai, Katsuhiko Iwakiri, and Choitsu Sakamoto. "Bactericidal/Permeability-Increasing Fold-Containing Family B Member 4 May Be Associated with NSAID-Induced Enteropathy." Digestive Diseases and Sciences 64, no. 2 (October 30, 2018): 401–8. http://dx.doi.org/10.1007/s10620-018-5349-0.

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Sulaieva, O. N., and J. L. Wallace. "Trends in development of gi-safe anti-inflammatory drugs." Clinical Medicine (Russian Journal) 95, no. 3 (May 10, 2017): 222–27. http://dx.doi.org/10.18821/0023-2149-2017-95-3-222-227.

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Despite the introduction of anti-inflammatory drugs that selectively inhibit cyclo-oxygenase-2 (COX-2), and potent inhibitors of gastric acid secretion, the gastrointestinal adverse effects of non-steroidal anti-inflammatory drugs (NSAIDs) remain a significant clinical problem. Combined use of antisecretory drugs and COX-2 inhibitors is helpful to limit the damage in the proximal gastrointestinal tract (stomach and duodenum), but it increases the risk of injury of small intestine and colon. It was proven that proton pump inhibitors and H2 receptor antagonists significantly worsen NSAID-induced small intestinal damage and microbiota balance. Nowadays, there is no proven effective preventative or curative treatment for NSAID-induced enteropathy. The new strategy of gastrointestinal protection is based on the discovery of endogenous cytoprotective molecules such as hydrogen sulfide (H2S). H2S is a gaseous mediator that produces strong cytoprotective and antioxidant effect on the gastrointestinal tract. The role of H2S in promoting mucosal integrity, healing of tissue injury and resolution of inflammation has been well documented. In addition, H2S stimulates productions of other cytoprotective molecules including prostaglandins, carbon monoxide and nitric oxide. Nowadays, the new generation of H2S-releasing non-steroidal anti-inflammatory drugs is developed and tested in clinical trials. H2S-NSAIDs possess enhanced anti-inflammatory activity and high gastrointestinal safety.

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Herstad, Kristin M. V., Hilde Vinje, Ellen Skancke, Terese Næverdal, Francisca Corral, Ann-Katrin Llarena, Romy M. Heilmann, Jan S. Suchodolski, Joerg M. Steiner, and Nicole Frost Nyquist. "Effects of Canine-Obtained Lactic-Acid Bacteria on the Fecal Microbiota and Inflammatory Markers in Dogs Receiving Non-Steroidal Anti-Inflammatory Treatment." Animals 12, no. 19 (September 21, 2022): 2519. http://dx.doi.org/10.3390/ani12192519.

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Non-steroidal anti-inflammatory drugs (NSAIDs) may cause enteropathy in dogs and probiotics may be one option to prevent this. The objective of this study was to determine whether the administration of canine-obtained lactic acid bacteria (LAB) has an effect on the frequency of diarrhea, the composition of the fecal microbiota, and/or markers of gastrointestinal inflammation in dogs receiving NSAIDs when compared to dogs given NSAIDs and a placebo. A total of 22 dogs treated with NSAIDs for various clinical indications were enrolled in a seven-day randomized, double-blinded placebo-controlled interventional study. Dogs were randomized to receive either placebo or LAB, a product containing Limosilactobacillus fermentum, Lacticaseibacillus rhamnosus, and Lactiplantibacillus plantarum. Fecal samples were collected on days one and seven. The fecal microbiota was evaluated using the fecal dysbiosis index (DI) and individual bacterial taxa. Fecal calprotectin (CP) and S100A12/Calgranulin C concentrations were used as markers of gastrointestinal inflammation. There was a difference in frequency of diarrhea between groups, with it affecting 4/12 dogs (33%) in the placebo group and 1/10 dogs (10%) in the LAB group, but this difference did not reach statistical significance (p = 0.32). There was a correlation between S100A12 and CP (p < 0.001), and Clostridium perfringens correlated with S100A12 (p < 0.015). Neither treatment significantly affected S100A12 (p = 0.37), CP (p = 0.12), or fecal DI (p = 0.65). This study suggests that LAB is a safe supplement to use for short-term treatment in NSAID-treated dogs, but further studies are needed to determine its potential to prevent NSAID-induced enteropathy in dogs.

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Bibik, E. Yu, A. V. Myazina, K. A. Frolov, V. V. Dotsenko, and S. G. Krivokolysko. "Influence of new 1,4‑dihydrothiopyridine derivatives with analgesic activity on the gastric mucosa." Glavvrač (Chief Medical Officer), no. 7 (July 1, 2022): 9–11. http://dx.doi.org/10.33920/med-03-2207-01.

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In clinical practice, such a side effect as gastrotoxicity can occur in patients taking NSAIDs with any route of administration. In this case, damage not only to the upper parts of the digestive tract, but also to the intestine as a whole is noted, since NSAID-induced enteropathy is manifested by a breach in the intestinal permeability with protein exudation and diapedesis of erythrocytes, as well as by the damage with the development of erosions, ulcers and life-threatening complications: bleeding, perforation, intestinal obstruction, the occurrence of circular structures [1]. The purpose of the study: to investigate the morphofunctional state of the stomach after exposure to non-steroidal anti-inflammatory drugs and new heterocyclic compounds synthesized by us with previously proven high analgesic activity in white rats.

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Oh, Dong Jun, Hyuk Yoon, Hyun Soo Kim, Yoon Jin Choi, Cheol Min Shin, Young Soo Park, Nayoung Kim, et al. "The effect of rebamipide on non-steroidal anti-inflammatory drug-induced gastro-enteropathy: a multi-center, randomized pilot study." Korean Journal of Internal Medicine 37, no. 6 (November 1, 2022): 1153–66. http://dx.doi.org/10.3904/kjim.2021.216.

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Background/Aims: Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly-used medications, and ailments such as arthritis or heart disease, require long-term use of these drugs, which can induce gastroenteropathy with bleeding and ulcers. This study investigated the associations between efficacy, safety, and gastrointestinal symptoms linked to rebamipide and proton pump inhibitor administration in patients requiring long-term NSAID use.Methods: This study was a multi-center, randomized, open-labeled, pilot design.Results: Thirty-three patients were included. Of these, 15 were included in the study group and 18 were in the control group. NSAID-induced gastric ulcers, which were the primary outcome of this study, did not occur in either the study or control group. Changes in the number of small bowel erosions and ulcers were –0.6 ± 3.06 in the study group and 1.33 ± 4.71 in the control group. The number of subjects with mucosal breaks (defined as multiple erosions and/or ulcers) was three (20%) in the study group and six (40%) in the control group (<i>p</i> = 0.427). No serious adverse events occurred in either group. However, dyspepsia and skin rashes occurred in six patients (31.58%) in the study group and 13 (65%) in the control group (<i>p</i> = 0.036).Conclusions: Although statistically significant differences were not generated, possibly as a result of the small sample size, mucosal breaks observed via capsule endoscopy revealed that rebamipide was likely to be more effective than lansoprazole in preventing small intestine damage caused by NSAIDs. Furthermore, fewer side-effects emerged with rebamipide.

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Bibik, E. Yu, A. V. Myazina, K. A. Frolov, V. V. Dotsenko, and S. G. Krivokolysko. "Impact of new 1,4‑dihydrothiopyridine derivatives with analgesic activity on gastric mucosa." Glavvrač (Chief Medical Officer), no. 9 (August 31, 2022): 16–18. http://dx.doi.org/10.33920/med-03-2209-04.

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In clinical practice, the occurrence of such a side effect as gastrotoxicity can occur in patients taking NSAIDs with any route of administration. In this case, damage not only to the upper parts of the digestive tract is noted, but also to the intestine as a whole, since NSAID-induced enteropathy is manifested by the intestinal permeability disorder with protein exudation and diapedesis of erythrocytes, as well as by the development of erosions, ulcers, and life-threatening complications: bleeding, perforation, intestinal obstruction, and the appearance of circular folds [1]. The purpose of the study: to investigate the morphofunctional state of the stomach after exposure to non-steroidal anti-inflammatory drugs and novel heterocyclic compounds synthesized by us which have been proven to have high analgesic activity in white rats.

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Said, Hyder, Yasutada Akiba, Kazuyuki Narimatsu, Koji Maruta, Ayaka Kuri, Ken-ichi Iwamoto, Atsukazu Kuwahara, and Jonathan D. Kaunitz. "FFA3 Activation Stimulates Duodenal Bicarbonate Secretion and Prevents NSAID-Induced Enteropathy via the GLP-2 Pathway in Rats." Digestive Diseases and Sciences 62, no. 8 (May 18, 2017): 1944–52. http://dx.doi.org/10.1007/s10620-017-4600-4.

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Peters, Timothy J., and Ingvar Bjarnason. "Uses and Abuses of Intestinal Permeability Measurements." Canadian Journal of Gastroenterology 2, no. 3 (1988): 127–32. http://dx.doi.org/10.1155/1988/867416.

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Intestinal permeability has been assessed with three different classes of permeability probes, viz various sugar mixtures,51Cr-EDTA and poly(ethylene glycol). The former two methods are having increasing clinical applications in the screening and assessment of small intestinal damage and51Cr-EDTA is now the preferred probe for routine clinical use. Poly(ethylene glycol)s have numerous disadvantages and are not recommended. Probes may be used both in vitro and in vivo and have been applied to a wide variety of clinical problems. In particular, NSAID induced enteropathy, a major complication of the chronic administration of these widely-used drugs, was recognized for the first time with51Cr-EDTA permeability measurements. The cytoprotective role of various prostanoids was also clearly demonstrated using51Cr-EDTA. It is anticipated that measurement of intestinal permeability will play an increasing role in clinical and research investigation and in the monitoring of intestinal disease.

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Sidhu, Reena, Ramesh P. Arasaradnam, Mark E. McAlindon, Kapil Kapur, Andrew D. Hopper, S. Jalil, and David S. Sanders. "Endoscopic Terminal Ileum Biopsies—Is Nonsteroidal Anti-Inflammatory Drug (NSAID) Induced Enteropathy Responsible for Some of the Macroscopic Abnormalities?" American Journal of Gastroenterology 102, no. 11 (November 2007): 2610–11. http://dx.doi.org/10.1111/j.1572-0241.2007.01514_10.x.

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Amagase, Kikuko, Akimu Ochi, Azusa Kojo, Ami Mizunoe, Masaya Taue, Naoya Kinoshita, Eiji Nakamura, and Koji Takeuchi. "New Therapeutic Strategy for Amino Acid Medicine: Prophylactic and Healing Promoting Effect of Monosodium Glutamate Against NSAID-Induced Enteropathy." Journal of Pharmacological Sciences 118, no. 2 (2012): 131–37. http://dx.doi.org/10.1254/jphs.11r03fm.

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Schoultz, Ida, Catherine M. McKay, Rabea Graepel, Van C. Phan, Arthur Wang, Johan Söderholm, and Derek M. McKay. "Indomethacin-induced translocation of bacteria across enteric epithelia is reactive oxygen species-dependent and reduced by vitamin C." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 5 (September 1, 2012): G536—G545. http://dx.doi.org/10.1152/ajpgi.00125.2012.

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Abstract:

The enteric epithelium must absorb nutrients and water and act as a barrier to the entry of luminal material into the body; this barrier function is a key component of innate immunity. Nonsteroidal anti-inflammatory drug (NSAID)-induced enteropathy occurs via inhibition of prostaglandin synthesis and perturbed epithelial mitochondrial activity. Here, the direct effect of NSAIDs [indomethacin, piroxicam (cyclooxygenase 1 and 2 inhibitors), and SC-560 (a cyclooxygenase 1 inhibitor)] on the barrier function of human T84 epithelial cell line monolayers was assessed by transepithelial electrical resistance (TER) and internalization and translocation of a commensal Escherichia coli . Exposure to E. coli in the presence and absence of drugs for 16 h reduced TER; however, monolayers cotreated with E. coli and indomethacin, but not piroxicam or SC-560, displayed significant increases in internalization and translocation of the bacteria. This was accompanied by increased reactive oxygen species (ROS) production, which was also increased in epithelia treated with E. coli only. Colocalization revealed upregulation of superoxide synthesis by mitochondria in epithelia treated with E. coli + indomethacin. Addition of antioxidants (vitamin C or a green tea polyphenol, epigallocathechin gallate) quenched the ROS and prevented the increase in E. coli internalization and translocation evoked by indomethacin, but not the drop in TER. Evidence of increased apoptosis was not observed in this model. The data implicate epithelial-derived ROS in indomethacin-induced barrier dysfunction and show that a portion of the bacteria likely cross the epithelium via a transcellular pathway. We speculate that addition of antioxidants as dietary supplements to NSAID treatment regimens would reduce the magnitude of decreased barrier function, specifically the transepithelial passage of bacteria.

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Journal articles on the topic 'NSAID-induced enteropathy'

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