Nonsteroidal Anti-inflammatory Gastropathy Research Articles

NSAID-induced gastropathy in a comorbid patient in a multidisciplinary hospital

The purpose of this case report is to demonstrate the importance of outpatient management of nonsteroidal anti-inflammatory drugs (NSAIDs) in patients, especially those at risk (elderly patients, alcohol abusers, patients with a history of peptic ulcer disease, patients taking glucocorticoids or anticoagulants) to avoid life-threatening complications. The following clinical case shows the association between gastric and duodenal mucosal barrier disruption and the use of nonsteroidal anti-inflammatory drugs. Methods: a complete blood count, blood biochemistry test, ultrasound, and abdominal radiography. Results. The clinical case describes a patient with coronary heart disease, ischemic cardiomyopathy, hypertension, permanent atrial fibrillation, impaired glucose tolerance, obesity, and a long history of smoking who had been taking 1–2 tablets of Nimesulide per day for a long time without doctor’s prescription; the intake of NSAIDs was not controlled on an outpatient basis. The reason for hospitalization was sharp pain in the epigastrium; the plain abdominal radiography in the emergency room revealed free gas below both domes of the diaphragm, and ultrasound examination of the abdominal cavity showed a level of inhomogeneous free fluid detected in all sloping areas and pneumatosis intestinalis. In this regard, the patient was urgently hospitalized to the department of surgery, where surgical intervention was performed, including upper-middle laparotomy, abdominoscopy, suture repair of the perforated gastric ulcer, and sanitation and drainage of the abdominal cavity. Conclusion. This clinical case draws attention to the problem of NSAID gastropathy in clinical practice. The task of a clinician is to prevent the development of NSAID-induced gastropathy, identify patients with risk factors for NSAID gastropathy at the earliest possible time, and carry out preventive and therapeutic measures. Patient management at the outpatient stage according to the clinical recommendations could have prevented the development of gastrointestinal bleeding associated with NSAID gastropathy.

НПВП-гастропатия — скрытая угроза при лечении боли

INTRODUCTION. NSAID gastropathy is one of the possible negative consequences of taking non-steroidal anti-inflammatory drugs (NSAIDs), characterized by pathological changes in the gastrointestinal tract. The disease is often asymptomatic, which is the reason for its low detectability during outpatient appointments. The risks of developing serious complications from the gastrointestinal tract (ulcers, bleeding, perforations) increase 3-fold already in the first days of NSAID use. Even a short course of NSAID therapy lasting 3–5 days carries a risk of gastrointestinal complications similar to that of long-term treatment. As a consequence, prevention strategies should be implemented regardless of the duration of therapy, especially in patients with more than one risk factor. CONCLUSION. The risks of complications when taking this group of drugs can be significantly reduced by drug prophylaxis in patients with risk factors for the development of NSAID-gastropathy. Proton pump inhibitors are the main means of preventing possible adverse drug reactions of NSAIDs from the upper gastrointestinal tract. Physicians should consider the need for prophylactic use of proton pump inhibitors throughout the duration of NSAID use. Omez® 20 mg has indications for both prevention and treatment of NSAID-associated gastropathy and can be recommended to such patients from the first day of NSAID intake regardless of the course duration of NSAID intake. KEYWORDS: pain, gastroenterology, geriatrics, gastrointestinal bleeding, gastrointestinal tract, proton pump inhibitors, neurology, adverse events, nonsteroidal anti-inflammatory drugs, NSAIDs, NSAID-associated complications, NSAID gastropathies, general surgery, prevention, therapy, risk factor, chronic pain

Efficacy of complementary medicine for nonsteroidal anti-inflammatory drug-induced small intestinal injuries

Nonsteroidal anti-inflammatory drug-induced small bowel injuries (NSIs) have been largely ignored for decades due to the focus on nonsteroidal anti-inflammatory drug gastropathy. With the visualization of the small intestines enabled by video capsule endoscopy, the frequency and severity of NSIs have become more evident. NSIs have a complex pathophysiology, and no effective preventive or treatment options have been proven. Complementary and alternative medicine (CAM) has been used to treat disorders of the small intestine, and more research on its effectiveness for NSIs has been conducted.We reviewed the current evidence and mechanisms of action of CAMs on NSI. Clinical and experimental studies on the effect of CAMs on NSIs were performed using 10 databases.Twenty-two studies (3 clinical and 19 in vivo experimental studies) were included in the final analysis involving 10 kinds of CAMs: bovine colostrum, Orengedokuto (coptis), muscovite, licorice, grape seed, wheat, brown seaweed, Ganoderma lucidum fungus mycelia, Chaenomeles speciosa (sweet) Nakai (muguasantie), and Jinghua Weikang capsule. The mechanisms of CAM include an increase in prostaglandin E2, reparation of the enteric nervous system, inhibition of pro-inflammatory cytokines, reduction of intestinal permeability and enteric bacterial numbers, decrease in oxidative stress, and modulation of small intestinal motility.CAM may be a novel alternative option for treating and preventing NSI, and further studies on human and animal models with relevant comorbidities are warranted.

Нестероидные противовоспалительные средства: современное представление о механизмах повреждения пищеварительного тракта, минусы препаратов патогенетического лечения и перспективы биологической терапии НПВС-индуцированной эзофагогастроэнтероколонопатии

Актуальность. Нестероидные противовоспалительные средства (НПВС) ежедневно применяют более чем 30 млн человек, а их арсенал насчитывает свыше 80 препаратов и около 1000 созданных на их основе лекарственных форм. Они широко используются во многих сферах медицины и являются одной из наиболее клинически значимых групп лекарственных средств. Однако при использовании НПВС достаточно часто могут возникать побочные реакции, наиболее распространенными из них являются повреждения желудочно-кишечного тракта. Цель: охарактеризовать со­временное представление о механизмах повреждения пищеварительного тракта НПВС, оценить недостатки существующих препаратов патогенетического лечения и перспективы биологической терапии НПВС-индуцированной эзофагогастроэнтероколонопатии криоконсервированным экстрактом плаценты человека. Материалы и методы. Проведен анализ работ, опубликованных в 2010–2020 гг., в которых освещались сведения об эпидемиологии, патогенезе, диагностике и тактике лечения поражений пищевода и желудочно-кишечного тракта, индуцированных НПВС, а также биологические свойства криоконсервированного экстракта плаценты человека как средства биологической терапии. Результаты. Лечение НПВС-индуцированной эзофагогастроэнтероколонопатии классически направлено на кислотосупрессивную терапию (ингибиторы протонной помпы, Н2-гистаминоблокаторы и др.), применение гастроцитопротекторов (де-нол, сукральфат и др.) и препаратов, восстанавливающих содержание простагландинов в слизистой оболочке (мизопростол, ребамипид и др.). Однако все указанные группы лекарственных средств недостаточно удовлетворяют клиницистов, поскольку направлены преимущественно на лечение НПВС-гастропатии и имеют побочные эффекты. Новым перспективным направлением повышения безопасности НПВС на сегодняшний день является применение средств биологической терапии, источниками которых выступают микроорганизмы, органы и ткани растительного или животного происхождения, клетки или жидкости (в том числе кровь и плазма) человеческого или животного происхождения и биотехнологические клеточные конструкции. Выводы. Использование НПВС значительно ограничивается присущими им побочными эффектами, наи­более распространенными являются нарушения со стороны желудочно-кишечного тракта. Криоконсервированный экстракт плаценты человека является перспективным средством биологической терапии ульцерогенных повреждений желудочно-кишечного тракта, индуцированных НПВС.

SHORT- AND LONG-TERM EFFECTS OF NSAIDS ON THE GASTROINTESTINAL MUCOSA: COMPLEX ANALYSIS OF BENEFITS AND COMPLICATIONS PREVENTION

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.

Peculiarities of management of patients with NSAID-induced gastropathy. Part II. A case of long-term treatment of elderly patients with comorbid pathology. Emphasis on cytoprotection

The paper present discussion of the risks of adverse events development in elderly patients with comorbid pathology, arising against the background of long‑term use of non‑steroidal anti‑inflammatory drugs (NSAIDs) for the relief of pain and inflammatory articular syndromes in combination with medications of other pharmaceutical groups (in particular acetylsalicylic acid and antiplatelet agents) used to treat concomitant diseases. The NSAIDs‑induced adverse events mostly often develop and have mostly intensive manifestations in the gastroduodenal zone. They are presented as clinical variants of NSAID‑induced gastropathies, including the forms of erosive and ulcerative lesions. When choosing NSAIDs for the treatment of elderly patients, especially with comorbid pathology, it is necessary to analyze risk factors, contributing to the development of adverse events, namely the gender and age of a patient, the presence of peptic ulcer and its complications in the anamnesis, H. pylori infection, the range of drugs taken, doses and duration of taking NSAIDs, their selectivity, combination with other drugs that have similar adverse effects on the mucous membranes of the gastrointestinal tract. Long‑term use of NSAIDs, in addition to undesirable gastrointestinal side effects, can lead to destabilization of arterial hypertension and heart failure, increase the risk of cardiovascular accidents, cause nephro‑ and hepatotoxic effects, hematological complications, allergic skin reactions and bronchospasm, the development of other adverse events. Based on a clinical example, a strategy for the prevention and treatment of NSAID gastropathy is proposed, caused by long‑term use of a combination of drugs that have an unfavorable effect on the gastroduodenal mucosa. The high clinical effectiveness has been demonstrated for the treatment regimen using pantoprazole as a representative of proton pump inhibitors with the longest acid‑suppressive effect and a low potential for adverse drug‑drug interactions in combination with colloidal bismuth subcitrate, which has a pronounced cytoprotective effect on the gastroduodenal mucosa. It can be recommended for elderly patients with comorbid pathology for prevention and treatment of NSAID‑induced gastropathies.

Modern opportunities for treatment and prevention of NSAID-induced enteropathies

Nonsteroidal anti-inflammatory drugs (NSAIDs) are currently actively used in real clinical practice and everyday life with a wide range of pathological conditions and diseases, and are part of the medicinal arsenal of doctors of various specialties. Along with high pharmacotherapeutic efficacy according to the main indications, a whole range of various complications is associated with the use of NSAIDs. Of particular relevance is the negative specific effect of NSAIDs on the mucous membrane of the gastrointestinal tract. The problem of NSAID gastropathy is widely discussed in the literature, which is largely due to the possibilities of its prevention and treatment using proton pump inhibitors. For a long time, much less attention was paid to the issues of NSAID-dependent bowel damage, which may be associated with less instrumental diagnostic capabilities of these lesions and the lack of effective means for their prevention and treatment. The review presented addresses the pathogenesis, clinical features and diagnosis of NSAID enteropathy. Proton pump inhibitors effectively prevent the development of dyspepsia, erosion and ulcers, as well as gastrointestinal bleeding when taking NSAIDs at the level of the upper gastrointestinal tract, but they are ineffective in preventing and treating NSAID enteropathy. A new approach is the use of rebamipide, which has proven its clinical effectiveness in the prevention of NSAID-mediated Lesions in the upper and Lower gastrointestinal tract. Currently, rebamipid is included in the recommendations of the leading specialized communities in Russia and is recommended not only for the prevention and treatment of NSAIDs induced gastrointestinal lesions, but also as part of the complex therapy of peptic ulcer and anti-heLicobacter therapy. The review reviewed studies showing the efficacy and safety of rebamipide for the treatment and prevention of NSAID enteropathy.

NSAID enteropathy

Nonsteroidal anti-inflammatory drugs (NSAIDs) are one of the most commonly used drugs in the world, and their side effects are very high. First of all, these are NSAID gastropathy, but in the long term, 5070% of NSAIDs cause damage to the small intestine (NSAID enteropathy), sometimes with serious consequences. To date, no drugs have been proposed with proven effectiveness to prevent this side effect. Apparently, this is not due to the fully clarified mechanism of pathogenesis. The most promising is the hypothesis of the participation of individual representatives of microflora in the development of enteropathy. Therefore, modulating the intestinal flora with the help of probiotics can be the basic therapeutic strategy for the prevention and treatment of such damage.

Small bowel injuries due to nonsteroidal anti-inflammatory drugs and antiplatelet therapy. Approaches to prevention and treatment

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.

CHRONIC GASTRITIS CLINICAL FEATURES AND STOMACH FUNCTIONAL STATE DURING NONSTEROIDAL ANTI-INFLAMMATORY DRUGS ADMINISTRATION IN PATIENTS WITH OSTEOARTHRITIS

Aim. Determination of chronic gastritis clinical features and stomach functional state during nonsteroidal anti-inflammatory drugs (NSAID) administration in patients with osteoarthritis (OA). Materials and methods. 122 patients with OA and verified chronic gastritis (CG) (50 males and 72 females) aged 42 to 64 years (mean age – 49.65±3.51) were observed. Depending on gastritis morphological form, patients were divided into 2 groups: 54 patients with OA in combination with non-atrophic gastritis (NAG) were included into the group I, 68 patients with OA in combination with atrophic gastritis (AG) – into group II. 40 patients with OA without concomitant gastroduodenal pathology in anamnesis were included into the group III. All patients obtained selective NSAID for OA treatment: Meloxicam 15 mg daily or Nimesulide 200 mg daily. The control group was formed by 20 persons, which were found to be healthy after a complex examination. Stomach acid-forming function was investigated using esophageal pH monitoring. In the gastric contents, which obtained by aspiration, concentration of sialic acids glycoproteins, fucose, and hexosamines was determined. Results. Clinical picture of NSAID gastropathy at NAG characterized by abdominal pain of varying intensity and not associated with eating, but in patients with AG severity and discomfort symptoms dominated over weakly expressed pain syndrome. As a result of NSAID, in the group I dyspepsia developed in 31 (57.4 %), and erosive gastropathy developed in 9 (16.7 %) patients. In the group II, erosive gastropathy and dyspepsia were observed in 15 (22.1%) and in 35 (51.5 %) patients, respectively. In the group III, erosive gastropathy was observed 3.3 times (c2=84.33; р=0.009) and 4.4 times (c2=36.78; р=0.002) less than in groups I and II, respectively. In 25% patients of the group I after NSAID therapy intragastric pH increased from normacid to hyperacid status. In the group II, NSAID administration led to stomach mucosal (SM) protective factors depletion, which was observed in 73.3 % and in 28.6 % of patients with erosive gastropathy and NSAID-associated dyspepsia, respectively. At AG with erosive gastropathy, unlike NAG, several protective factors simultaneous reduction was observed. Coonclusion. In anamnesis, CG factor at selective NSAID administration (Meloxicam and Nimesulide) in relation to OA significantly increases the risk of erosive gastropathy, compared with patients without CG in anamnesis. At OA NSAID administration in patients with NAG led to gastric contents acidification and in patients with AG – to SM protective factors depletion (glycoprotein, fucose, and hexosamine).

REBAMIPIDE: EFFECTIVE DRUG PREVENTION OF NSAID ENTEROPATHY IS POSSIBLE

Prevention of gastrointestinal tract (GIT) complications is the most important element for the rational use of nonsteroidal anti-inflammatory drugs (NSAIDs) and low-dose aspirin (LDA). Proton pump inhibitors (PPIs) have long been the only medication to prevent these complications. However, PPIs are only effective in preventing and treating upper GIT diseases (NSAID gastropathy) rather than small intestinal injury (NSAID enteropathy). Rebamipide has emerged as a novel agent to protect the gastrointestinal mucosa today. The effect of the drug differs from that of PPIs: it is a typical gastroand enteroprotector that enhances the synthesis of endogenous prostaglandins and possesses a significant anti-inflammatory potential. Rebamipide has long been widely used by doctors inJapan,South Korea, andChinaas an effective and safe agent for the treatment of many diseases of the digestive system. There is a strong evidence base for the efficacy of rebamipide in preventing and treating NSAID gastropathy and NSAID enteropathy (including LDA-induced injuries). Controlled studies have found that the drug is not inferior to the classic gastroprotective agent misoprostol, significantly outperforming the latter in its tolerability. This review describes the mechanism of action of rebamipide and main clinical trials of its therapeutic effect in NSAID gastropathy and NSAID enteropathy.

Adherence with proton pump inhibitor therapy, by continuously taking nonsteroidal anti-inflammatory drugs

To estimate the impact of adherence with proton pump inhibitor (PPI) therapy on the incidence of nonsteroidal anti-inflammatory drug (NSAID)-induced gastropathy (NSAID gastropathy) in patients with rheumatoid arthritis (RA). PPI pharmacotherapy adherence was estimated using the Medication Adherence Questionnaire (MAQ) in 92 patients with RA, including 32 patients did not take a PPI and 60 used a PPI. The groups were matched for age, disease duration, and used NSAIDs. All those asked underwent video esophagogastroduodenoscopy. According to the data of MAQ survey, low, moderate, and high adherence subgroups could be identified among the patients treated with a PPI. NSAID gastropathy was detected in 43.8% of the patients taking no PPI, in 50% of those with low PPI treatment adherence, in 12.5% with moderate adherence, and in 4.5% with high adherence. In the patients with low adherence to PPI therapy, NSAID gastropathy was recorded 11 times more frequently than in those with high adherence (c2 = 7.77; p = 0.005). This condition occurred in 28.6% of the patients taking NSAID without preventively using a PPI in the absence of risk factors for NSAID gastropathy. Only 36.7% patients who had been recommended to use a PPI for the prevention of NSAID gastropathy strictly observed their doctor's directions. Low PPI pharmacotherapy adherence may serve as an additional risk factor for NSAID gastropathy in patients in whom preventive antisecretory therapy used in combination with NSAID is indicated.

Prevention and Treatment of NSAID Gastropathy.

Nonsteroidal anti-inflammatory drug (NSAID) treatment will be necessary as part of our therapeutic armamentarium for many years to come. Therefore, safe prescription is mandatory in order to prevent adverse events. In the last two decades, new strategies and new drugs have been developed to reduce NSAID-associated upper gastrointestinal (GI) adverse events. Although the implementation of guidelines into clinical practice takes time, several studies have shown a recent and profound decrease in hospitalizations due to upper GI complications, which has been linked to widespread use of proton pump inhibitors (PPIs), better NSAID prescription, and decreased prevalence of Helicobacter pylori infection. This is encouraging.Safe NSAID prescription should be straightforward since the most relevant aspects are clinical in nature. Before issuing any prescription, three key questions should be considered:1) Is NSAID treatment necessary for this patient?2) What cardiovascular (CV) and GI risk factors does this patient have?3) What is the most suitable NSAID for this patient?GI and CV risk are easy to estimate, and we know that these risks are not the same for all NSAIDs. Selective cyclooxygenase (COX)-2 inhibitors, like celecoxib at usual doses, carry the lowest GI risk and are the best option in patients with moderate/high GI risk without high CV risk. Gastroprotective therapy (PPI as the drug of choice) should be considered if a non-selective NSAID is prescribed. For those at the highest risk, a combination of PPI plus a coxib is the best option. Also, eradication of H. pylori infection in patients with previous peptic ulcer or in NSAID-naïve users must be considered. Naproxen is the best option in patients with high CV risk and low/moderate GI risk.Patients taking aspirin represent a real challenge for treatment, since interaction with frequently prescribed NSAIDs (e.g. ibuprofen/naproxen) may alter its antiplatelet effect, representing a potential clinical problem. Switching treatment (e.g. taking aspirin before NSAID dosing) may not be an alternative since interaction may persist, especially when taking enteric-coated aspirin. Changing NSAID treatment to diclofenac/celecoxib/etoricoxib may also not be an option in patients with high or previous CV event history. Under these circumstances, careful prescription should be considered at the individual patient level.When dyspepsia develops in an NSAID user, PPI co-therapy plus reduction of the NSAID dose or a change in the type of NSAID are valid alternatives, but clinical experience shows that, for some patients, stopping NSAID therapy may be the only option. After a bleeding episode, most patients can be managed with alternative therapy to NSAIDs, but if needed, a coxib plus a PPI and H. pylori eradication is a safe alternative.

Coming to Terms with Nonsteroidal Anti-Inflammatory Drug Gastropathy

Despite well known complications, oral nonsteroidal anti-inflammatory drugs (NSAIDs) remain the most commonly prescribed medications in the US for musculoskeletal disorders such as osteoarthritis. Although there has been a recent focus on the cardiovascular and renal complications associated with these agents, NSAID gastropathy continues to be a particular concern in many patients, especially those at increased risk for serious adverse events, including the elderly. Complicating the diagnosis of NSAID gastropathy is its silent course, which, up to half of the time, is asymptomatic. Several strategies are currently employed by physicians to mitigate the risk of serious gastrointestinal events. These include either addition of a proton pump inhibitor to current nonselective NSAID therapy or the use of a cyclo-oxygenase-2-selective NSAID. Although these agents are effective at mitigating the overall risk of gastrointestinal adverse events, they fail to address NSAID-related cardiovascular and renal risks. Due to their reduced systemic absorption, topical NSAIDs may present a viable option for patients at increased risk for serious NSAID-related adverse events, including gastropathy.

Non-Steroidal Anti-Inflammatory Drugs and Gastroprotection with Proton Pump Inhibitors

Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most commonly prescribed agents for rheumatic disorders such as osteoarthritis (OA), rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Despite the known association between NSAID use and gastropathy, however, only around one-third of patients at risk of NSAID-induced gastrointestinal toxicity receive adequate gastroprotection, and as many as 44% of these patients are non-adherent. We review the co-prescription of proton pump inhibitors (PPIs) for the prevention of NSAID-induced gastropathy, with a particular focus on the first fixed-dose NSAID/PPI formulation: ketoprofen/omeprazole modified-release capsules. The ketoprofen/omeprazole fixed-dose combination is available in doses of 100 mg/20 mg, 150 mg/20 mg or 200 mg/20 mg as a single capsule for once-daily administration. Ketoprofen monotherapy has been shown to be generally equivalent to other NSAIDs when used in the treatment of OA. In RA, ketoprofen has demonstrated equivalent efficacy to diclofenac, indometacin, piroxicam, aceclofenac, phenylbutazone, naproxen and flurbiprofen. Studies comparing ketoprofen with ibuprofen and sulindac in patients with RA have, in general, favoured ketoprofen. Studies in AS have generally reported similar efficacy between ketoprofen and phenylbutazone and pirprofen. Prophylaxis with omeprazole is effective for the prevention of gastroduodenal ulcers, maintenance of remission and alleviation of dyspeptic symptoms in NSAID recipients. Omeprazole is well tolerated, and adverse events are generally gastrointestinal in nature. The fixed-dose combination of ketoprofen and omeprazole has demonstrated bioequivalence to the respective monotherapies. The incidence of digestive symptoms and the need for dose reduction was reported to be lower with the combination than with its components. Ketoprofen/omeprazole modified-release capsules are the first fixed-dose NSAID/PPI formulation to be approved. This formulation ensures compliance with the gastroprotective prophylaxis, as whenever the NSAID is taken, the PPI is co-administered. Additionally, the once-daily formulation has the potential to improve adherence to anti-inflammatory therapy.

NSAID gastropathy and enteropathy: distinct pathogenesis likely necessitates distinct prevention strategies

The mechanisms underlying the ability of nonsteroidal anti-inflammatory drugs (NSAIDs) to cause ulceration in the stomach and proximal duodenum are well understood, and this injury can largely be prevented through suppression of gastric acid secretion (mainly with proton pump inhibitors). In contrast, the pathogenesis of small intestinal injury induced by NSAIDs is less well understood, involving more complex mechanisms than those in the stomach and proximal duodenum. There is clear evidence for important contributions to NSAID enteropathy of enteric bacteria, bile and enterohepatic recirculation of the NSAID. There is no evidence that suppression of gastric acid secretion will reduce the incidence or severity of NSAID enteropathy. Indeed, clinical data suggest little, if any, benefit. Animal studies suggest a significant exacerbation of NSAID enteropathy when proton pump inhibitors are co-administered with the NSAID. This worsening of damage appears to be linked to changes in the number and types of bacteria in the small intestine during proton pump inhibitor therapy. The distinct mechanisms of NSAID-induced injury in the stomach/proximal duodenum versus the more distal small intestine likely dictate distinct strategies for prevention.

How dangerous is prescribing?

Nurse PrescribingVol. 9, No. 9 News AnalysisHow dangerous is prescribing?Steve AinsworthSteve AinsworthSearch for more papers by this authorSteve AinsworthPublished Online:16 Aug 2013https://doi.org/10.12968/npre.2011.9.9.426AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References Pirmohamed et al., 2004 Pirmohamed M, James S, Meakin S et al. (2004) Adverse drug reactions as cause of admission to hospital: Prospective analysis of 18820 patients. BMJ 329: 15–9 Crossref, Google ScholarCompass, 2008 Compass (2008) Adverse drug reactions wastes NHS £2BN reveals Compass. Available at: www.compassonline.org.uk/news/item.asp?n=1551 Google ScholarSingh, 1998 Singh G (1998) Recent considerations in nonsteroidal anti-inflammatory drug gastropathy. Am J Med 105: 31S–38S Crossref, Google Scholar FiguresReferencesRelatedDetails 1 September 2011Volume 9Issue 9ISSN (print): 1479-9189ISSN (online): 2052-2924 Metrics History Published online 16 August 2013 Published in print 1 September 2011 Information© MA Healthcare LimitedPDF download

NSAID GASTROPATHY: CHANGES OVER 12 YEARS

Система комплексной поддержки и сопровождения научного журнала Elpub позволяет запустить двуязычный сайт журнала со встроенной системой электронной редакции в соответствии с лучшими издательскими практиками, а так же предусматривает техническую и методическую поддержку со стороны специалистов НЭИКОН.

AN ASSOCIATION OF THE CLINICAL MANIFESTATIONS OF NSAID GASTROPATHY WITH UPPER GASTROINTESTINAL MOTOR DISORDERS IN PATIENTS WITH RHEUMATOID ARTHRITIS

Система комплексной поддержки и сопровождения научного журнала Elpub позволяет запустить двуязычный сайт журнала со встроенной системой электронной редакции в соответствии с лучшими издательскими практиками, а так же предусматривает техническую и методическую поддержку со стороны специалистов НЭИКОН.

Dyspepsia in Nonsteroidal Anti-inflammatory Drugs Gastropathy

Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) gastropathy is a common complication, which has characteristic symptoms of dyspepsia syndrome. Mostly, it includes epigastric discomfort with bloating and nausea. The aim of this study was to provide evidences that clinical symptoms of dyspepsia are related to macroscopic changes of gastric form in rats, which are expected to be applied in human. Method: The study was conducted in 20 white rats (Rattus norvegicus, Sprague-Dawley strain) at the Department of Pathology and Clinical Reproduction, Bogor Agricultural University between January and December 2008. The rats were divided to treatment group and control group and each group consisted of 10 rats. Acetyl salicylic acid (ASA/aspirin) was administered at 400 mg dose, diluted in distilled water and was given to the treatment group using gastric cannula, once daily for three days period; while the control group had received aquabidest only. Subsequently, necropsies were conducted for both groups, followed by macroscopic observation and measurement of sagittal and transversal diameter. Gastric incisions along the minor curvature were performed in both groups to recognize any macroscopic changes of gastric mucosa. ANOVA test was utilized for data analysis, which was followed by Duncan test when the results were significant. Results: Gastric diameters in treatment group with positive lesion were significantly different from the control group and the treatment group with negative lesion on anthrum/pylorus region, with p < 0.05. Conclusion: Prominent gastric dilatation at anthrum/pylorus region found in the treatment group may become the initial cause and signs of dyspepsia in human. Keywords: NSAID gastropathy, dyspepsia, NSAIDs/aspirin, gastric dilatation