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Efficacy and tolerability of naproxen/esomeprazole magnesium tablets compared with non-specific NSAIDs and COX-2 inhibitors: a systematic review and network analyses
Datto C, Hellmund R, Siddiqui MK
Open Access Rheumatology: Research and Reviews , 2013, DOI: http://dx.doi.org/10.2147/OARRR.S41420
Abstract: acy and tolerability of naproxen/esomeprazole magnesium tablets compared with non-specific NSAIDs and COX-2 inhibitors: a systematic review and network analyses Original Research (533) Total Article Views Authors: Datto C, Hellmund R, Siddiqui MK Published Date February 2013 Volume 2013:5 Pages 1 - 19 DOI: http://dx.doi.org/10.2147/OARRR.S41420 Received: 11 December 2012 Accepted: 14 January 2013 Published: 27 February 2013 Catherine Datto,1 Richard Hellmund,1 Mohd Kashif Siddiqui2 1AstraZeneca Pharmaceuticals LP, Wilmington, DE, USA; 2HERON PVT India, Chandigarh, UT, India Abstract: Non-steroidal anti-inflammatory drugs (NSAIDs), such as non-selective NSAIDs (nsNSAIDs) or selective cyclooxygenase-2 (COX-2) inhibitors, are commonly prescribed for arthritic pain relief in patients with osteoarthritis (OA), rheumatoid arthritis (RA), or ankylosing spondylitis (AS). Treatment guidelines for chronic NSAID therapy include the consideration for gastroprotection for those at risk of gastric ulcers (GUs) associated with the chronic NSAID therapy. The United States Food and Drug Administration has approved naproxen/esomeprazole magnesium tablets for the relief of signs and symptoms of OA, RA, and AS, and to decrease the risk of developing GUs in patients at risk of developing NSAID-associated GUs. The European Medical Association has approved this therapy for the symptomatic treatment of OA, RA, and AS in patients who are at risk of developing NSAID-associated GUs and/or duodenal ulcers, for whom treatment with lower doses of naproxen or other NSAIDs is not considered sufficient. Naproxen/esomeprazole magnesium tablets have been compared with naproxen and celecoxib for these indications in head-to-head trials. This systematic literature review and network meta-analyses of data from randomized controlled trials was performed to compare naproxen/esomeprazole magnesium tablets with a number of additional relevant comparators. For this study, an original review examined MEDLINE , Embase , and the Cochrane Controlled Trials Register from database start to April 14, 2009. Using the same methodology, a review update was conducted to December 21, 2009. The systematic review and network analyses showed naproxen/esomeprazole magnesium tablets have an improved upper gastrointestinal tolerability profile (dyspepsia and gastric or gastroduodenal ulcers) over several active comparators (naproxen, ibuprofen, diclofenac, ketoprofen, etoricoxib, and fixed-dose diclofenac sodium plus misoprostol), and are equally effective as all active comparators in treating arthritic symptoms in patients with OA, RA, and AS. Naproxen/esomeprazole magnesium tablets are therefore a valuable option for treating arthritic symptoms in eligible patients with OA, RA, and AS.
Efficacy and tolerability of naproxen/esomeprazole magnesium tablets compared with non-specific NSAIDs and COX-2 inhibitors: a systematic review and network analyses
Datto C,Hellmund R,Siddiqui MK
Open Access Rheumatology: Research and Reviews , 2013,
Abstract: Catherine Datto,1 Richard Hellmund,1 Mohd Kashif Siddiqui21AstraZeneca Pharmaceuticals LP, Wilmington, DE, USA; 2HERON PVT India, Chandigarh, UT, IndiaAbstract: Non-steroidal anti-inflammatory drugs (NSAIDs), such as non-selective NSAIDs (nsNSAIDs) or selective cyclooxygenase-2 (COX-2) inhibitors, are commonly prescribed for arthritic pain relief in patients with osteoarthritis (OA), rheumatoid arthritis (RA), or ankylosing spondylitis (AS). Treatment guidelines for chronic NSAID therapy include the consideration for gastroprotection for those at risk of gastric ulcers (GUs) associated with the chronic NSAID therapy. The United States Food and Drug Administration has approved naproxen/esomeprazole magnesium tablets for the relief of signs and symptoms of OA, RA, and AS, and to decrease the risk of developing GUs in patients at risk of developing NSAID-associated GUs. The European Medical Association has approved this therapy for the symptomatic treatment of OA, RA, and AS in patients who are at risk of developing NSAID-associated GUs and/or duodenal ulcers, for whom treatment with lower doses of naproxen or other NSAIDs is not considered sufficient. Naproxen/esomeprazole magnesium tablets have been compared with naproxen and celecoxib for these indications in head-to-head trials. This systematic literature review and network meta-analyses of data from randomized controlled trials was performed to compare naproxen/esomeprazole magnesium tablets with a number of additional relevant comparators. For this study, an original review examined MEDLINE , Embase , and the Cochrane Controlled Trials Register from database start to April 14, 2009. Using the same methodology, a review update was conducted to December 21, 2009. The systematic review and network analyses showed naproxen/esomeprazole magnesium tablets have an improved upper gastrointestinal tolerability profile (dyspepsia and gastric or gastroduodenal ulcers) over several active comparators (naproxen, ibuprofen, diclofenac, ketoprofen, etoricoxib, and fixed-dose diclofenac sodium plus misoprostol), and are equally effective as all active comparators in treating arthritic symptoms in patients with OA, RA, and AS. Naproxen/esomeprazole magnesium tablets are therefore a valuable option for treating arthritic symptoms in eligible patients with OA, RA, and AS.Keywords: non-steroidal anti-inflammatory drug, proton pump inhibitor, upper gastrointestinal tolerability, arthritis
Nonsteroidal anti-inflammatory drugs (NSAIDs), cyxlooxygenase-2 selective inhibitors (coxibs) and gastrointestinal harm: review of clinical trials and clinical practice
R Andrew Moore, Sheena Derry, Ceri J Phillips, Henry J McQuay
BMC Musculoskeletal Disorders , 2006, DOI: 10.1186/1471-2474-7-79
Abstract: We used a series of systematic literature searches to find full publications of relevant studies for evidence about the efficacy of these different gastroprotection strategies in clinical trials, and for evidence that they worked and were adhered to in clinical practice – whether they were effective. We chose to use good quality systematic reviews and meta-analyses when they were available.Evidence of efficacy of coxibs compared to NSAIDs for upper gastrointestinal bleeding was strong, with consistent reductions in events of about 50% in large randomised trials (34,460 patients), meta-analyses of randomised trials (52,474 patients), and large observational studies in clinical practice (3,093 bleeding events). Evidence on the efficacy of NSAID plus gastroprotection with acid suppressants (proton pump inhibitors, PPIs, and histamine antagonists, H2As) was based mainly on the surrogate measure of endoscopic ulcers. The limited information on damage to the bowel suggested that NSAID plus PPI was more damaging than coxibs.Eleven observational studies studied 1.6 million patients, of whom 911,000 were NSAID users, and showed that 76% (range 65% to 90%) of patients with at least one gastrointestinal risk factor received no prescription for gastroprotective agent with an NSAID. The exception was a cohort of US veterans with previous gastrointestinal bleeding, where 75% had gastroprotection with an NSAID. When gastroprotection was prescribed, it was often described as inadequate. A single study suggested that patient adherence to prescribed gastroprotection was low.Evidence for efficacy of gastroprotection strategies with NSAIDs is limited. In clinical practice few patients who need gastroprotection get it, and those who get it may not take it. For coxibs, gastroprotection is inherent, although probably not complete.Chronic pain affects one adult in five in Europe [1], limits functioning, and is an enormous problem for healthcare. Osteoarthritis, rheumatoid arthritis, and ba
Cardiovascular and gastrointestinal effects of COX-2 inhibitors and NSAIDs: achieving a balance
Jeffrey S Borer, Lee S Simon
Arthritis Research & Therapy , 2005, DOI: 10.1186/ar1794
Abstract: Conventional nonsteroidal anti-inflammatory drugs (NSAIDs; relatively nonselective in their inhibition of cyclo-oxygenase [COX]-1 and COX-2) are widely used for the treatment of pain and inflammation. However, the deleterious gastrointestinal effects potentially associated with their use can be a cause for concern, accounting for approximately 21% of adverse drug reactions reported in the USA [1]. Studies of the COX-2 selective agents (COX-2 inhibitors) have demonstrated that they are associated with a significantly reduced risk for upper and lower gastrointestinal complications compared with conventional NSAIDs, although recent evidence indicates that this effect is partially or totally ameliorated in patients who are receiving concomitant aspirin. Furthermore, recent evidence suggests that at least some of the COX-2 inhibitors are associated with cardiovascular adverse effects at certain doses; fewer relevant data are available for conventional NSAIDs (generally studied many years ago), although accumulating information suggests that at least some of these also increase risk for cardiovascular events.In clinical practice, patients who require NSAID or COX-2 inhibitor therapy most frequently are those at the highest risk for cardiovascular events and are also likely to be taking prophylactic low dose aspirin. Given the interaction between certain NSAIDs, COX-2 inhibitors, and aspirin, balancing the benefits and risks of each of these agents is of considerable importance. This article summarizes the effects of aspirin, nonaspirin NSAIDs, and COX-2 inhibitors on the gastrointestinal tract and cardiovascular system that must be considered when making treatment decisions in patients who require these therapies.The gastrointestinal adverse effects of aspirin and traditional NSAIDs are well known. Clinically important NSAID related events, such as bleeding, result in more than 100,000 hospitalizations and up to 16,500 excess gastrointestinal event related deaths each yea
Practical approaches to minimizing gastrointestinal and cardiovascular safety concerns with COX-2 inhibitors and NSAIDs
James M Scheiman, A Mark Fendrick
Arthritis Research & Therapy , 2005, DOI: 10.1186/ar1795
Abstract: Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most prescribed classes of medications worldwide, with over 111 million prescriptions written between September 1999 and August 2000 [1]. In addition, more than 30 billion over-the-counter (OTC) NSAID tablets are purchased annually. NSAID use is common in all age groups, with most frequent use among the elderly, of whom nearly 70% take NSAIDs at least weekly.The NSAIDs are highly effective in treating the pain and inflammation associated with osteoarthritis (OA) and rheumatoid arthritis (RA), but it is well recognized that these agents are associated with an increased risk for upper gastrointestinal toxicity, ranging from dyspepsia to gastroduodenal ulcers and bleeding. Although only a small proportion of patients who use these agents develops gastrointestinal complications, the widespread use of these agents magnifies the frequency into a large absolute number of clinical gastrointestinal events. Individually and together, NSAID related adverse events have an important impact on medical outcomes, patient quality of life, and health care costs.Treatment guidelines suggest that patients with one or more risk factors for NSAID associated upper gastrointestinal tract ulcer complications should be prescribed preventive treatment. Despite these recommendations, gastroprotective strategies (e.g. acid suppressive drugs, misoprostol, or selective cyclo-oxygenase [COX]-2 inhibitors) appear to be under-utilized in patients who receive NSAIDs. A retrospective observational cohort study conducted in The Netherlands [2], using data from early 1996 to mid-2002, found that only 7.9% of NSAID users during this time period received a preventive therapy. Of these, 6.6% received gastroprotective agents, and an additional 1.3% received COX-2 inhibitors. A greater percentage of patients with one or two risk factors for upper gastrointestinal injury received gastroprotective drugs, but well over 80% of these patients were provid
Comparative antiplatelet activity of COX1 NSAIDS versus aspirin, encompassing regimen simplification and gastroprotection: a call for a controlled study  [cached]
B. Rothschild
Reumatismo , 2011, DOI: 10.4081/reumatismo.2004.89
Abstract: The cardioprotective/platelet inhibitory role of non-steroidal antiinflammatory drugs (NSAIDs) has been controversial, perhaps in contrast to the accepted prophylactic role of aspirin (114). That cardioprotective effect is attributed to the platelet aggregation inhibitory effects of aspirin and COX 1 active NSAIDS (10, 11, 13) and can be studied without requirement for massive numbers of patients. Such cardioprotection, however, has its own risks. Significant gastrointestinal toxicity is still present with the 75-81 mg aspirin dose and appears no less than that found with the higher doses once routinely utilized in treatment of arthritis (2, 8, 9). One study even reported that 4% of patients receiving aspirin had moderate to severe bleeding (14). The challenge with aspirin is that even with a 75 mg dose, the frequency of severe gastrointestinal hemorrhage is double that of placebo (2, 8, 9) and not different from that observed with COX 1 NSAIDs, in the abse
Comparison of CD63 Upregulation Induced by NSAIDs on Basophils and Monocytes in Patients with NSAID Hypersensitivity  [PDF]
N. Abuaf,H. Rostane,J. Barbara,C. Toly-Ndour,H. Gaouar,P. Mathelier-Fusade,F. Leynadier,C. Francès,R. Girot
Journal of Allergy , 2012, DOI: 10.1155/2012/580873
Abstract: Background. An in vitro basophil activation test, based on the detection of CD63 upregulation induced by NSAIDs, has been described. Its clinical significance remains controversial. Objectives. In patients with a history of nonallergic NSAID hypersensitivity, stratified according to the severity of the symptoms, to assess with NSAIDs the predictive value of basophil (BAT) and monocyte (MAT) activation tests. Patients/Methods. Sixty patients who had NSAIDs-induced or exacerbated urticaria/angiooedema and 20 controls was included. After incubation with NSAIDs or acetaminophen, leukocytes were analysed for CD63 upregulation. Results. With aspirin, the sensitivity (37%) and specificity (90%) of BAT agree with already published results. In contrast, when patients had had cutaneous and visceral reactions, the frequency of positive BAT 14/22 (64%, ) or MAT 10/22 (46%, ) were increased. Conclusions. Positive tests were more frequent among patients having a severe hypersensitivity contrasting with the other patients who had results similar to controls. 1. Introduction Nonsteroidal anti-inflammatory drugs (NSAIDs) are after antibiotics, the second most frequently suspected agents causing drug hypersensitivity. The prevalence of acetyl salicylic acid (ASA, aspirin) hypersensitivity ranges from 0.6% to 2.5% in the general population, from 4.3% to 11% in asthmatic patients [1], and from 20 to 40% in chronic idiopathic urticaria (CIU) [2]. It also occurs in subjects with no known underlying disease, otherwise normal when they abstain from taking NSAID. Hypersensitivity may occur shortly, within 15 minutes or longer, up to 24 hours after NSAID intake. In general it develops within 1 to 4 hours [3]. Some patients might have life-threatening reactions, especially those with aspirin-exacerbated respiratory diseases (AERDs, Widal syndrome), which associate aspirin sensitivity, asthma, nasal polyposis, and airway remodelling [1]. In most patients the adverse reaction is nonallergic. Those with eicosanoid metabolism dysfunction or other alterations are prone to hypersensitivity when NSAIDs inhibit the enzyme cylooxygenase-1 (Cox-1) [3–14]. Selective NSAIDs strongly inhibit COX-2, but they are weak inhibitors of COX-1, so they are well tolerated in patients with NSAID-sensitive asthma or CIU [4, 5]. The concentration inhibiting efficiently COX-1 or COX-2 may differ as much as 3 logs between the strongest and weakest inhibitors (Table 1) [15–17]. Pharmacological profiles as well as hypersensitivity depend on their inhibitory activities. Table 1: Comparison of NSAIDs and
Balancing the gastrointestinal benefits and risks of nonselective NSAIDs
David A Peura, Lawrence Goldkind
Arthritis Research & Therapy , 2005, DOI: 10.1186/ar1793
Abstract: Gastrointestinal complications are strongly associated with the use of conventional nonsteroidal anti-inflammatory drugs (NSAIDs) and are recognized as the most prevalent and severe cause of drug toxicity in the USA [1]. Millions of patients use NSAIDs for the relief of various types of arthritis pain, stiffness, and related symptoms. Selective NSAIDs such as cyclo-oxygenase (COX)-2 inhibitors were first introduced with the purpose of providing symptomatic pain relief along with lesser gastrointestinal risk. Recent studies indicated that COX-2 inhibitors were prescribed more often than NSAIDs in patients who are older, sicker, and have risk factors associated with NSAID gastropathy [2].However, rofecoxib (Vioxx?; Merck & Co., Inc., Whitehouse Station, NJ, USA) was voluntarily withdrawn in September 2004; valdecoxib (Bextra?; Pfizer, Inc., New York, NY, USA) was withdrawn and a 'black box' warning was added for celecoxib (Celebrex?; Pfizer, Inc., New York, NY, USA) in April 2005; and a joint hearing of the US Food and Drug Administration Arthritis Committee and the Drug Safety and Risk Management Committee found that the use of COX-2 inhibitors is associated with increased risk for cardiovascular events [3]. These recent events have led many physicians to consider the use of traditional NSAIDs in combination with a proton pump inhibitor (PPI) to reduce the gastrointestinal side effects of NSAIDs. Indeed, major treatment guidelines recommend PPI prophylaxis in patients with a previous gastrointestinal event and in those at high risk for complications [4].NSAID-induced gastrointestinal complaints are among the most commonly reported adverse events. Balancing these benefits and risks is an important clinical goal in the post-Vioxx and post-Bextra era. Reducing the risk for gastrointestinal complications requires a thorough understanding of potential complications and underlying predisposing risk factors, which is a particularly important consideration in light of the fa
Molecular Mechanism for Various Pharmacological Activities of NSAIDS  [PDF]
Tohru Mizushima
Pharmaceuticals , 2010, DOI: 10.3390/ph3051614
Abstract: The anti-inflammatory action of non-steroidal anti-inflammatory drugs (NSAIDs) is mediated through their inhibitory effects on cyclooxygenase (COX) activity. On the other hand, NSAID use is often associated with gastrointestinal complications. The inhibition of COX by NSAIDs is not the sole explanation for the gastrointestinal side effects of NSAIDs. Furthermore, recent epidemiological studies have revealed that prolonged NSAID use reduces the risk of cancer and Alzheimer’s disease (AD) and a COX-independent unknown mechanism is suggested to be involved in these activities of NSAIDs. In this article, I review our recent work on the COX-independent mechanism involved in NSAID-induced gastric lesions and anti-tumor and anti-AD activities of NSAIDs. Using DNA microarray analysis, we found that NSAIDs affect expression of various genes in a COX-independent manner. We found that membrane permeabilization activity of NSAIDs and resulting NSAID-induced apoptosis are involved in NSAID-induced gastric lesions. On the other hand, induction of expression of tight junction-related genes and endoplasmic reticulum chaperones were suggested to be involved in anti-tumor and anti-AD, respectively, activities of NSAIDs. These results suggest that NSAIDs affect expression of various genes in a COX-independent manner, which is involved in various pharmacological activities of NSAIDs.
NSAID-Induced Enteropathy in Rheumatoid Arthritis Patients with Chronic Occult Gastrointestinal Bleeding: A Prospective Capsule Endoscopy Study  [PDF]
Ilja Tachecí,Petr Bradna,Tomá? Douda,Drahomíra Ba?tecká,Marcela Kopá?ová,Stanislav Rejchrt,Jan Bure?
Gastroenterology Research and Practice , 2013, DOI: 10.1155/2013/268382
Abstract: 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 with DRKS00004940. 1. Introduction Non-steroidal anti-inflammatory drugs (NSAIDs) are some of the most frequently prescribed medications in clinical practice for their analgesic, antipyretic, and anti-inflammatory effects, especially in rheumatic and other musculoskeletal disorders. The adverse effects of NSAIDs therapy are well recognised and described especially in the gastroduodenal area [1, 2]; however, the prevalence of small intestinal structural or functional abnormalities induced by NSAIDs can be much higher. The first description of NSAID (aspirin)-induced gastropathy identified by endoscopy was presented by Douthwaite and Lintott in 1938 [3]. Small bowel damage due to indomethacin was observed for the first time in humans in the 70s [4]. The complete NSAIDs mechanism of action is not still fully understood, but it is at least partially based on an inhibition of cyclooxygenase (COX) [5]. The pathogenesis of enteropathy was initially thought to be associated with COX-1 inhibition only. However, it has been proven that selective COX-1 inhibition (or absence) does not lead to gastrointestinal lesions, and selective COX-2
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