Prevention Of NSAID-induced Ulcers Research Articles

Evaluation of Provider Adherence to Clinical Guidelines for Gastroprotection in Patients at Increased Risk of NSAID Associated GI Bleeding, in Response to Education Intervention

Purpose: To evaluate provider adherence with ACG guidelines for gastroprotection (GP) in patients at increased risk of gastrointestinal (GI) complications of NSAIDs in the setting of coadministration of chronic anticoagulation. Methods: Two drug utilization reviews (DUR) were performed at the outpatient pharmacy at the National Naval Medical Center (NNMC). One DUR was performed prior to an educational intervention and the other after an educational intervention 6 months after the first DUR was performed. Each DUR was performed using the same methodology. First, the total number of patients who had received prescriptions for coumadin was identified. This cohort was then analyzed to identify the frequency of coadministration of NSAIDs (both COX-II selective NSAIDs and non-selective NSAIDs). These two cohorts were then further examined to determine the frequency of coadministration of GP agents such as H2RAs, PPIs or misoprostol to evaluate adherence rates relative to current recommendations for GP for patients coadministered warfarin and NSAIDs. The educational intervention was a flyer that was sent via mail and email to providers in clinics at NNMC who prescribe NSAIDs. The flyer contained provider adherence data based on the first DUR and outlined the ACG Guidelines on prevention of NSAID-induced ulcers. Results: In total, the number of patients included for each DUR was 1,016 patients at baseline and 1,043 patients post intervention. Each patient was included based on having been dispensed at least one 30 day prescription for coumadin between March 10, 2007 and June 14, 2007 for the first DUR, and between September 10, 2007 and December 14, 2007, for the second. At baseline, of 198 patients who should have been on GP, only 63 were on an appropriate regimen, indicating a compliance rate with GP recommendations of 31.8%. After the educational intervention, of 310 patients that should have been on GP, 195 were on an appropriate regimen, indicating a compliance rate of 62.9%. Conclusion: Our analysis reveals that approximately two-thirds of patients who received coumadin and concurrent NSAID therapy prior to an educational intervention were not on GP medication, placing them at increased risk for NSAID related GI complications. After an educational intervention, the compliance rate increased to 63%, demonstrating that prescriber patterns can be affected by simple and cost effective interventions. This data highlights the value of DURs and directed efforts to improve provider awareness of the risk of coadministration of coumadin and NSAIDs as well as the evidence surrounding the ACG guidelines. Future evaluations should look at whether this effect can be increased with more intensive educational initiatives.

Prevention of NSAID-induced ulcers

Cyclooxygenase-2 (COX-2) selective inhibitors were developed as gastrointestinal (GI) safer alternatives to nonselective NSAIDs--providing equivalent analgesic and anti-inflammatory efficacy. Their GI sparing is impaired by concomitant aspirin use, and concerns regarding adverse cardiovascular effects have emerged. Risk factors for NSAID-related complications include a history of ulcer disease or bleeding, concomitant corticosteroid or anticoagulant therapy, use of high-dose or multiple NSAIDs (including low-dose aspirin), advanced age, and certain chronic diseases. If an NSAID must be used in a patient at risk, the lowest-risk NSAID should be used with, in many cases, cotherapy to reduce the risk for ulcers. COX-2 drugs have been associated with a significantly higher risk of vascular events than placebo or naproxen. This increase may be shared by nonselective NSAIDs and appears to be medication- and dose-dependent. Prostaglandin depletion is a central mechanism for NSAID ulcer development, and replacement therapy with misoprostol reduces NSAID toxicity; however, it is rarely used due to side effects. The acid suppression provided by traditional doses of histamine 2-receptor antagonists (H(2)RAs) does not prevent most NSAID-related gastric ulcers. Despite a single study demonstrating that H(2)RAs at double the dose may be effective, studies comparing such high doses with misoprostol or proton pump inhibitors (PPIs) for preventing NSAID ulcers are not available. PPIs are effective at single daily doses, do not demonstrate tachyphylaxis, and are superior to H(2)RAs and misoprostol in reducing ulcers and NSAID-associated dyspepsia. NSAID choice should be predicated by an assessment of an individual's cardiovascular and GI risk. For those with competing cardiovascular and GI risks, the tradeoffs between reducing adverse GI events (COX-2 inhibitor instead of a nonselective NSAID) must be explicitly weighed against concerns about cardiovascular side effects (naproxen instead of other agents). Considering cost is appropriate because it may not be feasible to recommend the "safest" regimen in every circumstance. The cost effectiveness of risk-reducing therapies is intimately tied to the patient's underlying risk. For those at highest GI risk, using a PPI and a low-dose COX-2 inhibitor seems appropriate for those without high cardiovascular risk. For patients whose cardiovascular risk parallels or exceeds GI concerns, naproxen with a PPI is recommended when non-NSAID approaches fail.

Role of proton pump inhibitors in the prevention of NSAID-induced ulcers now emerging

Role of proton pump inhibitors in the prevention of NSAID-induced ulcers now emerging

Prevention of the gastrointestinal adverse effects of nonsteroidal anti-inflammatory drugs: the role of proton pump inhibitors.

The associations between nonsteroidal anti-inflammatory drugs (NSAIDs) and the presence and complications of gastroduodenal erosions and ulcers are well established. Evidence that acid aggravates NSAID-induced injury provides a rationale for minimising such damage by acid suppression. Other strategies discussed include avoidance of NSAIDs or minimising their dosage, selecting NSAIDs known to cause less damage, and co-prescription of various agents. Cytoprotection with misoprostol, a prostaglandin analogue, has been shown to be effective in reducing NSAID-related peptic ulcers and their complications. Unfortunately, adverse effects may limit compliance in some patients. Histamine H2 antagonists have only limited efficacy in the prevention of NSAID-induced ulcers in humans, particularly in the stomach, except at higher than standard dosages. This may relate to their relatively modest effect in elevating gastric pH, especially in comparison with proton pump inhibitors. Several studies now confirm the efficacy of proton pump inhibitors in the short and longer term prevention of NSAID-induced upper gastrointestinal injury. Placebo-controlled studies suggest reductions of over 70% in gastric and duodenal ulcer rates over 3 to 6 months. The recent ASTRONAUT (Acid Suppression Trial: Ranitidine versus Omeprazole for NSAID-Associated Ulcer Treatment) study documented the greater prophylactic efficacy of omeprazole over ranitidine at standard dosages for 6 months. The OMNIUM (Omeprazole versus Misoprostol for NSAID-Induced Ulcer Management) study showed omeprazole to be slightly more effective overall than misoprostol in preventing the upper gastrointestinal adverse effects of NSAIDs, with both substantially more effective than placebo, although misoprostol was somewhat less well tolerated. Although substantial reductions in NSAID ulceration are now achievable when co-therapy with a proton pump inhibitor is given, a few patients will still develop ulcers and their complications. Hence the judicious use of NSAIDs in the first instance cannot be overemphasised.

A guideline for the treatment and prevention of nsaid-induced ulcers

Guidelines for clinical practice are intended to indicate preferred approaches to medical problems as established by scientifically valid research. Double-blind, placebo-controlled studies are preferable, but compassionate use reports and expert review articles are used in a thorough review of the literature conducted through Medline with the National Library of Medicine. When only data that will not withstand objective scrutiny are available, a recommendation is identified as a consensus of experts. Guidelines are applicable to all physicians who address the subject without regard to specialty training or interests and are intended to indicate the preferable, but not necessarily the only, acceptable approach to a specific problem. Guidelines are intended to be flexible and must be distinguished from standards of care, which are inflexible and rarely violated. Given the wide range of specifics in any health care problem, the physician must always choose the course best suited to the individual patient and the variables in existence at the moment of decision. Guidelines are developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee and approved by the Board of Trustees. Each has been intensely reviewed and revised by the Committee, other experts in the field, physicians who will use them, and specialists in the science of decision analysis. The recommendations of each guideline are therefore considered valid at the time of their production based on the data available. New developments in medical research and practice pertinent to each guideline will be reviewed at a time established and indicated at publication to assure continued validity. INTRODUCTION

Pantoprazole vs placebo in prevention of NSAID-induced ulcers

Pantoprazole vs placebo in prevention of NSAID-induced ulcers

Prevention of NSAID-induced ulcers by the coadministration of misoprostol: implications in clinical practice.

The guiding principle of ulcer therapy for many years has been "No acid, no ulcer" and many still adhere to it. Nonsteroidal anti-inflammatory drugs (NSAIDs) appear to cause ulcers primarily through prostaglandin depletion rather than through an acid-based mechanism. These ulcers affect a large number of patients and give few warning signs, often none, until it is too late. The profound relief offered to arthritis patients by NSAIDs, in the absence of equally effective remedies, means that rheumatologists must continue to deal with specific and quantifiable risks of NSAID-related gastrointestinal (GI) ulceration and its associated complications. The prostaglandin analog, misoprostol, may address many of these concerns because it reverses the patient's prostaglandin depleted condition. It is effective in preventing NSAID-induced ulcers, and does not interfere with the desired analgesic or anti-inflammatory effects of NSAIDs. The tools to assess the risk of NSAID-related hospitalization or death due to GI complications are available and patients at greatest risk can be identified. Physicians whose patients are at risk may wish to consider therapy with misoprostol 400 to 800 micrograms/day in divided doses. It is recommended that misoprostol be coadministered with the NSAID after meals. The most common side effects that the patient may experience are some mild and transient diarrhea and cramps upon initiation of misoprostol therapy and these can be minimized by taking misoprostol with meals and avoiding magnesium-containing antacids. For misoprostol's protective role to be demonstrated, it should be coprescribed with the NSAID for the duration of the NSAID therapy.(ABSTRACT TRUNCATED AT 250 WORDS)