DOCSLIB.ORG

Quantifying the Impact of NSAID-Associated Adverse Events

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Quantifying the Impact of NSAID-Associated Adverse Events n REPORTS n Quantifying the Impact of NSAID-Associated Adverse Events Michael Fine, MD onsteroidal anti-inflammatory drugs (NSAIDs) are the cornerstone of pain management in patients Abstract who have inflammatory, acute pain (eg, headache, Nonsteroidal anti-inflammatory drugs postoperative pain, and orthopedic fractures), and (NSAIDs) are widely used among patients Nchronic pain (eg, rheumatoid arthritis, osteoarthritis, and gout).1,2 experiencing many different types of pain, Approximately 70% of people 65 years or older use NSAIDs at including inflammatory, acute pain (eg, injury, low back pain, headache, postopera- least once per week, with half of them taking at least 7 doses per tive pain), and chronic pain (eg, rheumatoid week. In 2000, more than 111 million prescriptions were written arthritis, osteoarthritis). However, both for NSAIDs in the United States, at an approximate cost of $4.8 traditional NSAIDs and second-generation billion.3 The use of NSAIDs is likely to increase even more as the NSAIDs (cyclooxygenase-2 inhibitors) can US population continues to age and experience painful condi- lead to very expensive and serious adverse events. Gastrointestinal, cardiovascular, and tions that are more common among older adults.4 renal complications associated with NSAIDs Both traditional© NSAIDs Managed and Carethe second & generation cyclo- have been shown to be dose-dependent. oxygenase-2Healthcare (COX-2) inhibitors Communications, offer superior efficacyLLC compared In 2005, to help minimize these risks, the with acetaminophen, but also carry significant risk for serious US Food and Drug Administration issued a gastrointestinal (GI), cardiovascular (CV), and renal adverse public health advisory stating that “NSAIDs events.1,5-7 A systematic review of 17 prospective observational should be administered at the lowest effec- tive dose for the shortest duration consistent studies found that 11% of preventable drug-related hospital with individual patient treatment goals.” This 8 admissions could be attributed to NSAIDs. Studies have docu- article reviews the undue clinical and eco- mented that the risk of adverse events associated with NSAIDs nomic burden associated with NSAID-related are both dose-dependent and duration dependent.1,7,9 serious adverse events. In 2005, the US Food and Drug Administration (FDA) issued Am J Manag Care. 2013;19(14 suppl):S267-S272 a public health advisory warning of an increased risk for serious CV events with NSAID use.10 In 2007, the FDA published a medication guide for NSAIDs that recommended using the lowest dose possible for treatment. The guide listed myocardial infarc- tion (MI), stroke, kidney problems, and GI bleeding as some of the serious potential side effects. Despite the emerging evidence, few studies have been conducted to help quantify the true burden of these side effects, especially when NSAIDs are used for acute pain. The Impact of Pain Management Acute pain is typically associated with an event, such as an injury or surgery, and usually resolves when the underlying event is treated or healed. Examples include headache, postoperative pain, fractures, low back pain, and neck pain.11,12 Approximately 40% of patient visits to primary care providers are due to mild to For author information and disclosures, see end of text. moderate acute pain.2 More than 70% of emergency department (ED) visits are for acute pain, making it the most common reason VOL. 19, NO. 14 n THE AMERICAN JOURNAL OF MANAGED CARE n S267 Reports why patients seek treatment. Among the over 115 million utilization that results from the morbidity and mortality asso- ED visits annually in the United States, headache alone ciated with these adverse events. accounts for 2.1 million.11,13 Considering that the average cost of a visit to the ED is $1349, the costs associated with Gastrointestinal Adverse Events acute pain are substantial.14 A meta-analysis published in 2012 examined the rela- Acute pain can also occur in the presence of chronic pain tive risk (RR) of upper GI complications (upper GI bleed- conditions such as osteoarthritis and low back pain; this type ing and/or perforation, or peptic ulcer) for both traditional of pain is referred to as breakthrough pain. Both osteoarthritis NSAIDs and COX-2 inhibitors using pooled data from 28 and low back pain have placed significant economic burden observational studies published between 1980 and May 2011. on the US healthcare system.12,15 Data from the National Researchers found an increased risk for upper GI complica- Health Interview Survey show that in 2011, 28.4% of tions across all 16 of the NSAIDs studied. Data showed that American adults reported experiencing low back pain within the risk was lowest for aceclofenac and celecoxib (RR, 1.4 the previous 3 months.16 Buurma et al (2012) estimated that and 1.5, respectively) and highest for ketorolac and azapropa- in 2011, there were 116.5 million cases of acute low back zone (RR, 11.5 and 18.5, respectively). Most of the NSAIDs and neck pain in the United States. By 2021, the number is were associated with an RR for upper GI complications expected to reach 128.5 million cases (or, a 10% growth over between approximately 2 and 4. Researchers also found that the next decade).17 the risk was dose-dependent. The use of high daily doses was Similarly, the number of Americans with osteoarthritis is associated with an approximately 2- to 3-fold increase in RR rising. Researchers estimate that the prevalence of arthritis in compared with low to medium doses for all NSAIDs except the United States among patients over 40 years of age grew celecoxib, for which the effect was not dose-dependent.1 from 10.1% in 1999 to 12.8% in 2008 (P = .011).18 Data from One of the more recent studies conducted regarding the the Medical Expenditure Panel Survey (MEPS) showed that GI side effects associated with NSAIDs was a 2013 meta- osteoarthritis was among the 5 most commonly treated con- analysis by the Coxib and traditional NSAID Trialists’ ditions in 2009, totaling $29.5 billion. MEPS data showed (CNT) Collaboration of 280 studies (124,514 participants). that 17.4 million adults between the ages of 40 and 64 years The study examined the relationship between the use of were treated for osteoarthritis in 2009.19 NSAIDs and upper GI complications, such as peptic ulcer perforations, obstructions, and bleeding. Data for naproxen, NSAIDs: The Hidden Costs ibuprofen, and diclofenac, as well as for the COX-2 inhibi- The cost of treating acute and chronic pain conditions is tors rofecoxib, etoricoxib, lumiracoxib, valdecoxib, and well documented. What is less well understood is the price tag GW403681, were analyzed. CNT researchers found an attached to the side effects associated with their treatment. elevated risk for upper GI complications across all of the Some estimates suggest that each year more than 100,000 medications studied. The RR was nearly twice as high for ibu- patients are hospitalized for NSAID-related GI complications profen and naproxen compared with diclofenac and COX-2 alone, with direct costs ranging from $1800 to $8500 per inhibitors (Figure 1).6 patient per hospitalization. Moreover, it has been reported A similar increased risk was found in a study among that 16,500 persons die annually from these complications. In Quebec residents. Patients using NSAIDs had a risk of devel- the elderly, the medical costs of adverse GI events associated oping GI adverse events that was 2.5 times (95% confidence with NSAID use likely exceed $4 billion per year.20 interval [CI], 2.04-3.00) that of patients not taking NSAIDs. NSAID use is also associated with costly adverse events In addition, researchers estimated that the average cost for GI impacting the CV and renal systems. For example, NSAID adverse events added an average of 66% to the cost of care. In use has been associated with increased risk for hospitaliza- patients over the age of 85 years with more than 5 physician tion due to MI as well as for heart failure (HF). According claims, the costs of management of adverse events associated to recent data from the Agency for Healthcare Research and with NSAIDs increased the cost of each prescription by a Quality, the average hospitalizations for acute MI and con- factor of 7.5.21 gestive HF cost $18,500 and $10,500, respectively. Likewise, acute renal failure, which is also associated with NSAID use, Cardiovascular Risks can ultimately lead to expensive dialysis treatment. The CNT study described above also examined the vas- Although direct cost data specific to NSAID adverse cular risk associated with NSAIDs. The primary outcome events are limited, several studies have examined healthcare was major vascular events, defined as nonfatal MI, nonfatal S268 n www.ajmc.com n NOVEMBER 2013 Quantifying the Impact of NSAID-Associated Adverse Events 6 n Figure 1. Relative Risk of Vascular and Upper GI Events by Drug Type: Results From the CNT Collaboration 4.5 a 4.22 3.97a 4 3.5 3 2.49a 2.5 2.28a a a 1.87a a 1.89 2 1.85 1.81 1.61 a 1.41a 1.44 Relative Risk Relative 1.37 1.5 a 1.22 1.20 1.03 0.93 1 0.5 0 Major Vascular Heart Failure Cause-Specific Upper GI Events Mortality COX-2 Inhibitors Diclofenac Ibuprofen Naproxen CNT indicates Coxib and traditional NSAID Trialists; COX-2, cyclooxygenase-2; GI, gastrointestinal; NSAID, nonsteroidal anti-inflammatory drug. aP <.05. stroke, or death from a vascular cause. The study also mea- the NSAIDs studied, there was a clear, dose-dependent risk sured the risk for major coronary events, stroke, hospitaliza- across all 3 end points. For example, high-dose diclofenac was tion for HF, and death.
Load more

Recommended publications
  • Studies in Laboratory Animals to Assess the Safety of Anti-Inflammatory Agents in Acute Porphyria
    Ann Rheum Dis: first published as 10.1136/ard.46.7.540 on 1 July 1987. Downloaded from Annals of the Rheumatic Diseases, 1987; 46, 540-542 Studies in laboratory animals to assess the safety of anti-inflammatory agents in acute porphyria KENNETH E L McCOLL, GEORGE G THOMPSON, AND MICHAEL R MOORE From the University Department of Medicine, Western Infirmary, Glasgow SUMMARY The safety of various anti-inflammatory drugs in acute porphyria was assessed by examining their effect on rat hepatic haem synthesis. Azapropazone, chloroquine, and gold increased 6-aminolaevulinic acid (ALA) synthase activity, indicating that they are liable to precipitate porphyric crises. Aspirin, ibuprofen, indomethacin, ketoprofen, flurbiprofen, phenylbutazone, naproxen, prednisolone, and penicillamine did not increase ALA synthase activity and should be safe in porphyria. Though these animal studies can be used as a guide to prescribing in patients with acute porphyria, some caution is still required as species may vary in their response to inducing agents. Key words: chloroquine, azapropazone, gold, b-aminolaevulinic acid synthase. copyright. The acute hepatic porphyrias which comprise acute controlling enzyme of haem biosynthesis 6- intermittent porphyria, hereditary coproporphyria, aminolaevulinic acid (ALA) synthase in rat hepatic and variegate porphyria are examples of pharma- tissue. To confirm the reliability of the animal cogenetic disease. They are the result of deficien- model, phenobarbitone was also tested. For each cies of individual enzymes in the pathway of haem drug examined six male Sprague-Dawley rats re- biosynthesis and are inherited in an autosomal ceived the test drug and six control rats received the dominant fashion.2 Subjects with the genetic trait appropriate placebo solution.
    [Show full text]
  • Drug-Induced Peptic Ulcer Disease
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by OAR@UM risk populations only.7 The prevalence of endoscopically confirmed gastrointestinal ulcers in NSAID users is quoted to be between 15% and 30%. Between 12% to 30% of NSAID-induced ulcers are gastric ulcers, whereas 2% to 19% are duodenal ulcers. NSAID-induced ulcers are symptomatic only in 1% of patients after three to six months and in 2 to 4% of patients after one year. Inappropriately they do not correlate well with pain because the analgesic action of NSAIDs may mask the ulcer pain.2 Drug-induced peptic Understanding the method by which NSAIDs cause gastric damage has helped in the development of prophylactic agents that ulcer disease 1 red uce their toxicity. The mechanism by which NSAIDs are thought to damage the Valerie Vella B Pharm(Hons), PgDip Clin Pharm (Aberdeen) gastrointestinal tract is four-fold. Clinical Pharmacist, St Luke’s Hospital, Guardamangia, Malta a) Topical injury Email: [email protected] Originally it was thought that NSAIDs damaged the gastric epithelium by Key words: Peptic ulcer, medicines, prostaglandins, gastrointestinal protection, intracellular accumulation of these drugs in gastrointestinal toxicity an ionised state.1 However the fact that enteric-coated formulations, pro-drugs, For more than a century, peptic ulcer disease has been a rectal and parenteral administration of 1 major cause of morbidity and mortality. Peptic ulcer disease NSAIDs still resulted in gastrointestinal is a heterogeneous group of disorders involving the damage despite the apparent absence of gastrointestinal tract and results from an imbalance between direct mucosal contact implies a minor role the aggressive forces of gastric acid and pepsin and the for topical injury1,2.
    [Show full text]
  • Individual Nsaids and Upper Gastrointestinal Complications a Systematic Review and Meta-Analysis of Observational Studies (The SOS Project)
    Drug Saf 2012; 35 (12): 1127-1146 SYSTEMATIC REVIEW 0114-5916/12/0012-1127 Adis ª 2012 Castellsague et al., publisher and licensee Springer International Publishing AG. This is an open access article published under the terms of the Creative Commons License ‘‘Attribution-NonCommercial-NoDerivative 3.0‘‘ (http://creativecommons.org/licenses/by-nc-nd/3.0/) which permits non-commercial use, distribution, and reproduction, provided the original work is properly cited and not altered. Individual NSAIDs and Upper Gastrointestinal Complications A Systematic Review and Meta-Analysis of Observational Studies (the SOS Project) Jordi Castellsague,1 Nuria Riera-Guardia,1 Brian Calingaert,2 Cristina Varas-Lorenzo,1 Annie Fourrier-Reglat,3 Federica Nicotra,4 Miriam Sturkenboom5 and Susana Perez-Gutthann1, on behalf of the investigators of the Safety of Non-Steroidal Anti-Inflammatory Drugs (SOS) Project 1 RTI Health Solutions, Barcelona, Spain 2 RTI Health Solutions, Research Triangle Park, NC, USA 3 Universite V. Segalen, Bordeaux, France 4 University Milan-Bicocca, Milan, Italy 5 Erasmus University Medical Center, Rotterdam, the Netherlands Abstract Background: The risk of upper gastrointestinal (GI) complications associated with the use of NSAIDs is a serious public health concern. The risk varies between individual NSAIDs; however, there is little information on the risk associated with some NSAIDs and on the impact of risk factors. These data are necessary to evaluate the benefit-risk of individual NSAIDs for clinical and health policy decision making. Within the European Community’s Seventh Framework Programme, the Safety Of non-Steroidal anti-inflammatory drugs (NSAIDs) [SOS] project aims to develop decision models for regulatory and clinical use of individual NSAIDs according to their GI and cardiovascular safety.
    [Show full text]
  • Long-Term Use of Anti-Inflammatory Drugs and Risk of Atrial Fibrillation
    ORIGINAL INVESTIGATION Long-term Use of Anti-inflammatory Drugs and Risk of Atrial Fibrillation Raffaele De Caterina, MD, PhD; Ana Ruigo´mez, MD, PhD; Luı´s Alberto Garcı´a Rodrı´guez, MD, MSc Background: Previous reports have described an asso- ratio [RR], 2.49; 95% confidence interval [CI], 1.56- ciation between the use of corticosteroids (steroidal anti- 3.97). However, we also found that the current use of inflammatory drugs [SAIDs]) and the risk of atrial fibril- NSAIDs was associated with an increased risk of chronic lation (AF). We sought to determine the existence of a AF (RR, 1.44; 95% CI, 1.08-1.91). Such risk was further similar association for non-SAIDs (NSAIDs). increased among long-term users with a treatment du- ration of longer than 1 year (RR, 1.80; 95% CI, 1.20- Methods: We identified patients aged 40 to 89 years with 2.72). The increased risk of chronic AF was not ex- a first-ever diagnosis of AF in 1996 in a United King- plained by the occurrence of heart failure. The use of dom primary care database and classified them as hav- NSAIDs was not associated with paroxysmal AF. ing paroxysmal or chronic AF. After validation with their primary care physicians, 1035 patients were confirmed Conclusions: The use of NSAIDs, as for SAIDs, is asso- as having incident chronic AF and 525 as having parox- ciated with an increased risk of chronic AF. Because the ysmal AF. Two separate nested case-control analyses es- use of anti-inflammatory drugs in general is a marker for timated the risk of first-time chronic and paroxysmal AF underlying inflammatory disorders, inflammation may among users of SAIDs and NSAIDs.
    [Show full text]
  • Non Steroidal Anti-Inflammatory Drugs
    Non Steroidal Anti‐inflammatory Drugs (NSAIDs) 4 signs of inflammation • Redness ‐ due to local vessel dilatation • Heat ‐ due to local vessel dilatation • Swelling – due to influx of plasma proteins and phagocytic cells into the tissue spaces • Pain – due to local release of enzymes and increased tissue pressure NSAIDs • Cause relief of pain ‐. analgesic • Suppress the signs and symptoms of inflammation. • Exert antipyretic action. • Useful in pain related to inflammation. Esp for superficial/integumental pain . Classification of NSAIDs • Salicylates: aspirin, Sodium salicylate & diflunisal. • Propionic acid derivatives: ibuprofen, ketoprofen, naproxen. • Aryl acetic acid derivatives: diclofenac, ketorolac • Indole derivatives: indomethacin, sulindac • Alkanones: Nabumetone. • Oxicams: piroxicam, tenoxicam Classification of NSAIDs ….. • Anthranilic acid derivatives (fenamates): mefenamic acid and flufenamic acid. • Pyrazolone derivatives: phenylbutazone, oxyphenbutazone, azapropazone (apazone) & dipyrone (novalgine). • Aniline derivatives (analgesic only): paracetamol. Clinical Classif. • Non selective Irreversible COX inhibitors • Non slective Reversible COX inhibitors • Preferential COX 2 inhibitors • 10‐20 fold cox 2 selective • meloxicam, etodolac, nabumetone • Selective COX 2 inhibitors • > 50 fold COX ‐2 selective • Celecoxib, Etoricoxib, Rofecoxib, Valdecoxib • COX 3 Inhibitor? PCM Cyclooxygenase‐1 (COX‐1): -constitutively expressed in wide variety of cells all over the body. -"housekeeping enzyme" -ex. gastric cytoprotection, hemostasis Cyclooxygenase‐2 (COX‐2): -inducible enzyme -dramatically up-regulated during inflammation (10-18X) -constitutive : maintains renal blood flow and renal electrolyte homeostasis Salicylates Acetyl salicylic acid (aspirin). Kinetics: • Well absorbed from the stomach, more from upper small intestine. • Distributed all over the body, 50‐80% bound to plasma protein (albumin). • Metabolized to acetic acid and salicylates (active metabolite). • Salicylate is conjugated with glucuronic acid and glycine. • Excreted by the kidney.
    [Show full text]
  • Variable in Their Efficacy? a Description of Ion Trapping
    Annals of the Rheumatic Diseases 1993; 52: 241-243 241 HYPOTHESIS Why are non-steroidal anti-inflammatory drugs so variable in their efficacy? A description of ion trapping G A Ellis, D R Blake Hypothesis Non-steroidal anti-inflammatory drugs vary in Our hypothesis is that acidic non-steroidal their aqueous solubility, but most are highly anti-inflammatory drugs (NSAIDs) undergo albumin bound and will be co-distributed with ion trapping in acidotic tissue and that this this protein. Diffusion of an NSAID into the affects not only their gastrotoxicity, which is cell follows Fick's law, as it is dependent on the well known, but also their selectivity for, and concentration gradient across the plasma their efficacy in, inflammatory joint disease. membrane and the lipid/water partition Tissue acidosis may not be a feature of all coefficient of the drug molecule. chronic inflammatory disease states, but it does For weak acids, such as most NSAIDs, the occur in inflammatory joint disease and is effective concentration gradient is that of the highly variable depending on the extent of the non-ionised form, as ionised molecules are not mismatch between synovial perfusion and lipid soluble metabolic demand. This mismatch is influ- HD D- + H+ enced not only by disease activity, but also by Non-ionised Ionised joint movement, which causes transient hypoxic episodes. Interventions, such as rest The position ofthe equilibrium depends on the and drug treatment, would serve to reduce ion intrinsic ionisation constant of the molecule trapping and, therefore, NSAID efficacy (pKa) and on the pH value of the aqueous through their effects on disease activity.
    [Show full text]
  • The Acceleration of Articular Cartilage Degeneration in Osteoarthritis by Nonsteroidal Anti-Inflammatory Drugs Ross A
    WONDER WHY? THE ACCELERATION OF ARTICULAR CARTILAGE DEGENERATION IN OSTEOARTHRITIS WONDER WHY? The Acceleration of Articular Cartilage Degeneration in Osteoarthritis by Nonsteroidal Anti-inflammatory Drugs Ross A. Hauser, MD A B STRA C T introduction over the past forty years is one of the main causes of the rapid rise in the need for hip and knee Nonsteroidal anti-inflammatory drugs (NSAIDs) are replacements, both now and in the future. among the most commonly used drugs in the world for the treatment of osteoarthritis (OA) symptoms, and are While it is admirable for the various consensus and taken by 20-30% of elderly people in developed countries. rheumatology organizations to educate doctors and Because of the potential for significant side effects of the lay public about the necessity to limit NSAID use in these medications on the liver, stomach, gastrointestinal OA, the author recommends that the following warning tract and heart, including death, treatment guidelines label be on each NSAID bottle: advise against their long term use to treat OA. One of the best documented but lesser known long-term side effects The use of this nonsteroidal anti-inflammatory of NSAIDs is their negative impact on articular cartilage. medication has been shown in scientific studies to accelerate the articular cartilage breakdown In the normal joint, there is a balance between the in osteoarthritis. Use of this product poses a continuous process of cartilage matrix degradation and significant risk in accelerating osteoarthritis joint repair. In OA, there is a disruption of the homeostatic breakdown. Anyone using this product for the pain state and the catabolic (breakdown) processes of of osteoarthritis should be under a doctor’s care and chondrocytes.
    [Show full text]
  • COX-2 Chronology C J Hawkey
    1509 LEADING ARTICLE Gut: first published as 10.1136/gut.2005.065003 on 13 October 2005. Downloaded from COX-2 chronology C J Hawkey ............................................................................................................................... Gut 2005;54:1509–1514. doi: 10.1136/gut.2005.065003 The role of selective cyclooxygenase (COX)-2 inhibitors in N 1859 Hammond Kolbe synthesises salicylic acid, with industrial scale production in 1874.7 medical practice has become controversial since evidence Salicylic acid is bitter and irritates the mouth emerged that their use is associated with an increased risk and stomach. of myocardial infarction. Selective COX-2 inhibitors were N 1863 Friedrich Bayer and Friedrich Weskott found a dye manufacturing company employ- seen as successor to non-selective non-steroidal anti- ing six people in Wuppertal-Barmen.8 inflammatory drugs, in turn successors to aspirin. The N 1886 Bayer manufacture phenacetin from a importance of pain relief means that such drugs have waste product of a benzo dye. What starts as a always attracted attention. The fact that they work through supplement to dye manufacture is to become the company’s more profitable and dominant inhibition of cyclooxygenase, are widespread, and have activity18 multiple effects also means that adverse effects that were unanticipated (even though predictable) have always THE ASPIRIN YEARS emerged. In this paper I therefore present an historical N 1897 Motivated by his father’s intolerance of perspective so that the lessons of the past may be applied salicylic acid, Felix Hoffman synthesises acetyl salicylic acid, named aspirin (derived from to the present. Acetyl Spirea).12910 This had been done ........................................................................... before in 1853 (Carl Friedrich Gerhardt) and 1869 (Kraut) but Hoffman’s method is quan- titative (mixing salicylic acid and acetic hydride 2:3 before adding acetic acid) and yields pure stable aspirin.12 Aspirin causes 1066 AND ALL THAT less dyspepsia than salicylic acid.
    [Show full text]
  • Prescription Medications, Drugs, Herbs & Chemicals Associated With
    Prescription Medications, Drugs, Herbs & Chemicals Associated with Tinnitus American Tinnitus Association Prescription Medications, Drugs, Herbs & Chemicals Associated with Tinnitus All rights reserved. No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form, or by any means, without the prior written permission of the American Tinnitus Association. ©2013 American Tinnitus Association Prescription Medications, Drugs, Herbs & Chemicals Associated with Tinnitus American Tinnitus Association This document is to be utilized as a conversation tool with your health care provider and is by no means a “complete” listing. Anyone reading this list of ototoxic drugs is strongly advised NOT to discontinue taking any prescribed medication without first contacting the prescribing physician. Just because a drug is listed does not mean that you will automatically get tinnitus, or exacerbate exisiting tinnitus, if you take it. A few will, but many will not. Whether or not you eperience tinnitus after taking one of the listed drugs or herbals, or after being exposed to one of the listed chemicals, depends on many factors ‐ such as your own body chemistry, your sensitivity to drugs, the dose you take, or the length of time you take the drug. It is important to note that there may be drugs NOT listed here that could still cause tinnitus. Although this list is one of the most complete listings of drugs associated with tinnitus, no list of this kind can ever be totally complete – therefore use it as a guide and resource, but do not take it as the final word. The drug brand name is italicized and is followed by the generic drug name in bold.
    [Show full text]
  • Oral Nonsteroidal Anti-Inflammatory Drugs for Neuropathic Pain
    Oral nonsteroidal anti-inflammatory drugs for neuropathic pain (Review) Moore RA, Chi CC, Wiffen PJ, Derry S, Rice ASC This is a reprint of a Cochrane review, prepared and maintained by The Cochrane Collaboration and published in The Cochrane Library 2015, Issue 10 http://www.thecochranelibrary.com Oral nonsteroidal anti-inflammatory drugs for neuropathic pain (Review) Copyright © 2015 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd. TABLE OF CONTENTS HEADER....................................... 1 ABSTRACT ...................................... 1 PLAINLANGUAGESUMMARY . 2 BACKGROUND .................................... 2 OBJECTIVES ..................................... 4 METHODS ...................................... 4 RESULTS....................................... 7 Figure1. ..................................... 8 Figure2. ..................................... 9 DISCUSSION ..................................... 10 AUTHORS’CONCLUSIONS . 11 ACKNOWLEDGEMENTS . 11 REFERENCES ..................................... 12 CHARACTERISTICSOFSTUDIES . 16 DATAANDANALYSES. 20 APPENDICES ..................................... 20 WHAT’SNEW..................................... 25 HISTORY....................................... 25 CONTRIBUTIONSOFAUTHORS . 25 DECLARATIONSOFINTEREST . 26 SOURCESOFSUPPORT . 26 DIFFERENCES BETWEEN PROTOCOL AND REVIEW . .... 26 NOTES........................................ 26 Oral nonsteroidal anti-inflammatory drugs for neuropathic pain (Review) i Copyright © 2015 The Cochrane Collaboration. Published by John Wiley
    [Show full text]
  • Reviewing the Major Risks of NSAIDS, the Most Commonly Used Class of Drugs in the U.S
    Reviewing the Major Risks of NSAIDS, the Most Commonly Used Class of Drugs in the U.S. Part 1: Introduction and Cardiovascular Complications By John Kiel, DO, MPH, CAQ-SM,1 Alexandra L. Mannix, MD,2 and Gregory Rubin, DO, CAQ-SM3 1Dept. of Emergency Medicine and Sports Medicine, University of Florida College of Medicine – Jacksonville, Jacksonville, FL 2Dept. of Emergency Medicine, University of Florida College of Medicine – Jacksonville, Jacksonville, FL 3Dept. of Internal Medicine, University of Central Florida and NCH Healthcare System Internal Medicine Residency, Naples, FL Address correspondence to: John Kiel DO, MPH, CAQ-SM University of Florida College of Medicine - Jacksonville 655 West 8th Street, Jacksonville, FL, 32209 904-244-6340 [email protected] Introduction Non-steroidal anti-inflammatory drugs (NSAIDs) are the most commonly used drug class in the United States according to the Centers for Disease Control and Prevention (CDC). NSAIDs address a wide range of maladies related to pain, as well as fever and inflammation. For this reason, they are commonly used to treat a broad spectrum of ailments. NSAID use is increasing over time; as recently as 2013, NSAIDs had accounted for more than 70 million prescriptions and 30 billion over-the-counter purchases.1 Ibuprofen is the 34th most prescribed drug in the United States followed by meloxicam (35th), aspirin (39th), naproxen (69th), diclofenac (84th), and celecoxib (109th) as of 2018.2 One study estimated that 36 million Americans use over the counter analgesia daily, with 23 million using NSAIDS and one-fourth of users exceeding the recommended dose.3 Users are generally unaware of the potential for adverse side effects.
    [Show full text]
  • Aceclofenac in Osteoarthritis - NSAID with Novel Mechanism of Action
    Acta Scientific Orthopaedics (ISSN: 2581-8635) Volume 3 Issue 12 December 2020 Review Article Aceclofenac in Osteoarthritis - NSAID with Novel Mechanism of Action Dilip Shah1, Ananda K Pal2, Gurinder Bedi3, Anu Grover4*, Amarjit October 06, 2020 Singh4, Indranil Purkait4, Apurva Jawdekar4 and Anil Pareek4 Received: Published: November 05, 2020 1Consultant Orthopedic Surgeon, Saifee Hospital, Mumbai, India © All rights are reserved by Anu Grover., 2Professor, Department of Orthopaedics and Traumatology, IPGMER, SSK Medical et al. College, Kolkata, West Bengal, India 3Director Orthopedics, Fortis Hospital, New Delhi, India 4Medical Affairs Department, Ipca Laboratories, Mumbai, India *Corresponding Author: Anu Grover, Medical Affairs Department, Ipca Laboratories, Mumbai, India. Abstract - tive and progressive disease which worsens over time, resulting in joint pain, swelling and stiffness. As the disease progresses, pain Osteoarthritis (OA) is the most common form of arthritis, affecting millions of people worldwide. It is an inflammatory, degenera and stiffness become severe making daily tasks difficult, thereby affecting the quality of life. The treatment of osteoarthritis mainly focuses on management of inflammation to control the symptoms as complete reversal of the disease is not practical. Non-steroidal Various NSAIDs are currently available in the market and looking into the co-morbidities associated with OA, there is a need for well anti-inflammatory drugs (NSAIDs) are most commonly used and are mainstay drugs in the symptomatic treatment of osteoarthritis. tolerated NSAID with proven efficacy and safety. Aceclofenac, although was a late entry in crowded NSAID market, but, now is a well established drug in management of OA pain. It predominantly inhibits the inflammatory COX-2 enzyme, and due to less inhibitory - action on gastroprotective COX-1 enzyme, it can be categorized as a preferential COX-2 inhibitor.
    [Show full text]