DOCSLIB.ORG

Mucosal Erosions in Longterm Non-Steroidal Anti

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Mucosal Erosions in Longterm Non-Steroidal Anti 334 Gut 1995; 36: 334-336 Mucosal erosions in longterm non-steroidal anti-inflammatory drug users: predisposition to ulceration and relation to Helicobacterpylori Gut: first published as 10.1136/gut.36.3.334 on 1 March 1995. Downloaded from A S Taha, R D Sturrock, R I Russell Abstract TABLE II Characteristics ofarthritis and details of The importance of erosions in longterm anti-rheumatoid second line drugs non-steroidal anti-inflammatory drug Erosions present Erosions absent (NSAID) users, their relevance to ulcera- (n=23) (n=27) tion and their relation to Helicobacter Osteoarthritis 3 5 pylori are unclear. This study assessed the Rheumatoid arthritis 20 22 Duration of arthritis (y) incidence of peptic ulcers in the presence median (interquartile range) 5 (3-11) 7 (3-11) or absence of erosions or H pylori in a Second line drugs Sulphasalazine 8 10 group of longterm NSAID users (n=50), Gold (intramuscular) 2 2 undergoing endoscopy at 0, 4, 12, and 24 Penicillamine 0 1 weeks while continuing with NSAIDs. Hydroxychloroquine 3 2 Ulcers diagnosed at baseline endoscopy were excluded. Ulcers developed in nine of 23 patients (390/o) with pre-existing erosions in longterm users is not clear. Also, erosions compared with six of 27 (22%) their link to ulceration has not been proved, without erosions (p<0.05). The group and their relation to Helicobacter pylori has not infected with H pylon (n=30) had a been defined. total of 18 patients (60%) with erosions, a We, therefore, aimed at investigating total of 12 ulcers (40/o), and eight ulcers the development of peptic ulcers in a group (27%) complicating previous erosions, of patients with chronic arthritis treated compared with five (25%, p<0-01), three with NSAIDs in the presence or absence of (15%, p<0.05), and one (5%/o, p<001) erosions, and to assess the relevance of respectively in patients not infected with H pylori to both erosions and ulcers in http://gut.bmj.com/ H pylori (n=20). Ulcer development was these patients. not influenced by the initial number of erosions but strongly associated with H pylori positive duodenal erosions. It is Patients and methods concluded that ulcers are more likely to Patients with osteoarthritis or rheumatoid develop in longterm NSAID users who arthritis, and aged 18 years or over, were have mucosal erosions or H pylori, or recruited from the Rheumatology Outpatient on September 28, 2021 by guest. Protected copyright. both. Clinic. NSAIDs had to be taken for at (Gut 1995; 36: 334-336) least four weeks before baseline endoscopy and to be continued throughout the study. Keywords: mucosal erosion, non-steroidal anti- Corticosteroids, cytotoxic drugs, or antiulcer inflammatory drug(s), Helicobacterpylori. treatment were not permitted. Endoscopy was performed after an overnight fast and intravenous midazolam was used for sedation. Gastric and duodenal erosions are the com- Patients with ulcers at baseline endoscopy monest endoscopic abnormalities related were excluded and those without ulcers were to acute exposure to non-steroidal anti-inflam- re-endoscoped at 4, 12, and 24 weeks. The matory drugs (NSAIDs).1 As they are primary end point was ulcer development at commonly repaired through processes of any stage of the study or the completion restitution and adaptation,2 erosions are often transient, and this in turn leads to the impres- TABLE III Details ofNSAID intake sion that they are comparatively trivial lesions.3 Erosions present Erosions absent Unlike the situation in subjects exposed to (n=23) (n=27) Departments of short courses of NSAIDs, the significance of Gastroenterology Type A S Taha Diclofenac 6 3 R I Russell Naproxen 5 6 TABLE I Demographic details of the study groups Indomethacin 4 7 and Rheumatology, Ketoprofen 2 2 Erosions absent Fenbufen 2 0 Royal Infirmary, Erosions present Nabumetone 1 3 Glasgow Number 23 27 Flurbiprofen 0 2 R D Sturrock Men 5 6 Others* 3 4 Women 18 21 Dosett 3 (2-3) 3 (2-3) Correspondence to: Age (y) median (interquartile Duration (years)4 2 (1-4) 2 (1-5) Dr A S Taha, GI Centre, range) 53 (43-59) 53 (43-61) Southem General Hospital, Smokers 10 11 *=One patient taking one of the following: ibuprofen, Glasgow G5 1 4TF. Alcohol drinkers 13 16 azapropazone, acematacin, or tiaprofenic acid. t=Dosage Accepted for publication Upper abdominal complaints 10 9 scale: 1, minimal dose; 2, submaximal; 3: maximal dose 24 June 1994 permitted. t=Median (interquartile range). Mucosal erosions in lonigterni nioni-steroidal anti-inflanmmatory dnig uisers: predisposition to ulceration and relation to Helicobacter pylori 335 TABLE IV Numbers ofpatients with erosionls or ulcers, in the presence (or absenice) of drugs (Table II), or in the types, doses, or H pylori at each endoscopy length of NSAID intake (Table III). Baseline 4 Weeks 12 Weeks 24 Weeks Table IV shows the numbers ofpatients with erosions or ulcers at each endoscopic assess- All erosions* 12 11 7 6 Gut: first published as 10.1136/gut.36.3.334 on 1 March 1995. Downloaded from All ulcers 0 8 5 2 ment. The study protocol excluded patients Ulcers plus erosions 0 2 3 1 with ulcers at baseline endoscopy. Erosions Erosions H pylon present (absent) 8 (4) 10 (1) 6 (1) 5 (1) were identified in 12 patients at the initial Ulcers endoscopy, and developed in 11 others on H pslon present (absent) 0 6 (2) 4 (1) 2 (0) subsequent examinations. They were recurrent * =Erosions developed in a total of 23 patients throughout the whole study, some of whom had in five patients, and disappeared altogether in lesions at more than one endoscopy (see text). eight patients. At each assessment, lesions were more likely to be found in patients of the required series of endoscopic examina- infected with H pylon. tions. An ulcer was defined as a mucosal Figure 1 shows ulcers developing in patients defect that is equal to or greater than 3 mm with or without previous erosions. Fifteen in diameter,4 5 and smaller lesions were con- ulcers were diagnosed in the study group as a sidered as erosions. Ulcers were described as whole (15 of 50, 30%0), with a median size of 4 deep (more than 3 mm) or comparatively mm (range 3-10 mm). Only five ulcers were superficial (2-3 mm in depth). Ulcer dimen- comparatively superficial and most (n= 10) sions were measured using the standard were deep. Ulcers affected the gastric body Olympus upper gastrointestinal endoscopy (n= 1), duodenum (n=5), gastric antrum biopsy forceps, with the fully open instrument (n=8), and both the duodenum and antrum being equivalent to 5 mm. The anatomical (n= 1). Most ulcers (nine of 15, 60%) locations of lesions were described as precisely developed in patients with previous or current as possible, their photographic appearances erosions. The median number of erosions (per recorded, and their distance from the teeth patient) appearing before an ulcer was measured. H pylorz was identified in gastric three (range 1-6) compared with four (1-12) antral biopsy specimens by both culture and erosions not followed by ulceration. Direct histological examination. The endoscopist was progression from an erosion to an ulcer was not aware of H pylon' status or the previous thought to have taken place in six of nine ulcer endoscopic findings, and the study patients patients with previous erosions. were re-endoscoped among a larger pool of Figure 2 shows ulcers and erosions classified arthritic patients to facilitate blinding and according to the presence or absence of further minimise familiarity between the H pylori. Patients with H pylori infection endoscopist and patients being repeatedly (n= 30) had significantly more erosions, ulcers, http://gut.bmj.com/ endoscoped. Statistical analyses included the and ulcers complicating previous erosions than X2 and Fisher's exact test where appropriate. patients not infected with Hpylori (n=20). It is The study was approved by the local ethics worth noting that of six patients with duodenal committee. erosions found in the study group as a whole five were positive for H pylon; all these five patients (100%) developed ulceration at Results subsequent endoscopic examinations (two on September 28, 2021 by guest. Protected copyright. A total of 50 patients were recruited. They gastric and three duodenal ulcers). This is were divided into two groups according to compared with only three ulcers developing in whether they had or had not had erosions at 13 patients (23%) with Hpylori positive gastric any stage of the study. Table I shows their erosions (p<0001) Also gastric submucosal demographic details. Patients in both groups haemorrhages were found in a total of five were comparable with respect to their ages, patients: three were infected with Hpylonr, and sex, smoking, and drinking habits. Also, there two of these three subsequently developed were no significant differences in the character- gastrlc eroslons. istics of patients' arthritis, use of second line Discussion 40 This study shows that longterm users of 35 NSAIDs with mucosal erosions are more likely to develop ulceration than patients without 30 these lesions. Also, the majority of both 0 25 - erosions and ulcers in longterm NSAID users 20 develop in patients infected with H pylon'. The (DI_.a) initial number of erosions in the individual 15 patient does not seem to influence the risk of 10 ulceration. In the presence of H pylori, 5 however, duodenal erosions have a stronger association with subsequent ulceration than All patients Patients with Patients without their gastric counterparts. (n=50) previous previous erosions erosions A variety of types of injury develop after the (n=23) (n=27) administration of NSAIDs, ranging from Figure 1: Ulcer development (%w) in patients with or petechial haemorrhages to erosions, and less without erosions.
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]