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Generic Name: Mefenamic Acid
Class: Other Nonsteroidal Anti-inflammatory Agents
VA Class: MS120
Chemical Name: N-(2,3-xylyl)anthranilic acid
Molecular Formula: C15H15NO2
CAS Number: 61-68-7

Medically reviewed by Last updated on Mar 25, 2019.


    Cardiovascular Risk
  • Increased risk of serious (sometimes fatal) cardiovascular thrombotic events (e.g., MI, stroke).125 500 502 508 b Risk may occur early in treatment and may increase with duration of use.500 502 505 506 508 (See Cardiovascular Thrombotic Effects under Cautions.)

  • Contraindicated in the setting of CABG surgery.505

    GI Risk
  • Increased risk of serious (sometimes fatal) GI events (e.g., bleeding, ulceration, perforation of the stomach or intestine).100 104 125 b Serious GI events can occur at any time and may not be preceded by warning signs and symptoms.100 101 104 125 b Geriatric individuals are at greater risk for serious GI events.125 b (See GI Effects under Cautions.)


Prototypical NSAIA; anthranilic acid derivative (fenamate); structurally and pharmacologically related to meclofenamate sodium.125 a

Uses for Ponstel

Consider potential benefits and risks of mefenamic acid therapy as well as alternative therapies before initiating therapy with the drug.125 b Use lowest possible effective dosage and shortest duration of therapy consistent with patient’s treatment goals.125 b


Relief of mild to moderate pain in patients ≥14 years of age when the duration of therapy ≤1 week.125 b


Treatment of primary dysmenorrhea.125 b


Has been used for reduction of fever associated with infection in children; routine use as an antipyretic not recommended because of potential adverse effects.a

Ponstel Dosage and Administration


  • Consider potential benefits and risks of mefenamic acid therapy as well as alternative therapies before initiating therapy with the drug.125 b


Oral Administration

Administer orally.125 May be administered in divided doses up to 4 times daily.125


To minimize the potential risk of adverse cardiovascular and/or GI events, use lowest effective dosage and shortest duration of therapy consistent with the patient’s treatment goals.125 b Adjust dosage based on individual requirements and response; attempt to titrate to the lowest effective dosage.125 b

Pediatric Patients


Adolescents ≥14 years of age should receive dosage recommended for adults.125 (See Adult Dosage.)



For mild to moderate pain in adults, 500 mg initially followed by 250 mg every 6 hours as necessary.125


For relief of primary dysmenorrhea in adults, 500 mg initially followed by 250 mg every 6 hours as necessary.125 Initiate at onset of bleeding and associated symptoms; treatment should not be necessary for >2–3 days.125

Prescribing Limits

Pediatric Patients


Duration of therapy usually should not exceed 1 week.125



Duration of therapy usually should not exceed 1 week.125


Therapy should not be necessary for more than 2–3 days.125

Special Populations

Hepatic Impairment

Dosage reduction may be required.125

Renal Impairment

Dosage reduction may be required if used in patients with renal impairment.125

Use not recommended in patients with preexisting renal disease or substantial renal impairment.125

Geriatric Patients

Select dosage carefully since may be more likely to have decreased renal function.125 b

Cautions for Ponstel


  • Known hypersensitivity to mefenamic acid or any ingredient in the formulation.125 b

  • History of asthma, urticaria, or other sensitivity reaction precipitated by aspirin or other NSAIAs.125 b

  • In the setting of CABG surgery.508

  • Active ulceration or chronic inflammation of upper or lower GI tract.125

  • Preexisting renal disease.125



Cardiovascular Thrombotic Effects

NSAIAs (selective COX-2 inhibitors, prototypical NSAIAs) increase the risk of serious adverse cardiovascular thrombotic events (e.g., MI, stroke) in patients with or without cardiovascular disease or risk factors for cardiovascular disease.500 502 508

Findings of FDA review of observational studies, meta-analysis of randomized controlled trials, and other published information500 501 502 indicate that NSAIAs may increase the risk of such events by 10–50% or more, depending on the drugs and dosages studied.500

Relative increase in risk appears to be similar in patients with or without known underlying cardiovascular disease or risk factors for cardiovascular disease, but the absolute incidence of serious NSAIA-associated cardiovascular thrombotic events is higher in those with cardiovascular disease or risk factors for cardiovascular disease because of their elevated baseline risk.500 502 506 508

Increased risk may occur early (within the first weeks) following initiation of therapy and may increase with higher dosages and longer durations of use.500 502 505 506 508

In controlled studies, increased risk of MI and stroke observed in patients receiving a selective COX-2 inhibitor for analgesia in first 10–14 days following CABG surgery.508

In patients receiving NSAIAs following MI, increased risk of reinfarction and death observed beginning in the first week of treatment.505 508

Increased 1-year mortality rate observed in patients receiving NSAIAs following MI;500 508 511 absolute mortality rate declined somewhat after the first post-MI year, but the increased relative risk of death persisted over at least the next 4 years.508 511

Some systematic reviews of controlled observational studies and meta-analyses of randomized studies suggest naproxen may be associated with lower risk of cardiovascular thrombotic events compared with other NSAIAs.133 134 135 136 500 501 502 503 506 FDA states that limitations of these studies and indirect comparisons preclude definitive conclusions regarding relative risks of NSAIAs.500

Use NSAIAs with caution and careful monitoring (e.g., monitor for development of cardiovascular events throughout therapy, even in those without prior cardiovascular symptoms) and at the lowest effective dosage for the shortest duration necessary.125 500 508 b

Some clinicians suggest that it may be prudent to avoid NSAIA use, whenever possible, in patients with cardiovascular disease.505 511 512 516 Avoid use in patients with recent MI unless benefits of therapy are expected to outweigh risk of recurrent cardiovascular thrombotic events; if used, monitor for cardiac ischemia.508 Contraindicated in the setting of CABG surgery.508

No consistent evidence that concomitant use of low-dose aspirin mitigates the increased risk of serious adverse cardiovascular events associated with NSAIAs.125 502 508 b (See Specific Drugs under Interactions.)

GI Effects

Serious GI toxicity (e.g., bleeding, ulceration, perforation) can occur with or without warning symptoms; increased risk in those with a history of GI bleeding or ulceration, geriatric patients, smokers, those with alcohol dependence, and those in poor general health.100 104 124 125 126 b

For patients at high risk for complications from NSAIA-induced GI ulceration (e.g., bleeding, perforation), consider concomitant use of misoprostol;124 127 h i alternatively, consider concomitant use of a proton-pump inhibitor (e.g., omeprazole)124 h i or use of an NSAIA that is a selective inhibitor of COX-2 (e.g., celecoxib).125 h


Hypertension and worsening of preexisting hypertension reported; either event may contribute to the increased incidence of cardiovascular events.125 b Use with caution in patients with hypertension; monitor BP.125 b

Impaired response to ACE inhibitors, angiotensin II receptor antagonists, β-blockers, and certain diuretics may occur.125 508 b (See Specific Drugs under Interactions.)

Heart Failure and Edema

Fluid retention and edema reported.125 508 b

NSAIAs (selective COX-2 inhibitors, prototypical NSAIAs) may increase morbidity and mortality in patients with heart failure.500 501 504 507 508

NSAIAs may diminish cardiovascular effects of diuretics, ACE inhibitors, or angiotensin II receptor antagonists used to treat heart failure or edema.508 (See Specific Drugs under Interactions.)

Manufacturer recommends avoiding use in patients with severe heart failure unless benefits of therapy are expected to outweigh risk of worsening heart failure; if used, monitor for worsening heart failure.508

Some experts recommend avoiding use, whenever possible, in patients with reduced left ventricular ejection fraction and current or prior symptoms of heart failure.507

Renal Effects

Direct renal injury, including renal papillary necrosis, reported in patients receiving long-term NSAIA therapy.125 b

Potential for overt renal decompensation.125 b Increased risk of renal toxicity in patients with renal or hepatic impairment or heart failure, in geriatric patients, in patients with volume depletion, and in those receiving a diuretic, ACE inhibitor, or angiotensin II receptor antagonist.125 128 b (See Renal Impairment under Cautions.)

Sensitivity Reactions

Hypersensitivity Reactions

Anaphylactoid reactions reported.125 b

Immediate medical intervention and discontinuance for anaphylaxis.125 b

Avoid in patients with aspirin triad (aspirin sensitivity, asthma, nasal polyps); caution in patients with asthma.125 b

Dermatologic Reactions

Serious skin reactions (e.g., exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis) reported; can occur without warning.125 b Discontinue at first appearance of rash or any other signs of hypersensitivity (e.g., blisters, fever, pruritus).125 b

General Precautions

Hepatic Effects

Severe reactions including jaundice, fatal fulminant hepatitis, liver necrosis, and hepatic failure (sometimes fatal) reported rarely with NSAIAs.125 b

Elevations of serum ALT or AST reported.125 b

Monitor for symptoms and/or signs suggesting liver dysfunction; monitor abnormal liver function test results.125 b Discontinue if signs or symptoms of liver disease or systemic manifestations (e.g., eosinophilia, rash) occur.125 b

Hematologic Effects

Anemia reported rarely.125 b Determine hemoglobin concentration or hematocrit in patients receiving long-term therapy if signs or symptoms of anemia occur.125 b

May inhibit platelet aggregation and prolong bleeding time.125 b

Ocular Effects

Visual disturbances reported; ophthalmic evaluation recommended if visual changes occur.125 a

Other Precautions

Not a substitute for corticosteroid therapy; not effective in the management of adrenal insufficiency.125 b

May mask certain signs of infection.125 b

Obtain CBC and chemistry profile periodically during long-term use.125 b

Specific Populations


Category C.125 b Avoid use in third trimester because of possible premature closure of the ductus arteriosus.125 b


Distributed into milk.125 c Discontinue nursing or the drug.125

Pediatric Use

Safety and efficacy not established in children <14 years of age.125

Geriatric Use

Use with caution in patients ≥65 years of age.125 b Geriatric adults appear to tolerate therapy less well (e.g., possible higher incidence of adverse GI effects, greater risk of developing renal decompensation) than younger individuals.125 b Fatal adverse GI effects reported more frequently in geriatric patients than younger adults.125 b

Substantially eliminated by kidneys; periodic monitoring of renal function may be useful since geriatric patients are more likely to have decreased renal function.125 (See Geriatric Patients under Dosage and Administration and Renal Impairment under Cautions.)

Renal Impairment

Use not recommended in patients with preexisting renal disease or substantial renal impairment.125

Common Adverse Effects

Abdominal pain,125 constipation,125 diarrhea,125 dyspepsia,125 flatulence,125 gross bleeding/perforation,125 heartburn,125 nausea,125 GI ulcers (gastric/duodenal),125 vomiting,125 abnormal renal function,125 anemia,125 dizziness,125 edema,125 elevated liver enzymes,125 headaches,125 increased bleeding time,125 pruritus,125 rashes,125 tinnitus.125

Interactions for Ponstel

Protein-bound Drugs

Possible pharmacokinetic interaction; potential for mefenamic acid to be displaced from binding sites by, or to displace from binding sites, other protein-bound drugs (e.g., oral anticoagulants, hydantoins, salicylates, sulfonamides, and sulfonylureas).125 a f Observe for adverse effects if used with other protein-bound drugs.a

Drugs Affecting Hepatic Microsomal Enzymes

Inhibitors of CYP2C9: possible altered safety and efficacy of mefenamic acid.125

Specific Drugs




ACE inhibitors

Reduced BP response to ACE inhibitor possible 125 128 b

Possible deterioration of renal function in individuals with renal impairment128

Monitor BP128

Angiotensin II receptor antagonists

Reduced BP response to angiotensin II receptor antagonist possible128

Possible deterioration of renal function in individuals with renal impairment128

Monitor BP128

Antacids (magnesium-containing)

Increased peak plasma concentrations and AUC of mefenamic acid125 d

Anticoagulants (e.g., warfarin)

Possible bleeding complications125 128 a b e

Use with caution; frequent monitoring of PT advised125 128 a e


Increased risk of GI ulceration or other complications 125 128 b

No consistent evidence that low-dose aspirin mitigates the increased risk of serious cardiovascular events associated with NSAIAs125 502 508 b

Concomitant use generally not recommended125 b

Diuretics (furosemide, thiazides)

Reduced natriuretic effects possible125 b

Monitor for diuretic efficacy and renal failure125 b


Increased plasma lithium concentrations105 125 b

Monitor for lithium toxicity105 125 b


Possible toxicity associated with increased plasma methotrexate concentrations during concomitant NSAIA use125 b

Caution advised125 b

Ponstel Pharmacokinetics



Rapidly absorbed following oral administration.125 a Peak plasma concentrations usually attained within 2–4 hours.125 a


Effect of food on rate and extent of absorption not known.125



Appears to cross the placenta.g

Distributed into milk in small amounts.125 c

Plasma Protein Binding




Metabolized by CYP2C9 to 3′-hydroxymethyl mefenamic acid; further oxidation to 3′-carboxymefenamic acid may occur. 125 Mefenamic acid and its metabolites also are glucuronidated.125

Elimination Route

Excreted in urine (52%) primarily as glucuronic acid conjugates of the drug and its metabolites and in feces (<20%).125


Mefenamic acid: approximately 2 hours.125 Half-lives of 3′-hydroxymethyl mefenamic acid and 3′-carboxymefenamic acid may be longer than parent compound.125

Special Populations

Half-life 5 times longer in preterm infants compared with adults.125

In patients with renal or hepatic impairment, clearance of metabolites may be decreased.125

Not substantially removed by hemodialysis.125 a





20–25°C (may be exposed to 15–30°C).125 a


  • Inhibits cyclooxygenase-1 (COX-1) and COX-2.117 118 119 120 121 122

  • Pharmacologic actions similar to those of other prototypical NSAIAs; exhibits anti-inflammatory, analgesic, and antipyretic activity.125 a

Advice to Patients

  • Importance of reading the medication guide for NSAIAs that is provided to the patient each time the drug is dispensed.125 b

  • Risk of serious cardiovascular events (e.g., MI, stroke).125 500 508 b Importance of seeking immediate medical attention if signs and symptoms of a cardiovascular event (chest pain, dyspnea, weakness, slurred speech) occur.125 500 508 b

  • Risk of GI bleeding and ulceration.100 104 125 b Importance of notifying a clinician if signs and symptoms of serious adverse GI effects occur.125 b

  • Importance of discontinuing mefenamic acid and contacting clinician if rash or other signs of hypersensitivity (blisters, fever, pruritus) develop.125 b Importance of seeking immediate medical attention if an anaphylactic reaction occurs.125 b

  • Risk of hepatotoxicity.125 b Importance of discontinuing therapy and contacting a clinician immediately if signs and symptoms of hepatotoxicity (nausea, fatigue, lethargy, pruritus, jaundice, upper right quadrant tenderness, flu-like symptoms) occur.125 b

  • Risk of heart failure or edema; importance of reporting dyspnea, unexplained weight gain, or edema.125 508 b

  • Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.125 Importance of avoiding mefenamic acid in late pregnancy (third trimester).125

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.125

  • Importance of informing patients of other important precautionary information.125 (See Cautions.)


Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

Mefenamic Acid


Dosage Forms


Brand Names




250 mg*

Mefenamic Acid Capsules



AHFS DI Essentials™. © Copyright 2019, Selected Revisions March 23, 2017. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

† Use is not currently included in the labeling approved by the US Food and Drug Administration.


100. Palmer JF. Letter sent to Lents CE, of Parke Davis, Division of Warner-Lambert Company regarding labeling revisions about gastrointestinal adverse reactions to Ponstel (mefenamic acid). Rockville, MD: Food and Drug Administration, Division of Oncology and Radiopharmaceutical Drug Products. 1988 Sep.

101. Food and Drug Administration. Labeling revisions for NSAIDs. FDA Drug Bull. 1989; 19:3-4.

102. Searle. Cytotec (misoprostol) prescribing information. Skokie, IL; 1989 Jan.

104. Soll AH, Weinstein WM, Kurata J et al. Nonsteroidal anti-inflammatory drugs and peptic ulcer disease. Ann Intern Med. 1991; 114:307-19.

105. Nonsteroidal anti-inflammatory drug interactions: Lithium. In: Hansten PD, Horn JR. Drug interactions and updates. Vancouver, WA: Applied Therapeutics, Inc; 1993:608-9.

106. Miller LG, Bowman RC, Bakht F. Sparing effect of sulindac on lithium levels. J Fam Prac. 1989; 28:592-3.

107. Corticosteroid interactions: nonsteroidal anti-inflammatory drugs (NSAIDs). In: Hansten PD, Horn JR. Drug interactions and updates. Vancouver, WA: Applied Therapeutics, Inc; 1993:562.

108. Garcia Rodriguez LA, Jick H. Risk of upper gastrointestinal bleeding and perforation associated with individual non-steroidal anti-inflammatory drugs. Lancet. 1994; 343:769-72.

109. Hollander D. Gastrointestinal complications of nonsteroidal anti-inflammatory drugs: prophylactic and therapeutic strategies. Am J Med. 1994; 96:274-81.

110. Schubert TT, Bologna SD, Yawer N et al. Ulcer risk factors: interaction between Helicobacter pylori infection, nonsteroidal use, and age. Am J Med. 1993; 94:413-7.

111. Bateman DN, Kennedy JG. Non-steroidal anti-inflammatory drugs and elderly patients: the medicine may be worse than the disease. BMJ. 1995; 310:817-8.

112. Piper JM, Ray WA, Daugherty JR et al. Corticosteroid use and peptic ulcer disease: role of nonsteroidal anti-inflammatory drugs. Ann Intern Med. 1991; 114:735-40.

113. Lithium interactions: diclofenac. In: Hansten PD, Horn JR. Drug interactions and updates. Vancouver, WA: Applied Therapeutics, Inc; 1993:607.

114. Ciba Geigy, Ardsley, NY: Personal communication on diclofenac 28:08.04.

115. Reviewers’ comments (personal observations) on diclofenac 28:08.04.

116. Searle. Cytotec (misoprostol) prescribing information. 1989 Jan.

117. Hawkey CJ. COX-2 inhibitors. Lancet. 1999; 353:307-14.

118. Kurumbail RG, Stevens AM, Gierse JK et al. Structural basis for selective inhibition of cyclooxygenase-2 by anti-inflammatory agents. Nature. 1996; 384:644-8.

119. Riendeau D, Charleson S, Cromlish W et al. Comparison of the cyclooxygenase-1 inhibitory properties of nonsteroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors, using sensitive microsomal and platelet assays. Can J Physiol Pharmaco. 1997; 75:1088-95.

120. DeWitt DL, Bhattacharyya D, Lecomte M et al. The differential susceptibility of prostaglandin endoperoxide H synthases-1 and -2 to nonsteroidal anti-inflammatory drugs: aspirin derivatives as selective inhibitors. Med Chem Res. 1995; 5:325-43.

121. Cryer B, Dubois A. The advent of highly selective inhibitors of cyclooxygenase—a review. Prostaglandins Other Lipid Mediators. 1998; 56:341-61.

122. Simon LS, Role and regulation of cyclooxygenase-2 during inflammation. Am J Med. 1999; 106(Suppl 5B):37-42S.

123. Morrison BW, Daniels SE, Kotey P et al. Rofecoxib, a specific cyclooxygenase-2 inhibitor, in primary dysmenorrhea: a randomized controlled study. Obstet Gynecol. 1999; 94:504-8.

124. Wolfe MM, Lichtenstein DR, Singh G. Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs. N Engl J Med. 1999; 340:1888-99.

125. First Horizon Pharmaceutical Corporation. Ponstel (mefenamic acid) capsules prescribing information. Alpharetta, GA; 2006 Jan.

126. Singh G, Triadafilopoulos G. Epidemiology of NSAID induced gastrointestinal complications. J Rheumatol. 1999; 26(suppl 56):18-24.

127. Lanza FL, and the Ad Hoc Committee on Practice Parameters of the American College of Gastroenterology. A guideline for the treatment and prevention of NSAID-induced ulcers. Am J Gastroenterol. 1998; 93:2037-46.

128. Merck & Co., Inc. Clinoril (sulindac) tablets prescribing information. Whitehouse Station, NJ; 2007 Feb.

129. Food and Drug Administration. Analysis and recommendations for agency action regarding non-steroidal anti-inflammatory drugs and cardiovascular risk. 2005 Apr 6.

130. Cush JJ. The safety of COX-2 inhibitors: deliberations from the February 16-18, 2005, FDA meeting. From the American College of Rheumatology website ( Accessed 2005 Oct 12.

131. Novartis Pharmaceuticals. Diovan (valsartan) capsules prescribing information (dated 1997 Apr). In: Physicians’ desk reference. 53rd ed. Montvale, NJ: Medical Economics Company Inc; 1999:2013-5.

132. Pharmacia. Daypro (oxaprozin) caplets prescribing information. Chicago, IL; 2002 May.

133. McGettigan P, Henry D. Cardiovascular risk and inhibition of cyclooxygenase: a systematic review of observational studies of selective and nonselective inhibitors of cyclooxygenase 2. JAMA. 2006; 296: 1633-44.

134. Kearney PM, Baigent C, Godwin J et al. Do selective cyclo-oxygenase-2 inhibitors and traditional non-steroidal anti-inflammatory drugs increase the risk of atherothrombosis? Meta-analysis of randomised trials. BMJ. 2006; 332: 1302-5.

135. Graham DJ. COX-2 inhibitors, other NSAIDs, and cardiovascular risk; the seduction of common sense. JAMA. 2006; 296:1653-6.

136. Chou R, Helfand M, Peterson K et al. Comparative effectiveness and safety of analgesics for osteoarthritis. Comparative effectiveness review no. 4. (Prepared by the Oregon evidence-based practice center under contract no. 290-02-0024.) . Rockville, MD: Agency for Healthcare Research and Quality. 2006 Sep. Available at:

500. Food and Drug Administration. Drug safety communication: FDA strengthens warning that non-aspirin nonsteroidal anti-inflammatory drugs (NSAIDs) can cause heart attacks or strokes. Silver Spring, MD; 2015 Jul 9. From the FDA web site. Accessed 2016 Mar 22.

501. Coxib and traditional NSAID Trialists' (CNT) Collaboration, Bhala N, Emberson J et al. Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials. Lancet. 2013; 382:769-79.

502. Food and Drug Administration. FDA briefing document: Joint meeting of the arthritis advisory committee and the drug safety and risk management advisory committee, February 10-11, 2014. From FDA web site

503. Trelle S, Reichenbach S, Wandel S et al. Cardiovascular safety of non-steroidal anti-inflammatory drugs: network meta-analysis. BMJ. 2011; 342:c7086.

504. Gislason GH, Rasmussen JN, Abildstrom SZ et al. Increased mortality and cardiovascular morbidity associated with use of nonsteroidal anti-inflammatory drugs in chronic heart failure. Arch Intern Med. 2009; 169:141-9.

505. Schjerning Olsen AM, Fosbøl EL, Lindhardsen J et al. Duration of treatment with nonsteroidal anti-inflammatory drugs and impact on risk of death and recurrent myocardial infarction in patients with prior myocardial infarction: a nationwide cohort study. Circulation. 2011; 123:2226-35.

506. McGettigan P, Henry D. Cardiovascular risk with non-steroidal anti-inflammatory drugs: systematic review of population-based controlled observational studies. PLoS Med. 2011; 8:e1001098.

507. Yancy CW, Jessup M, Bozkurt B et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013; 62:e147-239.

508. Lupin. Mefenamic acid capsules prescribing information. Baltimore, MD; 2016 Jun.

511. Olsen AM, Fosbøl EL, Lindhardsen J et al. Long-term cardiovascular risk of nonsteroidal anti-inflammatory drug use according to time passed after first-time myocardial infarction: a nationwide cohort study. Circulation. 2012; 126:1955-63.

512. Olsen AM, Fosbøl EL, Lindhardsen J et al. Cause-specific cardiovascular risk associated with nonsteroidal anti-inflammatory drugs among myocardial infarction patients--a nationwide study. PLoS One. 2013; 8:e54309.

516. Bavry AA, Khaliq A, Gong Y et al. Harmful effects of NSAIDs among patients with hypertension and coronary artery disease. Am J Med. 2011; 124:614-20.

a. AHFS drug information 2007. McEvoy GK, ed. Mefenamic acid. Bethesda, MD: American Society of Health-System Pharmacists; 2007:2096-9.

b. US Food and Drug Administration. Proposed NSAID Package Insert Labeling Template 1. From the FDA website ( Accessed 10 Oct 2005.

c. Buchanan RA, Eaton CJ, Koeff ST et al. The breast milk excretion of mefenamic acid. Curr Ther Res Clin Exp. 1968; 10: 592-7.

d. Neuvonen PJ, Kivistö KT. Enhancement of drug absorption by antacids: an unrecognized drug interaction. Clin Pharmacokinet. 1994; 27:120-8.

e. Chan TY. Adverse interactions between warfarin and nonsteroidal antinflammatory drugs: mechanisms, clinical significance, and avoidance. Ann Pharmacother. 1995; 29:1274-83.

f. Diana FJ, Veronich K, Kapoor AL. Binding of nonsteroidal anti-inflammatory agents and their effect on binding of racemic warfarin and its enantiomers to human serum albumin. J Pharm Sci. 1989; 78: 195-9.

g. MacKenzie IZ, Graf AK, Mitchell MD. Prostaglandins in the fetal circulation following maternal ingestion of a prostaglandin synthetase inhibitor during mid-pregnancy. Int J Gynaecol Obstet. 1985; 23: 455-8.

h. American College of Rheumatology Subcommittee on Rheumatoid Arthritis Guidelines. Guidelines for the management of rheumatoid arthritis; 2002 update. Arthritis Rheum. 2002; 46:328-46.

i. Anon. Drugs for rheumatoid arthritis. Med Lett Drugs Ther. 2000; 42:57-64.