Class: Other Nonsteroidal Anti-inflammatory Agents
VA Class: MS120
CAS Number: 6385-02-0
- Cardiovascular Risk
Increased risk of serious (sometimes fatal) cardiovascular thrombotic events (e.g., MI, stroke).146 147 500 502 508 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.508
- GI Risk
Increased risk of serious (sometimes fatal) GI events (e.g., bleeding, ulceration, perforation of the stomach or intestine).100 108 109 117 145 146 Serious GI events can occur at any time and may not be preceded by warning signs and symptoms.100 108 109 117 146 Geriatric individuals are at greater risk for serious GI events.100 146 (See GI Effects under Cautions.)
Prototypical NSAIA;100 a anthranilic acid derivative;100 a structurally related to diclofenac and mefenamic acid.100 a
Uses for Meclofenamate Sodium
Consider potential benefits and risks of meclofenamate sodium therapy as well as alternative therapies before initiating therapy with the drug.100 146 Use lowest effective dosage and shortest duration of therapy consistent with the patient’s treatment goals.100 146
Symptomatic treatment of acute and chronic osteoarthritis and rheumatoid arthritis.100 a
Has been used in a limited number of patients with psoriatic arthritis†.a
Relief of mild to moderate pain in adults.a 100 101 102 103 104 105 106
Dysmenorrhea and Menorrhagia
Treatment of primary dysmenorrhea.100 107 a
Treatment of idiopathic menorrhagia.100 112 a Use only for heavy menstrual flow that is idiopathic (i.e., no underlying pathophysiologic cause can be identified);100 112 do not use for the management of spotting or bleeding that occurs between menstrual cycles.100
Use for primary dysmenorrhea or idiopathic menorrhagia only when the potential benefits justify the possible risks.100
Meclofenamate Sodium Dosage and Administration
Consider potential benefits and risks of meclofenamate sodium therapy as well as alternative therapies before initiating therapy with the drug.100 146
Administer orally.100 a
Administration with meal, milk, or antacids may minimize adverse GI effects.100 146 a
Available as meclofenamate sodium; dosage expressed in terms of meclofenamic acid.100 a
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.100 146 a Adjust dosage based on individual requirements and response; attempt to titrate to the lowest effective dosage.100 146 a
Osteoarthritis or Rheumatoid ArthritisOral
200–400 mg daily in 3 or 4 equally divided doses.100 a Initiate at lower dosage and adjust dose and frequency as necessary based on severity of symptoms and clinical response (maximum 400 mg daily).100 146 a
50 mg every 4–6 hours.a 100 101 103 104 105 106 Some patients may require 100-mg doses for optimal pain relief (maximum 400 mg daily).a 100 101 102 103 104 105 106
Dysmenorrhea and Menorrhagia
100 mg 3 times daily.a 100 107 112 Initiated at onset of menses and continue ≤ 6 days or until cessation of menses.100 112 a
Osteoarthritis or Rheumatoid ArthritisOral
Maximum 400 mg daily.100 a
For mild to moderate pain, maximum 400 mg daily.100 101
Dysmenorrhea and Menorrhagia
Maximum 300 mg daily.100
Dosage reduction recommended in patients with renal impairment; monitor renal function.100 a
Use not recommended in patients with advanced renal disease.146
Consider reduced initial dosage; monitor carefully.a 100
Cautions for Meclofenamate Sodium
Known hypersensitivity to meclofenamate sodium or any ingredient in the formulation.100 146 a
History of asthma, urticaria, or other sensitivity reaction precipitated by aspirin or other NSAIAs.100 146 a
In the setting of CABG surgery.508
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.150 151 152 154 500 501 502 503 506 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.146 500 508
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.146 147 502 508 (See Specific Drugs under Interactions.)
Serious GI toxicity (e.g., bleeding, ulceration, perforation) can occur with or without warning symptoms;100 108 109 117 146 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.100 146 a
For patients at high risk for complications from NSAIA-induced GI ulceration (e.g., bleeding, perforation), consider concomitant use of misoprostol;111 120 134 135 alternatively, consider concomitant use of a proton-pump inhibitor (e.g., omeprazole) or use of an NSAIA that is a selective inhibitor of COX-2 (e.g., celecoxib).111 120 134
Hypertension and worsening of preexisting hypertension reported; either event may contribute to the increased incidence of cardiovascular events.146 Use with caution in patients with hypertension; monitor BP.146
Impaired response to ACE inhibitors, angiotensin II receptor antagonists, β-blockers, and certain diuretics may occur.146 508 509 (See Specific Drugs under Interactions.)
Heart Failure and Edema
Fluid retention and edema reported.146 508
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
Direct renal injury, including renal papillary necrosis, reported in patients receiving long-term NSAIA therapy.100 146
Potential for overt renal decompensation.100 146 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.100 146 149 a (See Renal Impairment under Cautions.)
Anaphylactoid reactions reported.146
Immediate medical intervention and discontinuance for anaphylaxis.146
Avoid in patients with aspirin triad (aspirin sensitivity, asthma, nasal polyps); caution in patients with asthma.100 146
Serious skin reactions (e.g., exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis) reported;100 146 can occur without warning.146 Discontinue at first appearance of rash or any other sign of hypersensitivity (e.g., blisters, fever, pruritus).146
Severe reactions including jaundice, fatal fulminant hepatitis, liver necrosis, and hepatic failure (sometimes fatal) reported rarely with NSAIAs.100 146 a
Elevations of serum ALT, AST, or alkaline phosphatase reported.100 146
Monitor for symptoms and/or signs suggesting liver dysfunction; monitor abnormal liver function test results.100 146 a Discontinue if signs or symptoms of liver disease or systemic manifestations (e.g., eosinophilia, rash) occur.100 146 a
Anemia reported.100 146 a Determine hemoglobin concentration or hematocrit in patients receiving long-term therapy if signs or symptoms of anemia occur.100 146 a
Leukopenia, thrombocytopenic purpura, neutropenia, and agranulocytosis reported rarely.100 a Decreased WBC counts usually transient and return to normal despite continued meclofenamate sodium therapy.100 a Further clinical evaluations are necessary if leukopenia, granulocytopenia, or thrombocytopenia persists; discontinuance of meclofenamate sodium therapy may be necessary.100 a
May inhibit platelet aggregation and prolong bleeding time.a 146
Ocular toxicity reported in patients receiving NSAIA therapy.100 a If visual difficulties develop during therapy, discontinue the drug and perform complete ophthalmologic examination.100 a
Sodium Content and Electrolyte Imbalance
100-mg meclofenamate sodium capsules each contain 0.34 mEq of sodium.a
Not a substitute for corticosteroid therapy; not effective in the management of adrenal insufficiency.146 a
May mask certain signs of infection or other conditions.146 a
Obtain CBC and chemistry profile periodically during long-term therapy.146 a
No FDA category rating.100 Safety not established; avoid use, particularly during first and third trimesters.100 146 a Avoid use in third trimester because of possible premature closure of the ductus arteriosus.a
Meclofenamic acid is distributed into milk.a 100 Discontinue nursing or the drug.100 146 a
Safety and efficacy not established in children <14 years of age.100 a
Use with caution in patients ≥65 years of age.100 146 a Geriatric adults appear to tolerate NSAIA-induced adverse effects less well than younger individuals.a 100 146 Fatal adverse GI effects reported more frequently in geriatric patients than younger adults.a 100
Metabolites eliminated principally via the kidney.100 a
Use with caution and close monitoring in patients with substantial renal impairment.100 a Use not recommended in patients with advanced renal disease; close monitoring of renal function advised if used.146
Common Adverse Effects
Diarrhea, nausea with or without vomiting, other GI disorders, abdominal pain, flatulence, pyrosis, dizziness, headache, rash.100 146 a
Interactions for Meclofenamate Sodium
Possible pharmacokinetic interaction; observe for adverse effects if used with other protein-bound drugs.100 a
Reduced BP response to ACE inhibitor possible146 153
Possible deterioration of renal function in individuals with renal impairment146
Angiotensin II receptor antagonists
Reduced BP response to angiotensin II receptor antagonist possible146 153
Possible deterioration of renal function in individuals with renal impairment146
Antacids (aluminum- and magnesium-containing)
No effect on meclofenamate sodium absorption100
May decrease plasma concentrations of meclofenamic acid100 a
Increased risk of GI ulceration and other complications100 137
No consistent evidence that low-dose aspirin mitigates the increased risk of serious cardiovascular events associated with NSAIAs147 502 508
Concomitant use not recommended146
Diuretics (furosemide, thiazides)
Reduced natriuretic effects146
Monitor for diuretic efficacy and renal failure146
Increased plasma lithium concentrations146
Monitor for lithium toxicity146
Possible toxicity associated with increased plasma methotrexate concentrations146
Pharmacokinetic interaction unlikely100
Possible bleeding complications and increases in PT100 146 a
Monitor PT, adjust warfarin dosage as needed, and observe for adverse effects100 146 a
Meclofenamate Sodium Pharmacokinetics
Rapidly and completely absorbed following oral administration.100 a Peak plasma concentrations usually attained within 0.5–2 hours following oral administration.2 100
Food decreases rate27 100 and extent100 of absorption.
Distribution into human body tissues and fluids not fully characterized.a In animals, the drug is distributed mainly into the plasma, liver, and kidneys, with lower concentrations being distributed into the heart, spleen, fat, skeletal muscle, and brain.a
Crosses the placenta.100 a Meclofenamic acid is distributed into milk.100 a
Plasma Protein Binding
>99% (mainly albumin).2 100 114 a
Excreted in urine (70%), mainly as glucuronide conjugates of the metabolites,2 27 100 114 and in feces (20–30%).2 27 100
40 minutes–5.3 hours.2 100 114
Tight, light-resistant containers at 15–30°C.100 a
Inhibits cyclooxygenase-1 (COX-1) and COX-2.127 128 129 130 131 132
Pharmacologic actions similar to those of other prototypical NSAIAs; exhibits anti-inflammatory, analgesic, and antipyretic activity.100 a
Advice to Patients
Importance of reading the medication guide for NSAIAs that is provided each time the drug is dispensed.146
Risk of serious cardiovascular events (e.g., MI, stroke).146 150 151 152 154 500 508 Importance of seeking immediate medical attention if signs and symptoms of a cardiovascular event (chest pain, dyspnea, weakness, slurred speech) occur.146 500 508
Risk of GI bleeding and ulceration.100 108 109 146 Importance of notifying a clinician if signs and symptoms of serious adverse GI effects occur.146
Risk of serious skin reactions.146 Importance of discontinuing meclofenamate sodium and contacting clinician if rash or other signs of hypersensitivity (blisters, fever, pruritus) develop.146
Risk of anaphylactoid and other sensitivity reactions.146 Importance of seeking immediate medical attention if an anaphylactic reaction occurs.146
Risk of hepatotoxicity.100 146 a 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.146
Risk of heart failure or edema; importance of reporting dyspnea, unexplained weight gain, or edema.100 146 508
Risk of dizziness and potential for drug to impair mental alertness; use caution when driving or operating machinery until effects on individual are known.a
Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.146 Importance of avoiding meclofenamate sodium in pregnancy, particularly during early and late pregnancy (first and third trimesters).100 146 a
Importance of advising women receiving meclofenamate sodium for menorrhagia to notify clinician if spotting or bleeding between menstrual cycles or worsening of menstrual blood flow occurs.100 a
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.100
Importance of informing patients of other important precautionary information.100 (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
50 mg (of meclofenamic acid)*
Meclofenamate Sodium Capsules
100 mg (of meclofenamic acid)*
Meclofenamate Sodium Capsules
AHFS DI Essentials. © Copyright 2017, Selected Revisions March 6, 2017. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.
2. Glazko AJ, Chang T, Borondy PE et al. Metabolic disposition of meclofenamic acid (Meclomen) in laboratory animals and in man. Curr Ther Res. 1978; 23(Suppl):S22-41.
27. Smith TC. Clinical pharmacology studies of sodium meclofenamate (Meclomen). Curr Ther Res. 1978; 23(Suppl):S42-50.
100. Mylan Pharmaceuticals Inc. Meclofenamate sodium capsules prescribing information. Morgantown, WV; 1998 Jun.
101. Markowitz NR, Young SK, Rohrer MD et al. Comparison of meclofenamate sodium with buffered aspirin and placebo in the treatment of postsurgical dental pain. J Oral Maxillofac Surg. 1985; 43:517-22. [PubMed 3859595]
102. Rowe NH, Aseltine LF, Turner JL. Control of pain with meclofenamate sodium following removal of an impacted molar. Oral Surg Oral Med Oral Pathol. 1985; 59:446-8. [PubMed 3892406]
103. Kempf KK, Konzelman JL, Schultz RE et al. Comparison of meclofenamate sodium with buffered aspirin and placebo for the relief of postoperative dental pain. Clin Ther. 1987; 9:594-601. [PubMed 3326678]
104. Hebertson RM, Storey N, Turner JL. Analgesic efficacy of meclofenamate sodium in episiotomy pain. Pharmacotherapy. 1986; 6:205-10. [PubMed 3540870]
105. Yonkeura ML, Petrone S, Turner JL et al. Double-blind comparison of meclofenamate sodium with codeine and placebo for the pain of episiotomy. Clin Ther. 1987; 9:578-84. [PubMed 3326676]
106. Gleason JA, Winer W, Turner JL. Comparison of meclofenamate sodium with codeine and placebo for the treatment of episiotomy pain. Clin Ther. 1987; 9:585-93. [PubMed 3326677]
107. Smith RP, Powell RJ. Simultaneous objective and subjective evaluation of meclofenamate sodium in the treatment of primary dysmenorrhea. Am J Obstet Gynecol. 1987; 157:611-8. [PubMed 3307421]
108. Palmer JF. Letter sent to Lents CE (Parke-Davis) regarding labeling revisions about gastrointestinal adverse reactions to Meclomen (meclofenamate sodium). Rockville, MD: Food and Drug Administration, Division of Oncology and Radiopharmaceutical Drug Products; 1988 Sep.
109. Food and Drug Administration. Labeling revisions for NSAIDs. FDA Drug Bull. 1989; 19:3-4.
110. Searle. Cytotec (misoprostol) prescribing information. Skokie, IL; 1989 Jan.
111. Anon. Drugs for rheumatoid arthritis. Med Lett Drugs Ther. 2000; 42:57-64. [PubMed 10887424]
112. Vargyas JM, Campeau JD, Mishell DR Hr. Treatment of menorrhagia with meclofenamate sodium. Am J Obstet Gynecol. 1987; 157:944-50. [PubMed 3314521]
113. Dawood MY. Nonsteroidal anti-inflammatory drugs and changing attitudes toward dysmenorrhea. Am J Med. 1988; 84(Suppl 5A):23-9. [PubMed 3287908]
114. Koup JR, Tucker E, Thomas DJ et al. A single and multiple dose pharmacokinetic and metabolism study of meclofenamate sodium. Biopharm Drug Dispos. 1990; 11:1-15. [PubMed 2322633]
115. Chan WY, Dawood MY, Fuchs F. Prostaglandins n primary dysmenorrhea: comparison of prophylactic and nonprophylactic treatment with ibuprofen and use of oral contraceptives. Am J Med. 1981; 70:535-41. [PubMed 7011011]
116. Dawood MY. Dysmenorrhoea and prostaglandins: pharmacological and therapeutic considerations. Drugs. 1981; 22:42-56. [PubMed 6790261]
117. Soll AH, Weinstein WM, Kurata J et al. Nonsteroidal anti-inflammatory drugs and peptic ulcer disease. Ann Intern Med. 1991; 114:307-19. [PubMed 1987878]
118. Ciba Geigy, Ardsley, NY: Personal communication on diclofenac 28:08.04.
119. Reviewers’ comments (personal observations) on diclofenac.
120. American College of Rheumatology Subcommittee on Rheumatoid Arthritis Guidelines. Guidelines for the management of rheumatoid arthritis: 2002 update. Arthritis Rheum. 2002; 46:328-46. [PubMed 11840435]
121. Corticosteroid interactions: nonsteroidal anti-inflammatory drugs (NSAIDs). In: Hansten PD, Horn JR. Drug interactions and updates. Vancouver, WA: Applied Therapeutics, Inc; 1993:562.
122. 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. [PubMed 7907735]
123. Hollander D. Gastrointestinal complications of nonsteroidal anti-inflammatory drugs: prophylactic and therapeutic strategies. Am J Med. 1994; 96:274-81. [PubMed 8154516]
124. 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. [PubMed 8475935]
125. 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. [PubMed 2012355]
126. 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. [PubMed 7711609]
127. Hawkey CJ. COX-2 inhibitors. Lancet. 1999; 353:307-14. [PubMed 9929039]
128. 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. [PubMed 8967954]
129. Riendeau D, Charleson S, Cromlish W et al. Comparison of the cyclooxygenase-1 inhibitory properties of nonsteroidal anti-inflammatory drug (NSAIDs) and selective COX-2 inhibitors, using sensitive microsomal and platelet assays. Can J Physiol Pharmacol. 1997; 75:1088-95. [PubMed 9365818]
130. 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; %:325-43.
131. Cryer B, Dubois A. The advent of highly selective inhibitors of cyclooxygenase—a review. Prostaglandins Other Lipid Mediators. 1998; 56:341-61. [PubMed 9990677]
132. Simon LS. Role and regulation of cyclooxygenase-2 during inflammation. Am J Med. 1999; 106(Suppl 5B):37-42S.
133. 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. [PubMed 10511349]
134. Wolfe MM, Lichtenstein DR, Singh G. Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs. N Engl J Med. 1999; 340:1888-99. [PubMed 10369853]
135. Lanza FL, and the members of 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. [PubMed 9820370]
136. Singh G, Triadafilopoulos G. Epidemiology of NSAID induced gastrointestinal complications. J Rheumatol. 1999; 26(suppl 56):18-24.
137. in’t Veld BA, Ruitenberg A, Hofman A et al. Nonsteroidal antiinflammatory drugs and the risk of Alzheimer’s disease. N Engl J Med. 2001; 345:1515-21. [PubMed 11794217]
138. Breitner JCS, Zandi PP. Do nonsteroidal antiinflammatory drugs reduce the risk of Alzheimer’s disease? N Engl J Med. 2001; 345:1567-8. Editorial.
139. McGeer PL, Schulzer M, McGeer EG. Arthritis and anti-inflammatory agents as possible protective factors for Alzheimer’s disease: a review of 17 epidemiologic studies. Neurology. 1996; 47:425-32. [PubMed 8757015]
140. Beard CM, Waring SC, O’sBrien PC et al. Nonsteroidal anti-inflammatory drug use and Alzheimer’s disease: a case-control study in Rochester, Minnesota, 1980 through 1984. Mayo Clin Proc. 1998; 73:951-5. [PubMed 9787743]
141. Veld BA, Launer LJ, Hoes AW et al. NSAIDs and incident Alzheimer’s disease: the Rotterdam Study. Neurobiol Aging. 1998; 19:607-11. [PubMed 10192221]
142. Stewart WF, Kawas C, Corrada M et al. Risk of Alzheimer’s disease and duration of NSAID use. Neurology. 1997; 48:626-32. [PubMed 9065537]
143. Pharmacia. Daypro (oxaprozin) caplets prescribing information. Chicago, IL; 2002 May.
144. Chan FKL, Hung LCT, Suen BY et al. Celecoxib versus diclofenac and omeprazole in reducing the risk of recurrent ulcer bleeding in patients with arthritis. N Engl J Med. 2002; 347:2104-10. [PubMed 12501222]
145. Graham DY. NSAIDs, Helicobacter pylori, and Pandora’s box. N Engl J Med. 2002; 347:2162-4. [PubMed 12501230]
146. US Food and Drug Administration. Proposed NSAID Package Insert Labeling Template 1. From the FDA website (). Accessed 10 Oct 2005.
147. Food and Drug Administration. Analysis and recommendations for agency action regarding non-steroidal anti-inflammatory drugs and cardiovascular risk. 2005 Apr 6.
148. 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.
149. 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.
150. 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. [PubMed 16968831]
151. 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. [PubMed 16740558]
152. Graham DJ. COX-2 inhibitors, other NSAIDs, and cardiovascular risk; the seduction of common sense. JAMA. 2006; 296:1653-6. [PubMed 16968830]
153. Merck & Co. Clinoril (sulindac) tablets prescribing information. Whitehouse Station, NJ; 2006 Feb.
154. 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. [PubMed 23726390]
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. [PubMed 21224324]
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. [PubMed 19171810]
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. [PubMed 21555710]
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. [PubMed 21980265]
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. [PubMed 23747642]
508. Mylan. Meclofenamate sodium capsules prescribing information. Morgantown, WV; 2015 Jul.
509. Cumberland Pharmaceuticals Inc. Caldolor (ibuprofen) injection prescribing information. Nashville, TN; 2016 Apr.
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. [PubMed 22965337]
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. [PubMed 23382889]
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. [PubMed 21596367]
a. AHFS drug information 2007. McEvoy GK, ed. Meclofenamate sodium. Bethesda, MD: American Society of Health-System Pharmacists; 2007:2091-95.
b. Ebner W, Poal Ballarin JM, Boussina I. Meclofenamate sodium in the treatment of ankylosing spondylitis: report of a European double-blind controlled multicenter study. Arzneimittelforschung. 1983; 33(Suppl 4A):660-3. [PubMed 6349653]
c. Eberl R, Dunky A. Meclofenamate sodium in the treatment of acute gout: results of a double-blind study. Arzneimittelforschung. 1983; 33(Suppl 4A):641-3. [PubMed 6349648]
More about meclofenamate
- Side Effects
- During Pregnancy or Breastfeeding
- Dosage Information
- Drug Images
- Drug Interactions
- Support Group
- Pricing & Coupons
- En Español
- 0 Reviews – Add your own review/rating
- Drug class: nonsteroidal anti-inflammatory agents