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MICRO LABS USA,
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42571025830

mefenamic acid 250 mg capsule (generic ponstel)

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Uses

Mefenamic acid is used for the management of mild to moderate pain and primary dysmenorrhea.

The potential benefits and risks of mefenamic acid therapy as well as alternative therapies should be considered prior to initiating mefenamic acid therapy. The lowest possible effective dosage and shortest duration of therapy consistent with treatment goals of the patient should be employed.

Pain

Mefenamic acid is used to relieve mild to moderate pain when the duration of therapy will not exceed 1 week. The drug has been used in the management of postoperative pain and pain following insertion of an intrauterine contraceptive device.

There are few published studies comparing the effectiveness of mefenamic acid with other analgesics, and long-term safety and efficacy of the drug have not been established. Therefore, determination of the relative value of mefenamic acid must await further studies. In the treatment of nonspecific pain associated with cancer, 250-mg oral doses of mefenamic acid appear to be at least as effective as 650-mg oral doses of acetaminophen, 650-mg oral doses of aspirin, 65-mg oral doses of codeine, or 50-mg oral doses of pentazocine.

Dysmenorrhea

Mefenamic acid is used in the management of primary dysmenorrhea. When used to relieve dysmenorrhea in one study, 250-mg doses of mefenamic acid administered 4 times daily beginning with the onset of menses or pain were more effective than placebo. In a controlled study of women with menorrhagia, administration of 500 mg of mefenamic acid 3 times daily resulted in a reduction in blood loss of up to 80% and was accompanied by a reduction in duration of dysmenorrhea and menstrually related headache.

Other Uses

Mefenamic acid has been used for its antipyretic effect in the management of fever associated with infection in children. In one study, the antipyretic effect of usual dosages of mefenamic acid was about equal to that of usual dosages of aspirin. The drug, however, should not be used routinely as an antipyretic because of its potential adverse effects.

Dosage and Administration

Administration

The potential benefits and risks of mefenamic acid therapy as well as alternative therapies should be considered prior to initiating mefenamic acid therapy.

Mefenamic acid is administered orally.

Dosage

The lowest possible effective dosage and shortest duration of therapy consistent with treatment goals of the patient should be employed. Dosage must be carefully adjusted according to individual requirements and response, using the lowest possible effective dosage.

Pain and Dysmenorrhea

For relief of acute, mild to moderate pain or primary dysmenorrhea in adults or children older than 14 years of age, the usual initial dose of mefenamic acid is 500 mg, followed by 250 mg every 6 hours as necessary. For relief of acute pain, the drug should not be administered for longer than 1 week. For relief of primary dysmenorrhea, mefenamic acid therapy should be initiated with the onset of bleeding and associated symptoms and should not be necessary for more than 2-3 days.

Cautions

Cardiovascular Effects

Congestive heart failure, hypertension, tachycardia, syncope, arrhythmia, hypotension, myocardial infarction, palpitations, and vasculitis have occurred in mefenamic acid-treated patients.

Nonsteroidal anti-inflammatory agents (NSAIAs), including selective cyclooxygenase-2 (COX-2) inhibitors and prototypical NSAIAs, increase the risk of serious adverse cardiovascular thrombotic events, including myocardial infarction and stroke (which can be fatal), in patients with or without cardiovascular disease or risk factors for cardiovascular disease. Use of NSAIAs also is associated with an increased risk of heart failure.

The association between cardiovascular complications and use of NSAIAs is an area of ongoing concern and study. Findings of an FDA review of published observational studies of NSAIAs, a meta-analysis of published and unpublished data from randomized controlled trials of these drugs, and other published information indicate that NSAIAs may increase the risk of serious adverse cardiovascular thrombotic events by 10-50% or more, depending on the drugs and dosages studied. Available data suggest that the increase in risk may occur early (within the first weeks) following initiation of therapy and may increase with higher dosages and longer durations of use. Although the relative increase in cardiovascular risk appears to be similar in patients with or without known underlying cardiovascular disease or risk factors for cardiovascular disease, 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.

Results from observational studies utilizing Danish national registry data indicated that patients receiving NSAIAs following a myocardial infarction were at increased risk of reinfarction, cardiovascular-related death, and all-cause mortality beginning in the first week of treatment. Patients who received NSAIAs following myocardial infarction had a higher 1-year mortality rate compared with those who did not receive NSAIAs (20 versus 12 deaths per 100 person-years). Although the absolute mortality rate declined somewhat after the first year following the myocardial infarction, the increased relative risk of death in patients who received NSAIAs persisted over at least the next 4 years of follow-up.

In 2 large controlled clinical trials of a selective COX-2 inhibitor for the management of pain in the first 10-14 days following coronary artery bypass graft (CABG) surgery, the incidence of myocardial infarction and stroke was increased. Therefore, NSAIAs are contraindicated in the setting of CABG surgery.

Findings from some systematic reviews of controlled observational studies and meta-analyses of data from randomized studies of NSAIAs suggest that naproxen may be associated with a lower risk of cardiovascular thrombotic events compared with other NSAIAs. However, limitations of these observational studies and the indirect comparisons used to assess cardiovascular risk of the prototypical NSAIAs (e.g., variability in patients' risk factors, comorbid conditions, concomitant drug therapy, drug interactions, dosage, and duration of therapy) affect the validity of the comparisons; in addition, these studies were not designed to demonstrate superior safety of one NSAIA compared with another. Therefore, FDA states that definitive conclusions regarding relative risks of NSAIAs are not possible at this time.

Data from observational studies also indicate that use of NSAIAs in patients with heart failure is associated with increased morbidity and mortality. Results from a retrospective study utilizing Danish national registry data indicated that use of selective COX-2 inhibitors or prototypical NSAIAs in patients with chronic heart failure was associated with a dose-dependent increase in the risk of death and an increased risk of hospitalization for myocardial infarction or heart failure. In addition, findings from a meta-analysis of published and unpublished data from randomized controlled trials of NSAIAs indicated that use of selective COX-2 inhibitors or prototypical NSAIAs was associated with an approximate twofold increase in the risk of hospitalization for heart failure. Fluid retention and edema also have been observed in some patients receiving NSAIAs.

There is no consistent evidence that use of low-dose aspirin mitigates the increased risk of serious cardiovascular events associated with NSAIAs.

GI Effects

Adverse reactions to mefenamic acid mainly involve the GI tract and may include diarrhea, nausea with or without vomiting, abdominal pain, dyspepsia, heartburn, flatulence, constipation, gross bleeding/GI perforation, and peptic ulcer with or without bleeding. Dry mouth, esophagitis, gastritis, glossitis, stomatitis, weight changes, appetite changes, eructation, and hematemesis have occurred in patients receiving mefenamic acid.

Adverse GI effects may be minimized by administering mefenamic acid with food. In one study, the amount of GI bleeding as determined by fecal blood loss was reported to be less with 2 g of mefenamic acid daily than with 2.6 g of aspirin daily. Although a causal relationship has not been directly determined, one case-control analysis suggests that NSAIAs may contribute to the formation of esophageal stricture in patients with gastroesophageal reflux.

Serious adverse GI effects (e.g., bleeding, ulceration, perforation) can occur at any time in patients receiving NSAIA therapy, and such effects may not be preceded by warning signs or symptoms. Only 1 in 5 patients who develop a serious upper GI adverse event while receiving NSAIA therapy is symptomatic. Therefore, clinicians should remain alert to the possible development of serious GI effects (e.g., bleeding, ulceration) in any patient receiving NSAIA therapy, and such patients should be followed chronically for the development of manifestations of such effects and advised of the importance of this follow-up. In addition, patients should be advised about the signs and symptoms of serious NSAIA-induced GI toxicity and what action to take if they occur. If signs and symptoms of a serious GI event develop, additional evaluation and treatment should be initiated promptly; the NSAIA should be discontinued until appropriate diagnostic studies have ruled out a serious GI event.

Results of studies to date are inconclusive concerning the relative risk of various prototypical NSAIAs in causing serious GI effects. In patients receiving NSAIAs and observed in clinical studies of several months' to 2 years' duration, symptomatic upper GI ulcers, gross bleeding, or perforation appeared to occur in approximately 1% of patients treated for 3-6 months and in about 2-4% of those treated for 1 year. Longer duration of therapy with an NSAIA increases the likelihood of a serious GI event. However, short-term therapy is not without risk. High dosages of any NSAIA probably are associated with an increased risk of such effects, although controlled studies documenting this probable association are lacking for most NSAIAs. Therefore, whenever use of relatively high dosages (within the recommended dosage range) is considered, sufficient benefit to offset the potential increased risk of GI toxicity should be anticipated.

Studies have shown that patients with a history of peptic ulcer disease and/or GI bleeding who are receiving NSAIAs have a substantially higher risk of developing GI bleeding than patients without these risk factors. In addition to a history of ulcer disease, pharmacoepidemiologic studies have identified several comorbid conditions and concomitant therapies that may increase the risk for GI bleeding, including concomitant administration of oral corticosteroids or anticoagulants, longer duration of NSAIA therapy, smoking, alcoholism, older age, and poor general health status. Most spontaneous reports of fatal GI effects have been in geriatric or debilitated patients.

For patients at high risk for complications from NSAIA-induced GI ulceration (e.g., bleeding, perforation), concomitant use of misoprostol can be considered for preventive therapy. Alternatively, some clinicians suggest that a proton-pump inhibitor (e.g., omeprazole) may be used concomitantly to decrease the incidence of serious GI toxicity associated with NSAIA therapy.

Hematologic Effects

The most common adverse hematologic effect of mefenamic acid is a decrease in hematocrit, principally in patients who have received the drug for prolonged periods. Leukopenia, eosinophilia, agranulocytosis, pancytopenia, ecchymosis, melena, purpura, rectal bleeding, thrombocytopenia, hemolytic anemia, aplastic anemia, and lymphadenopathy have also been reported occasionally. Since mefenamic acid can inhibit platelet aggregation, patients who may be adversely affected by a prolongation of bleeding time should be carefully observed during mefenamic acid therapy.

Nervous System Effects

Adverse nervous system effects occur occasionally in patients receiving mefenamic acid and may include drowsiness, dizziness, nervousness, headache, anxiety, asthenia, confusion, depression, dream abnormalities, malaise, paresthesia, somnolence, tremors, vertigo, and insomnia. Seizures, coma, hallucinations, or meningitis has occurred rarely in patient receiving mefenamic acid.

Ocular and Otic Effects

Blurred vision, tinnitus, conjunctivitis, and hearing impairment have occurred in patients receiving mefenamic acid. Patients who experience visual disturbances during therapy with the drug should have an ophthalmologic examination.

Renal Effects

Abnormal renal function, edema, cystitis, dysuria, hematuria, interstitial nephritis, oliguria/polyuria, proteinuria, and renal failure have been reported in mefenamic acid-treated patients. Long-term mefenamic acid therapy has resulted in renal papillary necrosis and other renal medullary changes.

Hepatic Effects

Mild hepatotoxicity has been reported during mefenamic acid therapy. Borderline elevations of one or more liver function test results may occur in up to 15% of patients treated with NSAIAs; meaningful (3 times the upper limit of normal) elevations of serum ALT (SGPT) or AST (SGOT) concentration have occurred in less than 1% of patients receiving NSAIAs in controlled clinical studies. These abnormalities may progress, may remain essentially unchanged, or may be transient with continued therapy. Hepatitis, jaundice, and liver failure have been reported in patients receiving mefenamic acid. Mefenamic acid should be discontinued if signs or symptoms of a severe hepatic reaction occur. (See Cautions: Precautions and Contraindications.)

Other Adverse Effects

Urticaria, rash, pruritus, alopecia, photosensitivity, and perspiration have been reported following mefenamic acid administration. Rarely reported adverse effects include death, angioedema, anaphylactoid reactions, toxic epidermal necrosis, erythema multiforme, exfoliative dermatitis, and Stevens-Johnson syndrome.

Asthma, dyspnea, respiratory depression, and pneumonia have been reported in patients receiving mefenamic acid. Other adverse effects reported in these patients include fever, infection, sepsis, hyperglycemia, and pancreatitis.

Precautions and Contraindications

Patients should be advised that mefenamic acid, like other NSAIAs, is not free of potential adverse effects, including some that can cause discomfort, and that more serious effects (e.g., myocardial infarction, stroke, GI bleeding), which may require hospitalization and may even be fatal, also can occur. Patients also should be informed that, while NSAIAs may be commonly employed for conditions that are less serious, NSAIA therapy often is considered essential for the management of some diseases, and the drugs have a major role in the management of pain. Clinicians may wish to discuss with their patients the potential risks and likely benefits of NSAIA therapy, particularly when consideration is being given to use of these drugs in less serious conditions for which therapy without an NSAIA may represent an acceptable alternative to both the patient and clinician.

Patients should be advised to read the medication guide for NSAIAs that is provided to the patient each time the drug is dispensed.

NSAIAs increase the risk of serious adverse cardiovascular thrombotic events.(See Cautions: Cardiovascular Effects.) To minimize the potential risk of adverse cardiovascular events, the lowest effective dosage and shortest possible duration of therapy should be employed. Some clinicians suggest that it may be prudent to avoid use of NSAIAs whenever possible in patients with cardiovascular disease. Patients receiving NSAIAs (including those without previous symptoms of cardiovascular disease) should be monitored for the possible development of cardiovascular events throughout therapy. Patients should be informed about the signs and symptoms of serious cardiovascular toxicity (chest pain, dyspnea, weakness, slurring of speech) and instructed to seek immediate medical attention if such toxicity occurs. Mefenamic acid should be avoided in patients with recent myocardial infarction unless the benefits of therapy are expected to outweigh the risk of recurrent cardiovascular thrombotic events; if mefenamic acid is used in such patients, the patient should be monitored for cardiac ischemia.

There is no consistent evidence that concomitant use of low-dose aspirin mitigates the increased risk of serious cardiovascular events associated with NSAIAs. Concomitant use of aspirin and an NSAIA increases the risk for serious GI events. Because of the potential for increased adverse effects, patients receiving mefenamic acid should be advised not to take aspirin.

Use of NSAIAs can result in the onset of hypertension or worsening of preexisting hypertension; either of these occurrences may contribute to the increased incidence of cardiovascular events. Patients receiving NSAIAs may have an impaired response to diuretics (i.e., thiazide or loop diuretics), angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor antagonists, or β-adrenergic blocking agents. NSAIAs should be used with caution in patients with hypertension. Blood pressure should be monitored closely during initiation of NSAIA therapy and throughout therapy.

Because NSAIAs increase morbidity and mortality in patients with heart failure, the manufacturer states that mefenamic acid should be avoided in patients with severe heart failure unless the benefits of therapy are expected to outweigh the risk of worsening heart failure; if mefenamic acid is used in such patients, the patient should be monitored for worsening heart failure. Some experts state that use of NSAIAs should be avoided whenever possible in patients with reduced ventricular ejection fraction and current or prior symptoms of heart failure. Patients receiving NSAIAs should be advised to inform their clinician if they experience symptoms of heart failure, including dyspnea, unexplained weight gain, and edema. Use of NSAIAs may diminish the cardiovascular effects of certain drugs used to treat heart failure and edema (e.g., diuretics, ACE inhibitors, angiotensin II receptor antagonists).(See Drug Interactions.)

The risk of potentially serious adverse GI effects should be considered in patients receiving mefenamic acid, particularly in patients receiving chronic therapy with the drug.(See Cautions: GI Effects.) Mefenamic acid should be used with caution in patients with a history of upper GI disease. Since peptic ulceration and/or GI bleeding have been reported in patients receiving the drug, patients should be advised to promptly report signs or symptoms of GI ulceration or bleeding to their clinician.

Mefenamic acid should be used with extreme caution and under close supervision in patients with a history of GI bleeding or peptic ulceration, and such patients should receive an appropriate ulcer preventive regimen. All patients considered at increased risk of potentially serious adverse GI effects (e.g., geriatric patients, those receiving high therapeutic dosages of NSAIAs, those with a history of peptic ulcer disease, those receiving anticoagulants or corticosteroids concomitantly) should be monitored closely for signs and symptoms of ulcer perforation or GI bleeding. To minimize the potential risk of adverse GI effects, the lowest effective dosage and shortest possible duration of therapy should be employed. For patients who are at high risk, therapy other than an NSAIA should be considered. The manufacturer states that mefenamic acid is contraindicated in patients with active ulceration or chronic inflammation of the upper or lower GI tract.

The possibility that the antipyretic and anti-inflammatory effects of NSAIAs may mask the usual signs and symptoms of infection or other diseases should be considered.

Elevations in serum ALT may be the most sensitive indicator of NSAIA-induced liver dysfunction. Patients who experience signs and/or symptoms suggestive of liver dysfunction or an abnormal liver function test result while receiving mefenamic acid should be evaluated for evidence of the development of a severe hepatic reaction. Severe reactions, including jaundice and fatal fulminant hepatitis, liver necrosis, and hepatic failure (sometimes fatal), have been reported in patients receiving NSAIAs. Although such reactions are rare, mefenamic acid should be discontinued if abnormal liver function test results persist or worsen, if clinical signs and symptoms consistent with liver disease develop, or if systemic manifestations occur (e.g., eosinophilia, rash).

Patients receiving mefenamic acid are at risk of developing adverse renal effects. Renal toxicity has been observed in patients in whom renal prostaglandins have a compensatory role in maintaining renal perfusion. Administration of an NSAIA to such patients may cause a dose-dependent reduction in prostaglandin formation and thereby precipitate overt renal decompensation. Patients at greatest risk of this reaction include those with impaired renal function, heart failure, or hepatic dysfunction; those with extracellular fluid depletion (e.g., patients receiving diuretics); those taking an ACE inhibitor or angiotensin II receptor antagonist concomitantly; and geriatric patients. Patients should be advised to consult their clinician promptly if unexplained weight gain or edema occurs. Recovery of renal function to pretreatment levels usually occurs following discontinuance of NSAIA therapy.

The manufacturer states that mefenamic acid should not be administered to patients with substantial renal impairment.

Mefenamic acid is not a substitute for corticosteroid therapy. Use of corticosteroids during NSAIA therapy may increase the risk of GI ulceration, and the drugs should be used concomitantly with caution. If corticosteroid dosage is decreased during mefenamic acid therapy, it should be done gradually and patients should be observed for adverse effects, including adrenocortical insufficiency or symptomatic exacerbation of the inflammatory condition being treated.

Mefenamic acid should be used with caution in patients who may be adversely affected by a prolongation of bleeding time (e.g., patients receiving anticoagulant therapy), because the drug may inhibit platelet function. If signs and/or symptoms of anemia occur during therapy with mefenamic acid, hemoglobin concentration and hematocrit should be determined.

Anaphylactoid reactions have been reported in patients receiving mefenamic acid. Patients receiving mefenamic acid should be informed of the signs and symptoms of an anaphylactoid reaction (e.g., difficulty breathing, swelling of the face or throat) and advised to seek immediate medical attention if an anaphylactoid reaction develops.

Serious skin reactions (e.g., exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis) can occur in patients receiving NSAIAs. These serious skin reactions may occur without warning; patients should be advised to consult their clinician if skin rash and blisters, fever, or other signs of hypersensitivity reaction (e.g., pruritus) occur. Mefenamic acid should be discontinued at the first appearance of rash or any other sign of hypersensitivity.

Patients receiving long-term NSAIA therapy should have a complete blood cell count and chemistry profile performed periodically.

The manufacturers state that mefenamic acid is contraindicated in patients with known hypersensitivity to the drug. In addition, NSAIAs generally are contraindicated in patients in whom asthma, urticaria, or other sensitivity reactions are precipitated by aspirin or other NSAIAs, since there is potential for cross-sensitivity between NSAIAs and aspirin, and severe, often fatal, anaphylactic reactions may occur in such patients. Although NSAIAs generally are contraindicated in these patients, the drugs have occasionally been used in NSAIA-sensitive patients who have undergone desensitization. Because patients with asthma may have aspirin-sensitivity asthma, NSAIAs should be used with caution in patients with asthma. In patients with asthma, aspirin sensitivity is manifested principally as bronchospasm and usually is associated with nasal polyps; the association of aspirin sensitivity, asthma, and nasal polyps is known as the aspirin triad. For a further discussion of cross-sensitivity of NSAIAs,

NSAIAs are contraindicated in the setting of CABG surgery.

Pediatric Precautions

Safety and efficacy of mefenamic acid in children younger than 14 years of age have not been established.

Geriatric Precautions

Caution should be observed if mefenamic acid is used in geriatric individuals. Many of the spontaneous reports of fatal adverse GI effects in patients receiving NSAIAs involve geriatric individuals.(See Cautions: GI Effects.)

Clinical studies of mefenamic acid did not include sufficient numbers of patients 65 years of age or older to determine whether geriatric patients respond differently than younger individuals.

Because geriatric patients are more likely to have decreased renal function and patients with renal impairment may be at increased risk of adverse reactions to mefenamic acid, the dosage should be selected carefully. It may be useful to monitor renal function in geriatric patients.

Pregnancy, Fertility, and Lactation

Pregnancy

Although there are no adequate and controlled studies to date in humans, mefenamic acid has been shown to have various adverse effects in animals during reproduction studies. Doses up to 10 times the usual human dose have resulted in a decreased rate of fetal survival-to-weaning in rats; these doses did not result in fetal abnormalities in rats or dogs. In rabbits, doses up to 2.5 times the usual human dose resulted in an increase in the number of fetal resorptions. Mefenamic acid inhibits prostaglandin synthesis which may result in prolongation of gestation and interference with labor if the drug is given late in pregnancy. Inhibitors of prostaglandin synthesis may have adverse effects on the fetal cardiovascular system (e.g., premature closure of the ductus arteriosus); therefore, administration of the drug during late pregnancy should be avoided. Mefenamic acid should be used during early pregnancy only when the potential benefits justify the possible risks to the fetus.

Fertility

Doses of mefenamic acid up to 10 times the usual human dose have resulted in decreased fertility in rats. The effect of the drug on fertility in humans is not known.

Lactation

Mefenamic acid is distributed into milk. Because of the potential for adverse effects from mefenamic acid on the cardiovascular system in infants, a decision should be made whether to discontinue nursing or the drug, taking into account the importance of the drug to the woman.

Drug Interactions

Protein-bound Drugs

Because mefenamic acid is highly protein bound, it theoretically could be displaced from binding sites by, or it could displace from binding sites, other protein-bound drugs such as oral anticoagulants, hydantoins, salicylates, sulfonamides, and sulfonylureas. Patients receiving mefenamic acid with any of these drugs should be observed for adverse effects.

Drugs Affecting Hepatic Microsomal Enzymes

Mefenamic acid is metabolized by cytochrome P-450 (CYP) isoenzyme 2C9, and concomitant use with drugs that inhibit this isoenzyme may result in altered safety and efficacy of mefenamic acid.

Angiotensin-converting Enzyme Inhibitors and Angiotensin II Receptor Antagonists

There is some evidence that concomitant use of NSAIAs with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor antagonists may reduce the blood pressure response to the antihypertensive agent.

Anticoagulants and Thrombolytic Agents

The effects of warfarin and NSAIAs on GI bleeding are synergistic. Concomitant use of NSAIAs and warfarin is associated with a higher risk of GI bleeding compared with use of either agent alone.

Mefenamic acid enhances the hypoprothrombinemic effect of warfarin. If the drugs must be used concurrently, prothrombin time should be determined frequently and anticoagulant dosage adjusted accordingly; the patient should be observed for adverse effects. In addition, the ulcerogenic potential of mefenamic acid and the effect of the drug on platelet function may further contribute to the hazard of concomitant therapy with any anticoagulant or thrombolytic agent (e.g., streptokinase).

Aspirin

Concomitant use of aspirin and an NSAIA increases the risk for serious GI events.Because of the potential for increased adverse effects, patients receiving mefenamic acid should be advised not to take aspirin. There is no consistent evidence that use of low-dose aspirin mitigates the increased risk of cardiovascular effects associated with NSAIAs.

Antacids

Concomitant administration of an antacid containing 1.7 g of magnesium hydroxide with mefenamic acid 500 mg increased the peak plasma concentration of mefenamic acid by 125% and the area under the plasma concentration-time curve (AUC) by 36% in a limited number of individuals.

Diuretics

NSAIAs can reduce the natriuretic effects of furosemide or thiazide diuretics. This effect may be related to inhibition of renal prostaglandin synthesis. Patients receiving concomitant NSAIA and diuretic therapy should be monitored for signs of renal failure and for efficacy of the diuretic.

Lithium

Mefenamic acid has been reported to reduce renal lithium clearance. The mechanism involved in the reduction of lithium clearance by NSAIAs is not known, but has been attributed to inhibition of prostaglandin synthesis, which may interfere with the renal elimination of lithium. If mefenamic acid and lithium are administered concurrently, the patient should be observed closely for signs of lithium toxicity, and serum lithium concentrations should be monitored carefully during initial stages of combined therapy. In addition, appropriate adjustment of lithium dosage may be required when therapy with mefenamic acid is discontinued.

Methotrexate

Because of the possibility of enhanced toxicity of methotrexate, caution is advised if methotrexate and an NSAIA are administered concomitantly.

Pharmacokinetics

Absorption

Mefenamic acid appears to be rapidly absorbed from the GI tract. Following oral administration of a single 1-g dose of mefenamic acid to healthy adults, peak plasma drug concentrations of approximately 10-20 mcg/mL are reached in 2-4 hours. Following oral administration of 1 g of mefenamic acid 4 times daily, steady-state concentrations of 20 mcg/mL are reached by the second day of administration. After multiple doses, plasma concentrations of mefenamic acid are 15proportional to the dose administered. The manufacturer states that there is no evidence of drug accumulation following multiple doses.

Distribution

Mefenamic acid is extensively bound to plasma proteins. It is not known if the drug or its metabolites cross the placenta. The drug is distributed into milk in very small amounts.

Elimination

The plasma half-life of mefenamic acid has been reported to be 2 hours.

Mefenamic acid is metabolized by cytochrome P-450 (CYP) isoenzyme 2C9 to 3'-hydroxymethyl mefenamic acid; further oxidation to 3'-carboxylmefenamic acid may occur. Glucuronic acid conjugates of the drug and its metabolites are also formed.

About 52% of a dose of mefenamic acid is excreted in urine as glucuronic acid conjugates of the drug and its metabolites. About 20% of a dose is excreted in feces. Mefenamic acid is apparently not dialyzable.

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