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PubMed1984

The treatment of premenstrual tension with mefenamic acid: analysis of prostaglandin concentrations.

Eighty patients with premenstrual tension were treated prospectively with mefenamic acid for a mean period of 13 months. Most of them (86%) reported significant relief of premenstrual tension. Symptoms of dysfunctional menorrhagia or primary dysmenorrhoea were also alleviated. In 19 patients, the plasma concentrations of prostaglandin (PG) E2, PGF2 alpha and 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) were measured at intervals throughout three menstrual cycles. During the first cycle the patients received no treatment; in the subsequent two cycles they received either mefenamic acid or placebo in a randomized double-blind crossover manner. Similar measurements were made in 22 matched control subjects. The plasma concentrations of PGE2, PGF2 alpha and PGFM were significantly lower in the 19 patients in all three menstrual cycles compared with the values in the control subjects. Excess synthesis of prostaglandins of the 1 series may occur in premenstrual tension and, by precursor depletion, result in decreased synthesis of the 2-series prostaglandins.

Adolescent↗
PubMed1999

Solubility behavior of polymorphs I and II of mefenamic acid in solvent mixtures.

The dissolution profile and solubility of two polymorphic forms of mefenamic acid were studied in solvent mixtures of ethanol-water and ethyl acetate-ethanol. The solubility parameter (delta) was used to study the effect of polarity on the solubility behavior of the two polymorphs. Differential scanning calorimetry and infrared spectroscopy were performed on the original powders and on the solid phases after contact with the solvent systems for the characterization and identification of the polymorphs. The dissolution rates of both polymorphs is greater in the less polar mixtures (ethyl acetate-ethanol) of lower solubility parameter values. Form II showed larger dissolution rates and saturation concentrations than Form I in all the solvent systems studied. The solid phase of Form II converts totally to Form I after equilibration with the solvents. The rate of conversion was faster in the least polar mixtures. The solubility of both polymorphs reaches a single maximum at 80% ethyl acetate in ethanol, delta = 20.09 MPa1/2. The modified extended Hildebrand method was used to predict the solubility profile of each polymorph. A single equation was obtained for both polymorphs which includes the solubility parameter of the mixtures and the logarithm of the solubility mole fraction of each polymorph in water. The Hildebrand solubility parameter of mefenamic acid is independent of the crystalline form and was determined from two methods giving quite similar values, delta 2 = 20-21 MPa1/2.

Acetates↗
PubMed1983

Double-blind comparison of piroxicam and mefenamic acid in the treatment of oral surgical pain.

Single doses of piroxicam (20 mg) and mefenamic acid (500 mg) were compared, double-blind, for analgesic effectiveness in the treatment of oral surgical pain in out-patients. Excluding placebo responders and patients with mild or no baseline pain, 118 cases (57 piroxicam, 61 mefenamic acid) were analyzed for efficacy. The treatments were statistically equivalent and highly effective; over 75% of patients in both groups reported a reduction of 2 points or more in pain severity. The percentage of patients reporting complete relief of severe pain was slightly higher for piroxicam, the onset of analgesic activity was equivalent, and side effects were infrequent (5%) and mild with both medications. Piroxicam was clearly efficacious in relieving post-exodontic pain. If these findings are confirmed in other painful conditions and safety on extended use is established, piroxicam should prove quite useful as a general analgesic for the treatment of a wide variety of painful conditions.

Adolescent↗
PubMed1988

Mefenamic acid nephropathy: an interstitial and mesangial lesion.

Six cases of acute renal failure associated with mefenamic acid therapy are described. Five patients were non-oliguric and five patients had clinical features of salt and water depletion. In these patients the presenting symptoms were abdominal pain, diarrhoea and vomiting. Renal biopsy in five patients showed interstitial nephritis and mesangial proliferation. All patients recovered without specific therapy after withdrawal of the drug, but in four patients mild renal impairment persisted. These findings indicate that both interstitial and mesangial changes are common features of acute renal failure due to mefenamic acid therapy.

Adult↗
PubMed1987

Effect of mefenamic acid on bronchial tone in vivo.

Prostaglandins (PG) are very potent mediators which can dilate or constrict the bronchi. In order to evaluate the role of PG in the homeostasis of bronchial tone, we studied the effects of mefenamic acid, a potent cyclooxygenase inhibitor, on the pulmonary function tests of 20 volunteers. The subjects were studied randomly in two sessions, one with a placebo and one with mefenamic acid. Tablets (drug or placebo) were taken for 2 days with the pulmonary function tests performed in the afternoon of the second day. Sessions were performed at least 2 days apart. Parameters measured, including forced vital capacity, forced expiratory volume in 1 s, expiratory flows, functional residual capacity and specific airway conductance (SGaw), were similar in both sessions. The SGaw, which was previously reported to increase with cyclooxygenase inhibitors, was 0.23 +/- 0.06 s-1 X cm H2O-1 in the placebo session and 0.24 +/- 0.06 in the mefenamic acid session (mean +/- SD). This study shows that cyclooxygenase inhibitors have no effect on airway tone and strongly suggests that endogenous PG do not participate in the homeostasis of normal bronchial tone.

Adolescent↗
PubMed2002

Sulfation of R(-)-apomorphine in the human liver and duodenum, and its inhibition by mefenamic acid, salicylic acid and quercetin.

1. The aims were to study the sulfation of R-(-)-apomorphine (hereafter apomorphine) in the human liver and duodenum, and to study the rate of inhibition of apomorphine sulphation by mefenamic acid, salicylic acid and quercetin also in the human liver and duodenum. 2. A rapid and sensitive method was developed to measure the sulfation rate of apomorphine in the human liver and duodenum. The method was based on the use of 0.4 micro M 3'-phosphoadenosine-5'-phosphosulfate-[(35)S] (PAPS) and 50 micro M apomorphine. The unreacted PAPS was precipitated with barium hydroxide, barium acetate and zinc sulfate. 3. The rate of apomorphine sulfation (mean +/- SD and median) was 261 +/- 82 and 242 pmol min(-1) mg(-1), respectively (liver), and 433 +/- 157 and 443 pmol min(-1) mg(-1), respectively (duodenum). The apomorphine sulfation rate was higher in the duodenum than in the liver (p = 0.0005). 4. Apomorphine sulfation was correlated with SULT1A1 activity in the liver (r(2) = 0.363, p = 0.005) and duodenum (r(2) = 0.494, p = 0.0005), but it did not correlate with SULT1A3 activity both in the liver and duodenum. 5. The K(m) estimate of apomorphine sulfation rate was 20 +/- 3.6 (liver) and 6.5 +/- 0.2 microM (duodenum, p = 0.024), and the V(max) estimate was 248 +/- 99 (liver) and 636 +/- 104 pmol min(-1) mg(-1) (duodenum, p = 0.018). 6. Mefenamic acid, salicylic acid and quercetin were potent inhibitors of apomorphine sulfation rate in the liver, and the IC(50) estimates were 16 +/- 0.2 nM, 54 +/- 8.6 microM and 18 +/- 2.8 nM, respectively. These compounds were poor inhibitors of apomorphine sulfation in the duodenum. 7. Apomorphine is sulfated by the human liver and duodenum, the highest activity being associated with the duodenum. The K(m) of apomorphine sulfotransferase is in the order of micro M both in the liver and duodenum. The non-steroidal anti-inflammatory drug mefenamic acid and the natural flavonoid quercetin inhibit the hepatic sulfation of apomorphine with an IC(50) in the order of nM.

Adult↗
PubMed2004

Liver injury induced by the non-steroidal anti-inflammatory drug mefenamic acid.

INTRODUCTION: Non-steroidal anti-inflammatory drugs (NSAIDs) are used to treat musculoskeletal disorders, inflammation and to control pain. Virtually all NSAIDs are capable of producing liver injury ranging from mild reversible elevation of liver enzymes to severe hepatic necrosis. METHODS: Mice were dosed intraperitoneally with mefenamic acid either one day at 100mg/kg and 200mg/kg, or 14 days dosing at 50mg/kg/day and 100mg/kg/day. Plasma was taken for alanine aminotransferase activity. Mice were sacrificed at the end of the study. Livers were removed and weighed. Liver samples were taken for histology. results: One-day doses of mefenamic acid revealed dose-dependent hepatocyte degeneration in the liver parenchyma. There were no significant changes in plasma alanine aminotransferase activity. Interestingly, 14-day daily doses induced hepatocellular necrosis, massive degeneration and inflammation. This was accompanied by a significant increase in plasma alanine aminotransferase activity and significant increase in the liver weight in the 100mg/kg/day mefenamic acid-dosed mice. CONCLUSION: Results from this study suggest that mefenamic acid is capable of producing hepatotoxicity and care should be taken when prescribing or using this drug.

Animals↗
PubMed2002

Crystal structure of the inclusion complex of beta-cyclodextrin with mefenamic acid from high-resolution synchrotron powder-diffraction data in combination with molecular-mechanics calculations.

The crystal structure of the inclusion complex of beta-cyclo-dextrin with mefenamic acid has been determined from a combination of high-resolution synchrotron powder-diffraction data and molecular-mechanics calculations. A grid search indicates two possible solutions, which are corroborated by molecular-mechanics calculations, while Rietveld-refinement results suggest the crystal structure that is more likely to be formed in the solid state. Mefenamic acid is partially included in beta-cyclodextrin with either the xylyl or the benzoic-acid moiety being inside its cavity. In both solutions mefenamic acid and beta-cyclodextrin form a monomeric complex in a herringbone packing scheme.

Journal Article↗
PubMed1976

Comparison of effectiveness of mefenamic acid and ibuprofen in treatment of rheumatoid arthritis.

This paper reports a double-blind crossover trial comparing mefenamic acid (1500 mg/day) with ibuprofen (1200 mg/day) in the treatment of patients with rheumatoid arthritis receiving maintenance salicylate therapy. Both drugs were used in three divided doses. Mefenamic acid compared favourably with ibuprofen. In the adopted dose regimes the side effects from both drugs were mild and almost exclusively gastrointestinal.

Arthritis, Rheumatoid↗
PubMed2005

The effects of mefenamic acid on the osmotic fragility of lacertilian erythrocytes.

Osmotic fragility of red cells is increased by the use of mefenamic acid. The use of this analgesic induces hemolytic anemia. Study of osmotic fragility of RBCs of control and test was observed following administration of 7.1 mg, 10.5 mg and 14 mg/day mefenamic acid to each lizard. Increased osmotic fragility was observed with increase in the amount of dose on day 6 and day 12.

Administration, Oral↗
PubMed1997

Diclofenac sodium and mefenamic acid: potent inducers of the membrane permeability transition in renal cortex mitochondria.

The ability of nonsteroidal anti-inflammatory drugs (NSAIDs) to induce Ca(2+)-mediated/cyclosporin A-sensitive mitochondrial membrane permeability transition (MMPT) was evaluated by monitoring swelling of isolated rat renal cortex mitochondria in the presence of 20 microM CaCl2. Dipyrone and paracetamol did not induce MMPT, while piroxicam and acetylsalicylic acid (and its metabolite salicylate) were poor inducers. In contrast, diclofenac sodium and mefenamic acid were potent triggering agents, inducing MMPT at 2 microM, a concentration below those previously shown to uncouple and/or inhibit oxidative phosphorylation. When compared to salicylate, a classical uncoupler and inducer of MMPT, the potency of diclofenac sodium and mefenamic acid was about 50-fold greater. Swelling was completely prevented by EGTA, cyclosporin A, or MgCl2, and only partially by ADP or dithiothreitol. Under the same experimental conditions as for the swelling assays, the drugs depressed the membrane potential of mitochondria, an effect prevented by cyclosporin A and restored by EGTA. Also, the drugs did not induce membrane lipid peroxidation or changes in GSSG levels, but led to a small decrease in protein thiol content, as well as to a substantial decrease in the NADPH levels of mitochondria. Hence, membrane depolarization and pyridine nucleotide oxidation seem to be involved in MMPT induction by these NSAIDs. The potency in eliciting the process, like the uncoupling activity, seems to be influenced by the lipophilic character of the molecules.

Animals↗
PubMed2006

Additive-induced metastable single crystal of mefenamic acid.

PURPOSE: To utilize additives to develop a strategy and a method to grow single crystals that allow structure determination of a metastable form of a drug. MATERIALS AND METHODS: The metastable form of mefenamic acid (MFA) was grown in the presence of various amounts of the structurally similar additive flufenamic acid (FFA) in ethanol. Single crystal X-ray analysis was performed on the single crystals of MFA II that were formed. The solubility of MFA in the presence of FFA was measured to elucidate the mechanism of MFA II formation. RESULTS: A supersaturated solution of MFA in ethanol produced the metastable form using FFA as an additive. Ethanol-water mixtures and toluene were also used to investigate the relationships between form produced and solvent since these two solvent systems do not produce MFA II. CONCLUSIONS: Additives can be used to obtain the metastable form of pharmaceutical compounds, and the relationships between molecules and solvent as well as between host and guest molecules are critical to obtaining the desired form.

Chromatography, High Pressure Liquid↗
PubMed1987

Effects of food on absorption of mefenamic acid from two commercial capsules differing in bioavailability under the fasting state.

The influence of food on the bioavailability of mefenamic acid from two commercial capsules (products A and B) differing in bioavailability was studied with four healthy male volunteers. The drug was administered as a single oral dose of 250 mg under fasting and nonfasting conditions. The study used a 4 X 4 Latin-square design. Seven blood samples were collected over a 9-h period following administration and the plasma concentrations of mefenamic acid were determined by a high performance liquid chromatographical method. The bioavailability was significantly different between the two products in the fasting condition, agreeing with the result of an in vitro dissolution study. However, in the nonfasting state, the difference was not significant because the product showing poor bioavailability, product A, in the nonfasting state showed marked improvement. On the other hand, the product showing good bioavailability, product B, was not affected by food.

Adult↗
PubMed1993

Effects of flunixin and mefenamic acid on cardiac pacemaker cells. Structure-activity relationship and comparison with clonixin.

1. The electrophysiological effects of flunixin and mefenamic acid, non-steroidal analgesics, on frog cardiac pacemaker cells, were studied by intracellular action potential recording. 2. Results show that flunixin (Flx) between 2 x 10(-6) and 1 x 10(-4) M, exerts a frequency, OS, APA and Vmax concentration-dependent decrease, similar to the effects of clonixin (Clx) reported elsewhere (Morales et al., Gen. Pharmac. 23, 515-521, 1992). 3. At 2.5 x 10(-4) M, Flx induces a complete cessation of the electrical activity of subsidiary pacemaker cells. 4. Mefenamic acid (Mef), in spite of its structural similarity with Clx and Flx, induces no appreciable electrophysiological changes. 5. Flx effects were partially reversed by increasing external calcium concentration and fully antagonized by BAY K-8644, a calcium L-type channel agonist. 6. By comparing the structures of the three fenamates studied, it is suggested that the nitrogen of the heterocycle and the electron-donor capacity of the bencenic ring are essential features for the calcium-antagonist activity of Clx and Flx.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Mefenamic acid in prevention of premature labour.

Women at risk of premature delivery were divided randomly into 2 groups of 80 each. Mefenamic acid 500mg 3 times a day or a placebo was given in a double blind fashion. Preterm delivery occurred in 15% of the treated group and 40% of the control group (p < 0.005). The mean birth weight in the test group was higher as compared to the controls. There were no cases of foetal malformations in either of the groups. The results support the use of Mefenamic acid in preventing premature labour.

Adolescent↗
PubMed1988

Inhibition of phospholipase A2 isoenzymes in human endometrium by mefenamic acid and indomethacin: modulation by calcium ions.

The inhibition of endometrial phospholipase A2 activity by the non-steroidal anti-inflammatory agents mefenamic acid and indomethacin was studied over the concentration range 1 mmol/1-0.1 mumol/l. Both phospholipase A2 type 1 (a calcium-dependent enzyme) and phospholipase A2 type 2 (a calcium-independent enzyme) were inhibited by mefenamic acid, but the magnitude of the inhibition was dependent on calcium concentration. Phospholipase A2 type 1 was inhibited 50% by 10 mumol mefenamic acid/l in the presence of 1.25-5 mmol calcium/l, but a concentration of 2.2 mmol mefenamic acid/l was required for 50% inhibition in the absence of calcium. On the other hand, phospholipase A2 type 2 was inhibited 50% by 22 mumol mefenamic acid/l in the absence of calcium and by 100 mumol mefenamic acid/l in the presence of calcium (2.5 mmol/l). Although indomethacin was a less effective inhibitor of phospholipase A2 activity, a similar relationship with calcium was demonstrated. However, indomethacin also had a stimulatory effect on phospholipase A2 type 1 activity in the absence of calcium. Our findings suggest that the two endometrial enzymes may be inhibited by different mechanisms and that the dependence of the enzyme on calcium for activation may be a contributing factor.

Calcium↗
PubMedDate not supplied

Preparation of mefenamic acid sustained release beads based on kappa-carrageenan.

Mefenamic acid (MA) is a nonsteroidal anti-inflammatory drug used as analgesic and antipyretic drug. Available conventional pharmaceutical forms are capsules and film-coated tablets given three times a day (t.t.d.). Natural polymers such as sodium alginate, pectin, chitosan and carregeenan, used as barriers to effect the drug release, are those of the main interest of researchers. The aim of the present study was to formulate sustained release MA-beads based on kappa-carrageenan in order to reduce daily dose and to minimize gastrointestinal disturbances caused by the drug.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2003

Investigations on mefenamic acid sustained release tablets with water-insoluble gel.

Mefenamic acid (MA) has analgesic, anti-inflammatory and antipyretic properties. Available conventional dosage forms are capsules and film-coated tablets. No commercial sustained release preparation of MA exists in the market. The usual oral dose is 250 or 500 mg and reported half-life is 2 h. Sodium alginate (NaAL) is the sodium salt of alginic acid, a natural polysaccharide extracted from marine brown algae. It has the ability to form a water-insoluble gel with a bivalent metal ions as calcium. Therefore, NaAL has been studied for preparing sustained release formulations in pharmaceutical technology. In this study, tablet formulations containing different ratios of NaAL and calcium gluconate (CaGL) were prepared by direct compression method. In vitro release studies were carried out using USP 23 basket method and release data were kinetically evaluated. According to release studies, it can be emphasized that NaAL and CaGL can be used for design of sustained release preparation of MA.

Anti-Inflammatory Agents, Non-Steroidal↗