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PubMed1989

[Nimesulide in the treatment of primary dysmenorrhea. Comparative clinical evaluation with mefenamic acid and fentiazac].

Sixty patients with primary dismenorrhea were treated: 20 with nimesulide, 20 with fentiazac and 20 with mefenamic acid during three consecutive cycles under double blind design. The doses used in each group were: nimesulide or fentiazac 100 mg, every 12 hrs., mefenamic acid 500 mg. every 8 hrs. in all cases during 5 days, beginning a day before the beginning, of the menstruation. The pain evolution and the symptoms were evaluated three times a day using a scale from 0 to 10, so measure its intensity. Concluding, the nimesulide is useful in the treatment of pain associated with primary dismenorrhea, answering with little statistical advantage over the fentiazac and with bigger statistical advantage over the mefenamic acid. The tolerance was excellent with the three drugs studied.

Acetates↗
PubMed1981

Efficacy of mefenamic acid in patients with a complaint of menorrhagia.

Sixty-nine patients with a convincing history of menorrhagia completed a 4-cycle double-blind randomized placebo-controlled crossover trial of mefenamic acid taken during menstruation. Only 30 of these patients demonstrated objective menorrhagia with a measured menstrual loss greater than 80 ml during the placebo cycles, but the remainder reported passing clots and/or using 2 pads at a time. Fourteen of these women (20%) had a loss of less than 35 ml while taking placebos. This raises serious questions about the establishment of menorrhagia based on history alone. Overall, there was a mean reduction of 28.1% in menstrual blood loss between placebo and mefenamic acid cycles (P less than .001). The greatest reduction recorded was 80%, and most of the large percentage reductions were seen in patients with high loss during placebo cycles. Significant reductions in blood loss (P less than .001) were seen in patients with ovulatory dysfunctional uterine bleeding and menorrhagia that developed after tubal interruption. There was also an indication based on small sample sizes that mefenamic acid reduced blood loss in women with anovulatory dysfunctional uterine bleeding, fibroids, intrauterine devices, and von Willebrand disease. No reduction was seen during the mefenamic acid cycle in the group with a loss of less than 35 ml during the placebo cycle. There was a significant shortening of duration of bleeding (P less than .003). Fifteen patients (21.7%) experienced no objective reduction in blood loss.

Adolescent↗
PubMed1980

The treatment of premenstrual symptoms with mefenamic acid.

Thirty-seven patients suffering from premenstrual symptoms were each studied through three menstrual cycles. After a control cycle, mefenamic acid and placebo were given during the luteal phase of the cycle in a random double-blind cross over manner, each patient serving as her own control. The dosage of mefenamic acid was 500 mg thrice daily. Medication significantly improved premenstrual symptoms, particularly tension, irritability, depression, pain and headache. It was not effective for breast symptoms. Most patients complaining of premenstrual symptoms also had menstrual symptoms, which were also improved by the mefenamic acid.

Adult↗
PubMed1987

A case of intravenous and oral mefenamic acid poisoning.

A 22 year old heroin addict was admitted with tonic-clonic seizures, confusion and agitation 10 hours after taking mefenamic acid 5 grams orally and 2.25 grams intravenously. This appears to be the first recorded case of intravenous mefenamic acid abuse and, although not fatal, is a cause of concern. This is a commonly used drug and its seizure inducing potential is well recognised. It may therefore be worthwhile considering the possibility of intravenous abuse of mefenamic acid in heroin addicts admitted with confusion or seizures.

Administration, Oral↗
PubMed1992

Effects of mefenamic acid on menstrual hemostasis in essential menorrhagia.

Prostaglandin synthesis inhibitors decrease menstrual blood loss by 30% to 50% in patients with essential menorrhagia. To obtain insight into their mechanism of action, we measured menstrual blood loss in menorrhagic women, who were receiving mefenamic acid (500 mg, three times daily) (n = 6) or placebo (n = 5) in a double-blind way. In addition we studied the morphology of early menstrual hemostasis. The subjects' uteri were extirpated in the first 24 hours of menstruation, and light and electron microscopy were used to perform morphologic and morphometric studies. In the group treated with mefenamic acid mean menstrual blood loss was decreased by 40%. In uteri of the women treated with mefenamic acid hemostatic plugs were further transformed, and fewer vessels without a plug were observed than in uteri of the group receiving placebo. These data suggest that mefenamic acid may act through an improvement of platelet aggregation and degranulation and through increased vasoconstriction.

Adult↗
PubMed1998

Determination of flufenamic, meclofenamic and mefenamic acids by capillary electrophoresis using beta-cyclodextrin.

The possibility of separating flufenamic, meclofenamic and mefenamic acids by capillary electrophoresis was studied. The best approach involved combining a suitable pH of the carrier electrolyte (pH 12.0) with the host-guest complexation effects of beta-cyclodextrin. A running buffer consisting of 30 mM phosphate buffer (pH 12.0), 2 mM beta-CD and 10% (v/v) acetonitrile was found to provide a very efficient and stable electrophoresis system for the analysis of fenamic acids by capillary zone electrophoresis. Responses were linear from 0.4 to 40 microg/ml for the three drugs with detection limits of about 0.3 ng/ml. Intra- and inter-day precision values of about 1-2% R.S.D. (n = 11) and 3-4% R.S.D. (n = 30), respectively, were obtained. The method is highly robust and no breakdowns of the current or capillary blockings were observed for several weeks. The general applicability of this rapid CZE procedure (migration times less than 12 min) is demonstrated for several practical samples, including serum, urine and pharmaceuticals.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1968

Autoimmune haemolytic anaemia and mefenamic acid therapy.

Three patients developed autoimmune haemolytic anaemia while being treated with mefenamic acid. In each case the autoimmune haemolytic anaemia was of the warm antibody gammaG type, and the antibodies had some rhesus specificity. All three patients recovered when the drug was withdrawn.Attempts to inhibit or enhance the activity of the antibody in vitro were unsuccessful.Direct antihuman globulin tests were made in.the red cells of 36 patients receiving long-term mefenamic acid therapy, but only one was found to be transitorily positive.

Anemia, Hemolytic, Autoimmune↗
PubMed1984

Comparison of the relative effects of aspirin, mefenamic acid, dihydrocodeine, dextropropoxyphene and paracetamol on visceral pain, respiratory rate and prostaglandin biosynthesis.

A comparison was made between the relative effects of aspirin, mefenamic acid, dihydrocodeine , dextropropoxyphene and paracetamol on visceral pain (chemically-inducing writhing), respiratory rate and prostaglandin (PG) biosynthesis (cyclo-oxygenase activity). A close correlation was found to exist between inhibition of PG biosynthesis and inhibition of visceral pain for mefenamic acid, aspirin and paracetamol. Analysis of the complete activity profiles derived from evaluation of the test parameters yielded the following rank order of overall ratios of their beneficial anti-writhing/anti-cyclo-oxygenase to respiratory depressive activities: (1) mefenamic acid, (2) aspirin, (3) dihydrocodeine , (4) dextropropoxyphene and paracetamol.

Acetaminophen↗
PubMed2005

Altered brain penetration of diclofenac and mefenamic acid, but not acetaminophen, in Shiga-like toxin II-treated mice.

It is well accepted that bacterial and virus infections elevate the levels of cytokines in serum and cerebrospinal fluids. Such high levels of cytokines might alter the integrity of the blood-brain barrier (BBB) and/or blood-cerebrospinal fluid barrier (BCSFB), subsequently affecting brain penetration of drugs. However, few reports have addressed this issue. Thus, we investigated brain penetration of cyclooxygenase (COX) inhibitors, commonly used as antipyretics, in mice treated with Shiga-like toxin II (SLT-II) derived from E. coli O157:H7, which significantly elevates cytokine levels. As antipyretics, we used diclofenac, mefenamic acid, and acetaminophen. We found that SLT-II significantly increased the brain-to-plasma concentration ratio (Kp) of diclofenac and mefenamic acid, but not of acetaminophen. Moreover, the Kp of diclofenac and mefenamic acid was increased by probenecid, an anionic compound. These results suggest that efflux anion transporters might be involved in the transport of diclofenac and mefenamic acid. Western blot analysis revealed that SLT-II decreased the expression of organic anion transporter-3, an efflux transporter located on the BBB and/or BCSFB. Taken together, these results suggest that SLT-II and/or SLT-II-stimulated cytokines might change brain penetration of drugs and could possibly increase the risk of their side-effects by altering the expression of transporters.

Acetaminophen↗
PubMed1986

Premenstrual syndrome in Cape Town. Part II. A double-blind placebo-controlled study of the efficacy of mefenamic acid.

Thirty patients suffering from the premenstrual syndrome were studied for five consecutive menstrual cycles. An untreated baseline cycle without medication was followed by four treatment cycles. Mefenamic acid or placebo was taken on days 11-26 of the cycle in a prospectively randomized double-blind cross-over manner, with each patient acting as her own control. On subjective assessment, there was a significant overall improvement on mefenamic acid compared with placebo. With the exception of gastro-intestinal symptoms, mefenamic acid was not significantly better than placebo for any of the individual symptoms assessed on the patients daily symptom checklists.

Clinical Trials as Topic↗
PubMed1986

A comparative crossover study of piroxicam vs. mefenamic acid and diclofenac in France.

A multicenter open crossover study compared piroxicam and mefenamic acid and piroxicam and diclofenac in the treatment of primary dysmenorrhea in 91 patients. Piroxicam 40 mg/day for two days followed by 20 mg/day was compared with mefenamic acid 500 mg t.i.d. and diclofenac 50 mg b.i.d. for two menstrual cycles on each drug. Assessment of efficacy found that piroxicam was more effective than either comparative drug. All three agents were well tolerated. It is concluded that piroxicam is a safe and effective drug for the treatment of primary dysmenorrhea.

Adult↗
PubMed1986

Double-blind comparison of ketoprofen and mefenamic acid in the treatment of primary dysmenorrhea.

Forty women with moderate to severe primary dysmenorrhea participated in a two-month, double-blind, crossover trial comparing ketoprofen with mefenamic acid. Treatment with ketoprofen provided rapid and marked pain relief similar to that afforded by mefenamic acid. This improvement in symptoms was accompanied by an amelioration of the disability score, which was equivalent for both drugs. There were no differences between the two treatments with respect to duration of menses or amount of menstrual flow. Patients rated both drugs as equally effective and had no preference for one treatment over the other. One patient dropped out because of a mild allergic reaction to ketoprofen. All other side effects were not severe, although slightly more gastrointestinal reactions were observed with ketoprofen. It is concluded that ketoprofen is as safe and effective as mefenamic acid in the treatment of primary dysmenorrhea.

Adolescent↗
PubMed1987

The effects of danazol, mefenamic acid, norethisterone and a progesterone-impregnated coil on endometrial prostaglandin concentrations in women with menorrhagia.

The effects of four medical treatments have been assessed on menstrual blood loss (MBL) and endometrial prostaglandin (PG) concentrations in 30 women with objectively confirmed menorrhagia. Patients were randomly treated with danazol, 200 mg daily (n = 6), mefenamic acid, 500 mg three times daily during menses (n = 8), norethisterone, 5 mg twice daily from day 15-25 of the cycle (n = 8) or a progesterone-impregnated coil releasing 65 micrograms progesterone daily (n = 8). Endometrial biopsies were obtained in the mid-luteal phase before and after treatment in 23 cases, and assayed for PG content using radioimmunoassay. Treatment with norethisterone had no effect on either MBL or the concentration of PGs in the endometrium. MBL was significantly reduced after treatment with mefenamic acid (P = 0.05, n = 6) and the progesterone coil (P less than 0.05, n = 6), and was reduced in each of 4 cases treated with danazol in whom endometrial biopsies were available. Although there was no consistent change in endometrial PG concentrations in either the mefenamic acid or danazol groups, the lower MBL after insertion of the progesterone coil was associated with a reduced endometrial content of PGE, PGF2 alpha and "total" PG (6oxo PGF1 alpha + PGE + PGF2 alpha)-P = 0.05. Whereas the cyclooxygenase inhibitor mefenamic acid is likely to exert its effect on endometrial PGs at the time of menstruation itself, the continuous administration of progesterone throughout the menstrual cycle could result in both an impairment in estrogen receptor generation leading to reduced estrogen-mediated cyclooxygenase activity, and an increase in endometrial PG metabolism.

Biopsy↗
PubMed1978

[Autoimmune hemolytic anemia induced by mefenamic acid].

A case of autoimmunohemolytic anemia following mefenamic acid therapy is described. A free anti-erythrocytic antibody of the IgG class was found in the serum of the patient. The same antibody was also found in the eluate of the patient's red cells. No blood group specificity could be demonstrated. Direct participation of the drug in the antibody red cell reaction could be ruled out by "facilitation" and "inhibition" tests.

Anemia, Hemolytic, Autoimmune↗
PubMed2004

Physicochemical and crystallographic characterization of mefenamic acid complexes with alkanolamines.

The preparation of mefenamic acid (MH)-alkanolamine (propanolamine, diethanolamine, triethanolamine) complexes was attempted to increase the transdermal flux of MH. Differential scanning calorimetry, Fourier transform infrared spectroscopy, and X-ray crystallographic studies demonstrated that MH and each alkanolamine formed an ion pair complex. The series of amine complexes had a lower melting point and higher solubility in water compared with pure MH.

Alkanes↗
PubMed1990

The effects of mefenamic acid and norethisterone on measured menstrual blood loss.

Although there are numerous medical treatments for menorrhagia, in many instances neither the precise diagnosis nor the response to therapy have been assessed objectively. Menorrhagia (menstrual blood loss more than 80 mL per cycle) was diagnosed objectively in 32 (44%) of 72 women with a subjective complaint of heavy menses. All of the 32 women had ovulatory cycles. After random allocation to treatment with either mefenamic acid (500 mg three times daily during menses, N = 17) or norethisterone (5 mg twice daily on days 19-26 of the cycle, N = 15) for two additional cycles, the median menstrual blood loss was reduced from 123 mL (range 86-237) to 81 mL (22-193) (P less than .001) and from 109 mL (81-236) to 92 mL (43-189) (P less than .002) with mefenamic acid and norethisterone, respectively. Apart from a decrease in the median number of days of bleeding, from 7 (5-8) to 5 (3-8) in those women treated with mefenamic acid, no other differences were seen between the groups. We conclude that mefenamic acid and norethisterone were similarly effective in reducing the degree of menstrual blood loss in women with proved menorrhagia, but that 52 and 67% of the women, respectively, remained menorrhagic after 2 months of treatment.

Adult↗
PubMed1995

Bromoacetamido analogs of indomethacin and mefenamic acid as affinity-labeling agents and mechanistic probes for prostaglandin H2 synthase.

Affinity-labeling agents, 1-[4-(bromoacetamido)benzyl]-5-methoxy-2-methylindole-3-acetic acid (I) and 4-(bromoacetamido)-N-(2,3-dimethylphenyl)anthranilic acid (II), were synthesized on the basis of their respective nonsteroidal anti-inflammatory drugs (NSAIDs), indomethacin and mefenamic acid [Askonas & Penning (1991) Biochemistry 30, 11553-11560]. Compounds I and II are now shown to inhibit homogeneous ram seminal vesicle prostaglandin H2 (PGH2) synthase by two kinetically distinct complexes. They are competitive inhibitors versus arachidonic acid via the formation of high-affinity E.I complexes, and they cause time-dependent inactivation of the holoenzyme via low-affinity E.I complexes. Compounds I and II, unlike classical NSAIDs, were found to inactivate both the cyclooxygenase and peroxidase reactions of the synthase in a parallel manner. Inactivation was accompanied by the incorporation of 2 mol of either radiolabeled I or II per synthase monomer. The covalent bonds that result were stable to boiling in SDS, indicating that I and II offer alternatives to aspirin in locating NSAID binding sites. Incubation of aspirin-treated PGH2 synthase with radiolabeled I reduced the stoichiometry of incorporation to 1.0, suggesting that one of the sites modified corresponds to the cyclooxygenase site. By saturating the cyclooxygenase site with mefenamic acid, I and II only abolished the peroxidase activity of the enzyme, suggesting that the second site of modification corresponds to the peroxidase site. When PGH2 synthase was incubated with mefenamic acid and I or II, only the peroxidase activity was inactivated. Subsequent removal of all drugs by dialysis gave a preparation of PGH2 synthase that could perform the cyclooxygenase reaction, but lacked the ability to cleave ethyl hydroperoxide to ethanol and water.(ABSTRACT TRUNCATED AT 250 WORDS)

Affinity Labels↗
PubMed2006

Effects of aspirin and mefenamic acid on soman poisoning-induced neuropathology in mice.

The efficacy of aspirin and mefenamic acid to counteract soman-induced brain damage was investigated in mice. Neuronal damage was evaluated in the hippocampus and amygdala by performing omega3 receptor density measurements and hemalun-phloxin staining. The effect of both drugs on the proliferation of neural progenitors after soman exposure was also assessed. Mefenamic acid aggravated the soman-induced hippocampal neuropathology. On the other hand, aspirin recorded a weak neuroprotective effect in the amygdala. However, this drug also diminished the proliferation of neural precursor cells. The possible neurochemical mechanisms underlying such differences in the efficacy of the two drugs are also reviewed.

Animals↗