PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Mefenamic Acid”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1990

Flufenamic acid, mefenamic acid and niflumic acid inhibit single nonselective cation channels in the rat exocrine pancreas.

The non-steroidal anti-inflammatory drugs, flufenamic acid, mefenamic acid and niflumic acid, block Ca2(+)-activated non-selective cation channels in inside-out patches from the basolateral membrane of rat exocrine pancreatic cells. Half-maximal inhibition was about 10 microM for flufenamic acid and mefenamic acid, whereas niflumic acid was less potent (IC50 about 50 microM). Indomethacin, aspirin, diltiazem and ibuprofen (100 microM) had not effect. It is concluded that the inhibitory effect of flufenamate, mefenamate and niflumate is dependent on the specific structure, consisting of two phenyl rings linked by an amino bridge.

Animals↗
PubMed1992

A comparison of tiaprofenic acid, mefenamic acid and placebo in the treatment of dysmenorrhoea in general practice.

The efficiency and side-effects of tiaprofenic acid, mefenamic acid and placebo were compared in the treatment of primary dysmenorrhoea. The trial was a double-blind prospective randomized 3-way crossover study during 6 successive menstrual cycles following a 2-cycle run-in period and involved 50 women with primary dysmenorrhoea selected from 96 volunteers between 16 and 35 years of age. Overall pain was significantly less (p less than 0.05) on treatment with tiaprofenic acid than on treatment with mefanemic acid, placebo, or the women's usual treatments. Both active treatments were well tolerated but more side-effects were reported during treatment with mefenamic acid.

Adolescent↗
PubMed1986

Investigation of dressings designed for treatment of alveolitis sicca dolorosa ("dry socket"). Part 3: Influence of mannitol and sorbitol on properties of tablets and dressings comprising acetylsalicylic acid, mefenamic acid and aseptin P.

In the dressings for dry tooth sockets, mannitol and sorbitol as solid hydrophilizers have been applied. Increase of concentrations of these hydrophilizers in the tablets results in dressings with increased swelling ability and pharmaceutical availability but decreased viscosity and resistance to washing out. These properties of the dressings are also influenced by medicinal substances present. The dressing fills the tooth socket within several min, removes pain and remain there for 24-48 h.

Anti-Infective Agents↗
PubMed1985

The effect of activated charcoal and hyoscine butylbromide alone and in combination on the absorption of mefenamic acid.

Mefenamic acid 500 mg orally was administered to nine healthy volunteers on four occasions 7 days apart. On two occasions allocated at random, activated charcoal (2.5 g of medicoal) was administered 1 h after the drug. Hyoscine butylbromide (20 mg intramuscularly) was given immediately after mefenamic acid on one of these occasions, and on one occasion after mefenamic acid without charcoal. Hyoscine significantly delayed the time to maximum mefenamic acid concentrations but did not affect the area under the plasma concentration-time curve. Charcoal reduced the area under the plasma concentration curve by 36% and charcoal and hyoscine reduced the area under the plasma concentration curve by 42% from their respective control values. We conclude that early charcoal administration in a ratio of 5 g to 1 g of drug effectively reduces the area under the plasma concentration-time curve after oral mefenamic acid administration. Early charcoal administration may be of value therefore in reducing the toxicity of mefenamic acid after deliberate or accidental overdosage.

Adolescent↗
PubMed1986

Effect of 16,16-dimethyl PGE2 on renal papillary necrosis and gastrointestinal ulcerations (gastric, duodenal, intestinal) produced in rats by mefenamic acid.

Mefenamic acid, given orally to rats at a single dose of 1200 mg/kg, produced renal papillary necrosis (RPN) in 63% of animals. The incidence was reduced to 27% by 16,16-dimethyl PGE2 (dmPGE2), given at an oral dose of 0.75 mg/kg t.i.d. RPN is likely to be caused by the renal prostaglandin depletion elicited by mefenamic acid, an inhibitor of prostaglandin cyclooxygenase. Substitution with dmPGE2 reduces RPN presumably by preventing the prostaglandin depletion. We conclude that the prostaglandin used is cytoprotective for the kidney. Mefenamic acid, like most nonsteroidal anti-inflammatory compounds (NOSAC), produced ulcerations of the small intestine (jejunum and ileum). These were prevented by dmPGE2 (intestinal cytoprotection). Unlike most other NOSAC, however, mefenamic acid produced duodenal ulcers in nearly all animals (80%). Of these ulcers, 88% were perforated. Twenty-five of the twenty-six animals that died had a perforated ulcer. These duodenal ulcers were also prevented by dmPGE2. Mefenamic acid-induced ulcers could be used as an experimental model for testing agents with a potential for preventing or healing duodenal ulcers.

16,16-Dimethylprostaglandin E2↗
PubMed2000

Some physicochemical properties of mefenamic acid.

Mefenamic acid is a problematic drug in granulation, tableting, and dissolution due to its poor solubility, hydrophobicity, and tendency to stick to surfaces. In most cases, the specifications of a drug by the pharmacopoeia include identification and purity, but they do not describe the physicochemical drug properties precisely. To characterize the mefenamic acid particle size, surface area measurements, X-ray pattern, differential scanning calorimetry (DSC), wettability, crystal habit, and compression behavior of different batches from two manufacturers were investigated. Due to larger particle size and better wettability, mefenamic acid of Il Yang type was easier to handle in a granulation process. The compression behavior of both types was nearly the same, although particle size, crystal habit, and wettability were very different.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2001

Acute renal failure from hemoglobinuric and interstitial nephritis secondary to iodine and mefenamic acid.

Mefenamic acid ingestion, usually in excess and over prolonged period is known to produce interstitial nephritis, or less commonly papillary necrosis, with acute renal failure. However, it is not dose-dependent for the induction of tubulointerstitial damage. Excess iodine ingestion is known to produce toxicity and possible death, but acute renal failure is rare. There is evidence from clinical and experimental data that iodine has toxic effect on tubular epithelial cells. Iodine has not been documented to produce red cell hemolysis and hemoglobinuria. We present a unique case of acute renal failure from hemoglobinuric and acute interstitial nephritis secondary to suicidal ingestion of potassium iodide solution and also ingestion of a few mefenamic acid tablets. These agents led to potentiation of the renal injury from hemoglobinuric tubulopathy, probably from the iodine, and renal dysfunction from alteration of renal perfusion by selective COX-1 inhibition of prostaglandin production, and induction of acute interstitial nephritis from mefenamic acid, leading to acute renal failure which was reversible by hemodialysis and supportive therapy.

Acute Disease↗
PubMed1978

Oral antipyretic therapy: evaluation of the N-aryl-anthranilic acid derivatives mefenamic acid, tolfenamic acid and flufenamic acid.

The antipyretic activity of three N-aryl-anthranilic acid derivatives, mefenamic acid, tolfenamic acid and flufenamic acid, was compared and their optimal antipyretic dose determined in a trial in 87 children (aged 5 months to 15 years), who suffered from infections and fever exceeding 38.5 degrees C. Tolfenamic acid proved to be the most potent antipyretic agent of the three drugs; it was eight times more powerful than mefenamic acid and three times more powerful than flufenamic acid. The optimal antipyretic doses were: mefenamic acid 4 mg/kg, tolfenamic acid 0.5 mg/kg and flufenamic acid 1.5 mg/kg. It is evident that the antipyretic activity of these anthranilic acid derivatives is even greater than their antirheumatic effect, the difference being most noticeable in the case of tolfenamic acid.

Adolescent↗
PubMed1980

Cortical facilitatory effect of mefenamic acid.

Mefenamic acid intravenously injected or locally applied upon the cerebral cortex increases the amplitude of the evoked responses recorded in the somatosensory S1 cortex. This facilitatory effect supports previous EEG studies showing that this drug also has central actions. In light of the present result it is suggested that the central action induced by mefenamic acid occurs at the cortical level.

Animals↗
PubMed1994

Tolfenamic acid and mefenamic acid in the treatment of primary dysmenorrhoea.

The clinical efficacy of tolfenamic acid and mefenamic acid in the treatment of primary dysmenorrhoea was studied in a prospective, controlled, double-blind, cross-over study comprising 73 patients aged 13-39 with an average body weight of 56 kilos. The patients were randomized to receive either tolfenamic acid (200 mg t.i.d.) or mefenamic acid (500 mg t.i.d.) for 3 days, during 3 consecutive menstrual cycles each, in a sequential design A-B or B-A. At the beginning and at the end of each treatment period, 13 dysmenorrhoeic symptoms were evaluated on a visual analogue scale (lower back pain, interference with daily activities, nausea, vomiting, diarrhoea, headache, dizziness, fatigue, sweating, chills, hot flashes, depressant states, and mood swings). The data were analyzed by using two statistical models. The first one, for the 73 patients, by making paired comparisons regardless of treatment sequence. With respect to the initial values, the results showed that both drugs were statistically significant (P < 0.05) in reducing the intensity of the evaluated symptoms. When comparing both treatments, tolfenamic acid showed a significant difference as to interference with daily activities (P < 0.025) and hot flashes (P < 0.005). In the result analysis with the second model, the groups were divided according to the first assigned treatment and paired comparisons were made. It was observed that the group receiving tolfenamic acid in the last sequence reached a higher level of response and statistical significance was demonstrated in 8 of 13 evaluated symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1999

Subunit-selective modulation of GABAA receptors by the non-steroidal anti-inflammatory agent, mefenamic acid.

Mefenamic acid (MFA) has anti-convulsant and pro-convulsant effects in vivo, and has been shown to potentiate and inhibit GABAA (gamma-aminobutyric acid) receptors in vitro. In this study, whole-cell currents were recorded from Xenopus oocytes and human embryonic kidney (HEK) cells expressing human recombinant GABAA receptors to resolve the molecular mechanisms by which MFA modulates GABAA receptor function. We demonstrate that MFA potentiated GABA-activated currents for alpha1beta2 gamma2S (EC50 = 3.2 +/- 0.5 microM), but not for alpha1beta1 gamma2S receptors. MFA also enhanced GABA-activated responses and directly activated alpha1beta2/beta3 GABAA receptors, but inhibited responses to GABA on alpha1beta1 constructs (IC50 = 40 +/- 7.2 microM). A comparison of beta1, beta2 and beta3 subunits suggested that the positive modulatory action of MFA involved asparagine (N) 290 in the second transmembrane domain (TM2) of the beta2 and beta3 subunits. Mutation of N290 to serine (S) markedly reduced modulation by MFA in alpha1beta2(N290S)gamma2S receptors, whereas alpha1beta1(S290N)gamma2S constructs revealed potentiated responses to GABA (EC50 = 7.8 +/- 1.7 microM) and direct activation by MFA. The potentiation by MFA displayed voltage sensitivity. The direct activation, potentiation and inhibitory aspects of MFA action were predominantly conferred by the beta subunits as the spontaneously active homomeric beta1 and beta3 receptors were susceptible to modulation by MFA. Molecular comparisons of MFA, loreclezole and etomidate, agents which exhibit similar selectivity for GABAA receptors, revealed their ability to adopt similar structural conformations. This study indicates that N290 in TM2 of beta2 and beta3 subunits is important for the regulation of GABAA receptor function by MFA. Our data provide a potential molecular mechanism for the complex central effects of MFA in vivo.

Amino Acid Sequence↗
PubMed1977

Oral antipyretic therapy. Evaluation of mefenamic acid (short communication).

The capacity of N-(2,3-xylyl)anthranilic acid (mefenamic acid) to reduce fever in children was compared with that of acetylsalicylic acid, paracetamol and amino-phenazone. The series of cases consisted of 71 patients in the age range from 3 months to 15 years and with rectal temperatures above 38.5 degrees C. Temperatures were recorded at 15 and 30 min, and 1, 2, 4 and 6 h after challenge with the drug. The antipyretic effect of mefenamic acid in a dose of 4 mg/kg was optimal: it was 2.5 times that of acetyl-salicylic acid or paracetamol and nearly similar to that of aminophenazone. It seems possible that the antipyretic effect of mefenamic acid is stronger than its anti-inflammatory and analgetic properties.

Acetaminophen↗
PubMed2003

Inactivation of creatine kinase during the interaction of mefenamic acid with horseradish peroxidase and hydrogen peroxide: participation by the mefenamic acid radical.

Creatine kinase (CK) was used as a marker molecule to examine the side effects of damage to tissues by mefenamic acid, an effective drug to treat rheumatic and arthritic diseases, with horseradish peroxidase and hydrogen peroxide (HRP-H(2)O(2)). Mefenamic acid inactivated CK during its interaction with HRP-H(2)O(2). Also, diphenylamine and flufenamic acid caused a loss of CK activity, indicating the imino group, not substituent groups, in the phenyl rings have a crucial role in CK inactivation. Rapid change in mefenamic acid spectra was detected, suggesting that mefenamic acid is efficiently oxidized by HRP-H(2)O(2). Peroxidases oxidize xenobiotics to free radicals by a one-electron transfer. However, direct detection of mefenamic acid radicals by electron spin resonance (ESR) was unsuccessful. Reduced glutathione and 5,5-dimethyl-1-pyrroline-1-oxide (DMPO) in the reaction mixture containing mefenamic acid with HRP-H(2)O(2) produced ESR signals consistent with a DMPO-glutathionyl radical adduct. These results suggest that inactivation of CK is probably caused through formation of mefenamic acid radicals. Sulfhydryl groups and tryptophan residues of CK were diminished by mefenamic acid with HRP-H(2)O(2). Other SH enzymes, including alcohol dehydrogenase and glyceraldehyde-3-phosphate dehydrogenase, were very sensitive to mefenamic acid with HRP-H(2)O(2). Inactivation of SH enzymes may explain some deleterious actions of mefenamic acid.

Amino Acid Substitution↗