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Non-steroidal anti-inflammatory drugs (NSAIDs) have been widely used to reduce the inflammation and pain in patients suffering from arthritis. There is a possible use for these drugs in the treatment of inflammation associated with periodontitis. However, the propensity of NSAIDs to cause serious side effects, including gastrointestinal bleeding, has reduced their usefulness. The local application of NSAIDs can avoid these side effects by delivering low doses of drug directly to the affected site. Three NSAIDs (indomethacin, tolmetin and mefenamic acid) were incorporated into polymethylmethacrylate bone cement (PM MA) strips in a range of concentrations and their cytotoxicity, pattern of drug release and ability to suppress elevated levels of prostaglandin E2 (PGE2) in cultured human periodontal ligament fibroblasts (HPLF) assessed. The strips released between 10 and 30% of the total incorporated drug over 7 days, with the highest levels released by strips containing 20% w/w of drug. Strips containing 20% indomethacin and mefenamic acid released in excess of toxic levels in the first 24 h. Strips containing 20, 10 and 5% w/w NSAID significantly (P < 0.05) reduced the level of PGE2 expression by E. coli lipopolysaccharide (LPS) challenged cells, with only the 20% mefenamic acid strip performing significantly better than the other drugs. We conclude that local delivery of NSAIDs using PMMA as a sustained release vehicle is a possible additional tool in the treatment of periodontitis.
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In this randomized clinical trial, 122 female students with moderate to severe dysmenorrhea were assessed and were placed in either the exercise or mefenamic acid group. The exercise program was performed for 15 minutes, three times a week and included a five-minute warm up and six belly and pelvic stretching exercises for 10 minutes. The mefenamic acid group received 250 mg capsules every eight hours from the onset of menstruation until pain relief. Both interventions were performed during two consecutive menstrual cycles. Pain intensity was measured using a 10 cm visual analog scale.
A new analytical method was developed for simultaneous determination of 12 pharmaceuticals using ultrasound-assisted dispersive liquid-liquid microextraction (DLLME) followed by ultra-high performance liquid chromatography with tandem mass spectrometry (UHPLC-MS/MS). Six nonsteroidal anti-inflammatory drugs (NSAIDs, ketoprofen, mefenamic acid, tolfenamic acid, naproxen, sulindac, and piroxicam) and six antibiotics (tinidazole, cefuroxime axetil, ciprofloxacin, sulfamethoxazole, sulfadiazine, and chloramphenicol) were extracted by ultrasound-assisted DLLME using dichloromethane (800 μL) and methanol/acetonitrile (1:1, v/v, 1200 μL) as the extraction and dispersive solvents, respectively. The factors affecting the extraction efficiency, such as the type and volume of extraction and dispersive solvent, vortex and ultrasonic time, sample pH, and ionic strength, were optimized. The ultrasound-assisted process was applied to accelerate the formation of the fine cloudy solution by using a small volume of dispersive solvent, which increased the extraction efficiency and reduced the equilibrium time. Under the optimal conditions, the calibration curves showed good linearity in the range of 0.04-20 ng mL(-1) (ciprofloxacin and sulfadiazine), 0.2-100 ng mL(-1) (ketoprofen, tinidazole, cefuroxime axetil, naproxen, sulfamethoxazole, and sulindac), and 1-200 ng mL(-1) (mefenamic acid, tolfenamic acid, piroxicam, and chloramphenicol). The LODs and LOQs of the method were in the range of 0.006-0.091 and 0.018-0.281 ng mL(-1), respectively. The relative recoveries of the target analytes were in the range from 76.77 to 99.97 % with RSDs between 1.6 and 8.8 %. The developed method was successfully applied to the extraction and analysis of 12 pharmaceuticals in five kinds of water samples (drinking water, running water, river water, influent and effluent wastewater) with satisfactory results. Graphical Abstract Twelve pharmaceuticals in water samples analyted by UHPLC-MS/MS using ultrasound-assisted DLLME.
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A novel magneto multiwalled carbon nanotube/carbon paste electrode (MMW/CPE) for the determination of mefenamic acid (MFA) was introduced. Magnetic molecularly imprinted polymer nanoparticles (MMIPNPs) were synthesized and then added to the solution of MFA. After stirring for 20 min, the MMW/CPE was immersed in the solution of MFA (contain MMIPNPs) and the MMIPNPs were captured by it. Then oxidation of MFA was analyzed by differential pulse voltammetry (DPV). Electrochemical impedance spectroscopy, cyclic voltammetry, and DPV were employed to characterize the MMW/CPE. The MMIPNPs exhibited a high selectivity and sensitivity toward MFA. The effect of various experimental parameters including pH, MMIPNPs dosage, stirring time, accumulation potential and time on the voltammetric response of MFA were investigated. Under the optimal conditions, selective detection of MFA in a linear concentration range of 2.0-1000.0 nmol L(-1) was performed with the detection limit of 1.2 nmol L(-1) (3S/N). To further study the practical applicability of this method, it was applied to the analysis of some real samples and the obtained results were satisfactory.
A 52 year old man developed bullous pemphigoid, Coombs' positive haemolytic anaemia and diarrhoea related to the use of mefenamic acid. Clinical manifestation of the bullous pemphigoid, haemolytic anaemia and diarrhoea resolved following discontinuation of the mefenamic acid. Mefenamic acid should be added to the list of agents that are known to induce bullous pemphigoid.
A high-performance liquid chromatographic (HPLC) method for simultaneous determination of mefenamic acid (MFA), flufenamic acid (FFA) and tolfenamic acid (TFA) is presented for application to pharmaceuticals and human urine. Isocratic reversed-phase HPLC was employed for quantitative analysis using tetra-pentylammonium bromide (TPAB) as an ion-pair reagent. Urine samples were purified by solid-phase extraction using a silica-based strong anion-exchanger, Bond-Elut SAX cartridge. The HPLC assay was carried out using a Wakosil ODS 5C18 column (5 microm, 150x4.6 mm I.D.). The mobile phase consisted of 1.9 g of TPAB dissolved in 1:1 of a mixture of acetic acid-sodium acetate buffer solution, pH 5.0, and acetonitrile (11:9, v/v). The calibration curves of MFA, FFA and TFA showed good linearity in the concentration range of 33-167 microg/ml with a wavelength of 280 nm for pharmaceuticals, and in the low concentration range (1.7-30.1 microg/ml) with a wavelength of 230 nm for biological fluids. The correlation coefficients were better than 0.9999 in all cases. The lower limits of detection (defined as a signal-to-noise ratio of about 3) were approximately 2 ng for MFA, 3.5 ng for FFA and 2.5 ng for TFA. The procedure described here is rapid, simple, selective and is suitable for routine analysis of pharmaceuticals and pharmacokinetic studies in human urine samples.
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A rapid screening method for detecting the inhibitory potential of various drugs against UGT2B7 was established using a LC-MS/MS system. The effects of nine NSAIDs (acetaminophen, diclofenac, diflunisal, indomethacin, ketoprofen, mefenamic acid, naproxen, niflumic acid, and salicylic acid) against UGT2B7-catalyzed 3'-azido-3'-deoxythymidine glucuronidation (AZTG) were investigated in human liver microsomes (HLM) and recombinant human UGT2B7.
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Electronic searches for relevant randomised controlled trials of the Cochrane Menstrual Disorders and Subfertility Group Register of Trials, MEDLINE, EMBASE, PsychLIT, Current Contents, Biological Abstracts, Social Sciences Index and CINAHL were performed. Attempts were also made to identify trials from citation lists of review articles and drug companies were approached for unpublished data. In most cases, the first author of each included trial was contacted for additional information.
Randomised controlled trial.
The treatment of primary spasmodic dysmenorrhea with prostaglandin synthetase/receptor site inhibitors such as mefenamic acid (Ponstel) is becoming accepted. Recent improvements in intrauterine pressure recording have made the acquisition of reliable, physiologic data possible. These data have been used to provide objective evaluation of the effectiveness of drug therapy as part of a larger subjective investigation. Analysis of these data shows that mefenamic aid causes rapid, dramatic reductions in parameters of uterine pressure and work. Complete loss of uterine contractile activity was found in 46.2% of patients. Subjective relief was obtained in all patients receiving mefenamic acid in this sample.
The inhibitory effects of selected drugs on the Arthus reaction, a model of immune-complex-induced tissue injury, were studied. The reverse passive Arthus reaction (RPAR) was elicited in the dorsal skin of rats, using bovine serum albumin and the gamma-globulin fraction of rabbit anti-BSA. The optimal amounts of antigen and antibody required to elicit the reaction, as well as the reaction kinetics, were examined. Chlorpheniramine, cyproheptadine, d-penicillamine, chloroquine, indomethacin, phenylbutazone, naproxen, and mefenamic acid were found to be inactive despite high doses; aspirin and ibuprofen were only weakly active. Hydrocortisone and colchicine were strong inhibitors of the RPAR: the calculated ED50 values were 13 mg/kg p.o. and 0.3 mg/kg i.v., respectively. The RPAR exhibits a different sensitivity to drug inhibition than conventional models of inflammation (e.g., carrageenin paw edema) end may be useful to detect new types of anti-inflammatory agents.
Antifibrinolytic therapy compared to placebo showed a significant reduction in mean blood loss (WMD -94.0 [-151.4, -36.5]) and significant change in mean reduction of blood loss (WMD -110.2 [-146. 5, -73.8]). This objective improvement was not mirrored by a patient perceived improvement in monthly menstrual blood loss (RR 2.5 [0.9, 7.3]) in the one study which recorded this outcome ( approximately approximately Edlund 1995 approximately approximately ). Antifibrinolytic agents were compared to only three other medical (non-surgical) therapies: mefenamic acid, norethisterone administered in the luteal phase and ethamsylate. In all instances, there was a significant reduction in mean blood loss (WMD -73.0 [-123.4, -22.6], WMD -111.0 [-178.5, -43.5] and (WMD -100 [-143.9, -56.1] respectively) and a strong, although non-significant trend in favour of tranexamic acid in the participants' perception of an improvement in menstrual blood loss. There were no significant differences in the frequency of reported gastrointestinal side effects with tranexamic acid when compared to either NSAIDs (RR 0.9 [0.4, 2.1], oral luteal phase progestagens (RR 0.4 [0.1, 1.2]) or ethamsylate (RR 0.88 [0.3, 2.9]) when these treatments were used for heavy menstrual bleeding. (ABSTRACT TRUNCATED)
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To determine the effectiveness of oral contraceptive pills compared with other medical therapies, placebo or no therapy in the treatment of heavy menstrual bleeding.
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Desmopressin may be a useful therapeutic tool for many women with IUD-related menorrhagia. Its mechanism of action lies in an ability to enhance local haemostasis, without affecting uterine blood flow.
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Prospective observational study.
There were no differences between two groups for demographic or descriptive variables. Comprising the VAS showed that the participants in T. polium and mefenamic acid groups had lower significant pain in the 1st and the 2nd months after the treatment (P < 0.05). No side effects were reported in the T. polium and Mefenamic Acid groups.
Ninety OSA patients were enrolled for surgical treatments in this study. Forty-five patients (group 1) were randomized to receive intravenous ketorolac and another 45 patients (group 2) were given the conventional regimen of oral mefenamic acid and intramuscular meperidine after OSA surgeries for 3 days at hospital. Postoperative discomfort was measured by a self-assessment questionnaire on the 1st and 3rd days after surgery. Any adverse effect of pain treatment was carefully monitored. Patients' satisfaction with postoperative pain treatment was evaluated 1 month postoperatively.
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Over an 18-month period at a single clinic, 43 new cases of colonic inflammation have been diagnosed (19 proctitis only). Crohn's colitis has been excluded from this analysis. In all these subjects a careful drug history has been taken in a prospective manner and in 4 of these 43 patients colonic inflammation appeared to be directly related to non-steroidal anti-inflammatory drug (NSAID) administration (mefenamic acid, 2; piroxicam, 2). In all 4 patients there was a time interval (mean 3 months) between initiation of treatment with NSAID and presentation with diarrhoea and weight loss. Pathological findings were minor and biochemical changes insignificant, in contrast to the protracted troublesome symptoms. Resolution of symptoms was very rapid on discontinuation of NSAID medication but 2 patients experienced immediate return of symptoms following inadvertent rechallenge. Approximately 10% of newly diagnosed colitis may be related to NSAID administration. Subjects taking NSAID medications appear to be five times more likely to develop colonic inflammation than the general population.
In humans, orally administered 4-(5-pyridin-4-yl-1H-[1,2,4]triazol-3-yl) pyridine-2-carbonitrile (FYX-051) is excreted mainly as triazole N(1)- and N(2)-glucuronides in urine. It is important to determine the enzyme(s) that catalyze the metabolism of a new drug to estimate individual differences and/or drug-drug interactions. Therefore, the characterization and mechanism of these glucuronidations were investigated using human liver microsomes (HLMs), human intestinal microsomes (HIMs), and recombinant human UDP-glucuronosyltransferase (UGT) isoforms to determine the UGT isoform(s) responsible for FYX-051 N(1)- and N(2)-glucuronidation. FYX-051 was metabolized to its N(1)- and N(2)-glucuronide forms by HLMs, and their K(m) values were 64.1 and 72.7 microM, respectively; however, FYX-051 was scarcely metabolized to its glucuronides by HIMs. Furthermore, among the recombinant human UGT isoforms, UGT1A1, UGT1A7, and UGT1A9 catalyzed the N(1)- and N(2)-glucuronidation of FYX-051. To estimate their contribution to FYX-051 glucuronidation, inhibition analysis with pooled HLMs was performed. Mefenamic acid, a UGT1A9 inhibitor, decreased FYX-051 N(1)- and N(2)-glucuronosyltransferase activities, whereas bilirubin, a UGT1A1 inhibitor, did not affect these activities. Furthermore, in the experiment using microsomes from eight human livers, the N(1)- and N(2)-glucuronidation activity of FYX-051 was found to significantly correlate with the glucuronidation activity of propofol, a specific substrate of UGT1A9 (N(1): r(2) = 0.868, p < 0.01; N(2): r(2) = 0.775, p < 0.01). These results strongly suggested that the N(1)- and N(2)-glucuronidation of FYX-051 is catalyzed mainly by UGT1A9 in human livers.
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We report a case of steatorrhoea and sub-total villous atrophy, occurring during therapy with mefenamic acid. The patient recovered on cessation of the drug while continuing a normal diet.
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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.
AUTOANTIBODY PRODUCTION: The production of autoantibodies can only occur if immune tolerance is circumvented. Thus drug-induced autoimmune hemolytic anemia requires that the drug have an effect on both autoantigens and on the immune system. AN EXAMPLE, METHYLDOPA: Methyldopa is a hypotensive agent which induces major production of anti-Rh IgG anti-erythrocyte autoantibodies, anti-nuclear antibodies and anti-actin antibodies. These autoantibodies generally appear 6 months after treatment onset and are observed in 20% of treated patients. Hemolysis is however exceptional and is only clinically or biologically perceptible in 1 to 2% of the patients who become immunized. Induced lupus has been reported as have been several dozen cases of drug-induced hepatitis with anti-actin autoantibodies. DRUGS INDUCING HEMOLYTIC ANEMIA: Besides methyldopa, other drugs known to induce hemolytic anemia include levodopa used for Parkinson's disease, mefenamic acid, a nonsteroidal antiinflammatory drug, interferon-alpha, used in chronic viral hepatitis, cyclosporin used for the prevention of graft rejection and the treatment of certain autoimmune diseases, and fludarabin, used in chronic lymphoid leukemia.
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The effect of various antacids on the absorption of tolfenamic and mefenamic acids has been investigated in three separate crossover studies, each consisting of four phases. Single doses of magnesium hydroxide (85 mg, 425 mg and 1700 mg) or of water (150 ml) were given by mouth to 6 healthy volunteers immediately after tolfenamic acid 400 mg (Study 1), and, using an identical study design, after mefenamic acid 500 mg (Study 3). In Study 2 sodium bicarbonate 1 g, aluminium hydroxide 1 g, an antacid preparation containing both aluminium and magnesium hydroxides, or water alone were ingested with tolfenamic acid 400 mg. Plasma concentrations of tolfenamic and mefenamic acids and their cumulative excretion in urine were determined up to 24 h. Magnesium hydroxide greatly accelerated, in a dose-dependent manner the absorption of both tolfenamic and mefenamic acids. The peak times in plasma were shortened by about 1 h by 425 mg and 1700 mg magnesium hydroxide, and the peak plasma concentrations of both fenamates were elevated up to 3-fold. The area under the plasma concentration-time curve between 0 and 1 h of tolfenamic acid was increased up to 7-fold and that of mefenamic acid up to 3-fold. The total bioavailability of tolfenamic and mefenamic acids was only slightly increased. Aluminium hydroxide alone and in combination with magnesium hydroxide significantly retarded the absorption and lowered the peak plasma concentration of tolfenamic acid. Sodium bicarbonate had no significant effect on its absorption. The interaction with magnesium hydroxide leads to higher and earlier peak plasma concentrations of the fenamates.(ABSTRACT TRUNCATED AT 250 WORDS)
Regulation of avidin accumulation by prostaglandins (PGs) and their inhibitors was studied in chick oviduct organ culture. Avidin was induced neither by progesterone nor PGF2 alpha in the oviduct of immature chicks. By progesterone and PGs, a high avidin synthesis was induced when the chicks received diethylstilbestrol (DES) for 7 days. Enhanced avidin production was observed by PGF2 alpha, PGE1 and PGE2, whereas PGA2 and PGB2 had a slight inhibitory effect and PGA1 and PGB1 had no effect on avidin production. PGF2 alpha was most effective at a concentration of 10-20 micrograms/ml. The effects of progesterone and PGF2 alpha were not additive. Mefenamic acid, at concentrations of 40 and 60 micrograms/ml, inhibited 50 and 85%, respectively, of the avidin synthesis induced by progesterone, whereas the inhibition of the total protein synthesis was only 20%, and this only by the higher concentration of the drug. Tolfenamic and meclofenamic acid were also inhibitory in the case of progestin-induced avidin synthesis. These studies indicate that the PGs (F2 alpha, E1 and E2) might be involved in the avidin induction in the chick differentiated oviduct. The specific inhibition of the progesterone-dependent avidin synthesis by the PG inhibitors suggests that PGs may be connected with the progesterone action in the oviduct. We propose that the avidin synthesis by the chick oviduct might be considered as a model system for studying PG effects on the synthesis of a specific protein.
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Ileal blood flow was significantly reduced in NEC animals as compared with CONTROLs. The addition of DPR to the peritoneum increased ileal blood flow significantly in all groups in spite of blockade of these known vasoactive mechanisms. Direct peritoneal resuscitation may be a novel strategy to improve intestinal blood flow in NEC.
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The methods for quantitative determination of meloxicam and mefenamic acid in pharmaceuticals by classic spectrophotometry - zero order derivative, first and second order derivatives spectrophotometry is described, using "peak - peak" (P-P) and "peak - zero" (P-O) measurements. The calibration curves are linear within the concentration range of 4.0 - 14.0 microg/mL for meloxicam and 14.0 - 24.0 microg/mL for mefenamic acid. The procedure is simple, rapid and the results are reliable.
The effects of aspirin, salicylate formulations and substitutes, smoking (nicotine), indomethacin, corticosteroids, phenylbutazone, ethanol, caffeine and reserpine on the gastric mucosa are discussed. The damaging effects of the drugs are considered in terms of the gastric mucosal barrier, gastric erosions, microbleeding and haematemesis and melaena and finally whether they cause peptic ulcer. There is suggestive evidence that unbuffered aspirin is a cause of haematemesis and melaena and of gastric ulcer but the incidence rates for hospital admission are low, being 10 to 15 per 100,000 heavy users per year. Aspirin in solution as acetylsalicylate buffered to maintain a neutral pH protects against gastric damage. Newer aspirin substitutes (mefenamic acid, fenoprofen, naproxen, tolmetin and ibuprofen) appear to cause less faecal blood loss than aspirin but their long-term effects have not been fully evaluated. Smoking is definitely associated with peptic ucler but the mechanism is unknown. Corticosteroids are probably not ulcerogenic despite clinical bias that they are. Indomethacin and phenylbutazone may be ulcerogenic but there is insufficient evidence to make firm judgements. Ethanol, caffeine and reserpine, on available evidence, are probably not ulcerogenic.
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Selected patients suffering from menorrhagia may be treated with the HTA device using local anesthesia in an outpatient setting.
Rat pups were assigned by litter to experimental NEC or CONTROL groups. Laser Doppler flowmetry evaluation of intestinal microvascular blood flow was studied at baseline, with mediator blockade (endothelin-A receptor, endothelin-B receptor, PG synthesis, or NO synthase) and with DPR. Repeated-measures analysis of variance test was applied with Tukey-Kramer honestly significant difference test (P < .05).