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Ponstel (Mefenamic Acid)

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Ponstel is in a group of drugs called nonsteroidal anti-inflammatory drugs (NSAIDs). Ponstel is used for treating menstrual pain. It may be used for short-term (not more than 7 days) treatment of mild to moderate pain. Ponstel blocks the effect of certain substances in the body that are associated with pain and inflammation.

Other names for this medication:

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Also known as:  Mefenamic Acid.


Ponstel is used for treating menstrual pain. It may be used for short term (not more than 7 days) treatment of mild to moderate pain.

Ponstel blocks certain substances in the body that are linked to inflammation. NSAIDs treat the symptoms of pain and inflammation.

Ponstel is also known as Mefenamic acid, Ponstan.

Generic name of Ponstel is Mefenamic Acid.

Brand name of Ponstel is Ponstel.


Take Ponstel orally.

Take Ponstel with or without food.

Take Ponstel with a full glass of water.

If you want to achieve most effective results do not stop taking Ponstel suddenly.


If you overdose Ponstel and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Ponstel if you are allergic to Ponstel components or to aspirin.

Do not take Ponstel if you are pregnant, planning to become pregnant, or are breast-feeding.

Do not take Ponstel if you have had a severe allergic reaction (e.g., severe rash, hives, trouble breathing, growths in the nose, dizziness) to aspirin or a nonsteroidal anti-inflammatory drug (NSAID) (e.g., ibuprofen, celecoxib).

Do not take Ponstel if you have had recent or will be having bypass heart surgery.

Do not take Ponstel if you have kidney problems.

Do not take Ponstel if you have ulcers or inflammation of the stomach or bowel.

Do not use Ponstel with aspirin.

Be careful with Ponstel when it is used by children younger than 14 years old and by elderly people.

Avoid machine driving.

Avoid drinking alcohol.

It can be dangerous to stop Ponstel taking suddenly.

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Cyclooxygenase-2 (COX-2) catalyzes the oxygenation of arachidonic acid (AA) and endocannabinoid substrates, placing the enzyme at a unique junction between the eicosanoid and endocannabinoid signaling pathways. COX-2 is a sequence homodimer, but the enzyme displays half-of-site reactivity, such that only one monomer of the dimer is active at a given time. Certain rapid reversible, competitive nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to inhibit COX-2 in a substrate-selective manner, with the binding of inhibitor to a single monomer sufficient to inhibit the oxygenation of endocannabinoids but not arachidonic acid. The underlying mechanism responsible for substrate-selective inhibition has remained elusive. We utilized structural and biophysical methods to evaluate flufenamic acid, meclofenamic acid, mefenamic acid, and tolfenamic acid for their ability to act as substrate-selective inhibitors. Crystal structures of each drug in complex with human COX-2 revealed that the inhibitor binds within the cyclooxygenase channel in an inverted orientation, with the carboxylate group interacting with Tyr-385 and Ser-530 at the top of the channel. Tryptophan fluorescence quenching, continuous-wave electron spin resonance, and UV-visible spectroscopy demonstrate that flufenamic acid, mefenamic acid, and tolfenamic acid are substrate-selective inhibitors that bind rapidly to COX-2, quench tyrosyl radicals, and reduce higher oxidation states of the heme moiety. Substrate-selective inhibition was attenuated by the addition of the lipid peroxide 15-hydroperoxyeicosatertaenoic acid. Collectively, these studies implicate peroxide tone as an important mechanistic component of substrate-selective inhibition by flufenamic acid, mefenamic acid, and tolfenamic acid.

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This study aimed to investigate the combined effect of magnesium oxide (MgO) as an alkalizer and polyethylene glycol (PEG) as a plasticizer and wetting agent in the presence of Kollidon® 12 PF and 17 PF polymer carriers on the release profile of mefenamic acid (MA), which was prepared via hot-melt extrusion technique. Various drug loads of MA and various ratios of the polymers, PEG 3350 and MgO were blended using a V-shell blender and extruded using a twin-screw extruder (16-mm Prism EuroLab, ThermoFisher Scientific, Carlsbad, CA) at different screw speeds and temperatures to prepare a solid dispersion system. Differential scanning calorimetry and X-ray diffraction data of the extruded material confirmed that the drug existed in the amorphous form, as evidenced by the absence of corresponding peaks. MgO and PEG altered the micro-environmental pH to be more alkaline (pH 9) and increased the hydrophilicity and dispersibility of the extrudates to enhance MA solubility and release, respectively. The in vitro release study demonstrated an immediate release for 2 h with more than 80% drug release within 45 min in matrices containing MgO and PEG in combination with polyvinylpyrrolidone when compared to the binary mixture, physical mixture and pure drug.

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Television microscopy was used to observe the responses of in vivo arterioles and venules of the rat cremaster muscle to the topical application of angiotensin II (10(-8) and 10(-6) M). Neither the first- (A1) or second-order arterioles (A2) nor the first- (V1) or second-order venules (V2) constricted significantly to angiotensin II. However, after the inhibition of local prostaglandin synthesis with either mefenamic acid or indomethacin, both A1 and A2, but not the venules, gave a significant constrictor response to angiotensin II (10(-6) M). Arterioles and venules, which were preconstricted with norepinephrine, dilated to their initial baseline diameters after angiotensin II (10(-6) M), a response not observed when the microvessels were pretreated with either an angiotensin antagonist or a prostaglandin synthesis inhibitor. These observations indicate that endogenous prostaglandins exert a significant dilator influence on the larger arterioles, that this dilator influence appears to oppose the constrictor effect of angiotensin II, and that angiotensin II acts on specific receptors to induce synthesis and/or release of dilator prostaglandins in large arterioles. However, prostaglandins cannot account for the absence of a venular constriction to angiotensin.

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Hepatotoxicity is a known side effect of nonsteroidal anti-inflammatory drugs (NSAIDs). In the present study, the effects of N-phenylanthranilic acid (NPA) scaffold NSAIDs on rat liver mitochondria were examined. Mefenamic acid (MEF, 200 µM) induced mitochondrial swelling, which was inorganic phosphate (Pi)-dependent and suppressed by cyclosporin A (CsA, 2.5 µM), similar to calcium-induced swelling. Mitochondrial swelling was also observed following the addition of 200 µM flufenamic acid (FLU), meclofenamic acid (MCL), and tolfenamic acid (TOL). Less swelling was observed with the addition of 200 µM diclofenac (DIC) or NPA. Diphenylamine (DPA)-induced swelling occurred in a Pi-independent manner and was not sensitive to CsA. The mechanism by which DPA interacted with the mitochondrial inner membrane differed from those of the other NPA scaffold NSAIDs. The addition of 50 µM MEF, MCL, TOL, and FLU had uncoupling effects in mitochondrial inner membrane. These NSAIDs dose-dependently obstructed electron transport in the respiratory chain. NSAIDs are known to have various dynamic structures, and the solvation free energies (dGWs: an index of stereo-hydrophobicity) of the conformers obtained were determined using a molecular orbital analysis. The relationship between the dynamic structures and swelling induced by NPA scaffold NSAIDs was also examined.

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Acyl glucuronides have been implicated in the toxicity of many xenobiotics and marketed drugs. These toxicities are hypothesized to be a consequence of covalent binding of the reactive forms of the acyl glucuronide to proteins. Reactive intermediates of the acyl glucuronide arise from the migration of the aglycone leading to other positional and stereoisomers under physiological conditions. In order to screen for the potential liabilities of these metabolites during the early phase of pharmaceutical development, an NMR method based on the disappearance of the anomeric resonance of the O-1-acyl glucuronide was used to monitor the degradation kinetics of 11 structurally diverse acyl glucuronides, including those produced from the known nonsteroidal anti-inflammatory drugs (NSAIDs). The acyl glucuronides were either chemically synthesized or were isolated from biological matrices (bile, urine, and liver microsomal extracts). The half-lives attained utilizing this method were found to be comparable to those reported in the literature. NMR analysis also enabled the delineation of the two possible pathways of degradation: acyl migration and hydrolytic cleavage. The previously characterized 1H resonances of acyl migrated products are quite distinguishable from those that arise from hydrolysis. The NMR method described here could be used to rank order acyl glucuronide forming discovery compounds based on the potential reactivity of the conjugates and their routes of decomposition under physiological conditions. Furthermore, we have shown that in vitro systems such as liver microsomal preparations can be used to generate sufficient quantities of acyl glucuronides from early discovery compounds for NMR characterization. This is particularly important, as we often have limited supply of early discovery compounds to conduct in vivo studies to generate sufficient quantities of acyl glucuronides for further characterization.

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Three fenamates (flufenamate, meclofenamate and mefenamate) were examined for their protective effect on neurons under ischemic (glucose/oxygen deprivation) or excitotoxic conditions, using the isolated retina of chick embryo as a model. Retinal damage was evaluated by histology and lactate dehydrogenase assay. Whole-cell recording was used to examine the direct effect of the fenamates on glutamate receptor-mediated currents. The fenamates protected the retina against the ischemic or excitotoxic insult. Part of the neuroprotection by the fenamates derived from inhibition of N-methyl-D-aspartate receptor-mediated currents. However, kainate receptor-mediated currents were not blocked by the fenamates, which nonetheless reduced kainate receptor-mediated retinal damage. Our results raise the possibility that fenamates may serve as lead structures in the development of novel therapeutic agents against brain ischemia.

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The diagnosis of DUB is made by the exclusion of organic disease as a cause of the abnormal menses; the condition accounts for about 80% of cases of menorrhagia. Of these, over 80% will have no abnormality of the hypothalamo-pituitary-ovarian axis, and it is likely that the disorder is the result of local endometrial factors. There appears to be not only a preponderance of vasodilatory prostaglandins in the endometrium of women with menorrhagia, but also an excessive increase in fibrinolytic activity within the uterine cavity. Once a diagnosis has been reached with the aid of history, examination, haematological and endocrine investigations, and dilatation and curettage when appropriate, medical treatment is the usual first line approach. Non-steroidal anti-inflammatory drugs such as mefenamic acid, or antifibrinolytic agents such as tranexamic or epsilon aminocaproic acids, will reduce blood loss by between 25 and 50%. Though the former drugs are relatively free from side-effects in healthy women, intracranial thrombosis has been reported with the latter (Agnelli et al, 1982). Medications which suppress ovarian function, such as danazol or gonadotrophin releasing hormone analogues, are highly effective in lessening, or inhibiting, menstrual loss, but at the expense of side-effects and convenience respectively. The combined contraceptive pill may reduce blood loss by 50% but is not appropriate for older women. Cyclical gestagens such as norethisterone have been widely employed, particularly for the treatment of anovulatory cycles, but their place in the management of ovulatory DUB is less clear. If medical treatment fails hysterectomy should be considered, though less invasive surgical methods of endometrial ablation are being developed. Finally, it should be remembered that in the absence of associated signs or symptoms of iron-deficiency anaemia, heavy menstrual bleeding is a subjective complaint and up to 50% of women describing menorrhagia will have a measured monthly blood loss within normal limits.

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The use of a zinc supplement in combination with mefenamic acid was superior in reducing primary dysmenorrhea compared to mefenamic acid alone.

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There are no studies verifying that mefenamic acid is more effective than other NSAID (= non-steroidal anti-inflammatory drugs). However, there are several notions in the literature that this drug is less well-tolerated than other NSAID because over a prolonged period of application more lesions of the upper gastro-intestinal tract are induced as well as occasionally renal insufficiency. Compared to other NSAID the systemic toxicity starts already with relatively low doses above the maximal daily dose. Considering current knowledge there is no reason to prefer mefenamic acid to other NSAID.

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There is no treatment proven to limit the growth of abdominal aortic aneurysms, in which the histological hallmarks include inflammation and medial atrophy, with apoptosis of smooth muscle cells and destruction of elastin.

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To assess whether use of tranexamic acid is associated with an increased risk of venous thromboembolism (VTE).

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Differences in the inhibitory potentials against UDP-glucuronosyltransferase (UGT) between species have been reported only rarely, even though the information would be useful for the precise characterization of drug candidates. In this study, the inhibition potentials of nonsteroidal anti-inflammatory drugs (NSAIDs) against UGT-catalyzed estradiol 3beta-glucuronidation (E3G) in the liver microsomes of rats, dogs, and humans were compared. Rat liver microsomes (RLMs) and human liver microsomes (HLMs) exhibited homotropic activation kinetics with S(50) values of 22 and 12 microM, respectively. However, dog liver microsomes (DLMs), exhibited Michaelis-Menten kinetics with no activation. Among the NSAIDs investigated (diclofenac, diflunisal, fenoprofen, flurbiprofen, ibuprofen, indomethacin, ketoprofen, mefenamic acid, niflumic acid, and sulindac), only niflumic acid and mefenamic acid inhibited E3G potently in all three species. The IC(50) values of NSAIDs against E3G in RLMs and HLMs were within a threefold difference of each other, while those in DLMs was more than three times higher than the other two. In conclusion, RLMs showed an inhibitory pattern similar to that of HLMs, whereas DLMs presented a distinct pattern. These results indicate that a rat animal model would be useful for evaluating the inhibitory potentials of drugs against estradiol glucuronidation, but a dog model would not.

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Thiopurine S-methyltransferase (TPMT) is a biotransformation phase II enzyme responsible for the metabolic inactivation of thiopurine drugs. The present study was carried out to investigate the inhibitory potential of 15 nonsteroidal anti-inflammatory drugs (NSAIDs) on human TPMT activity in vitro. TPMT activity was measured in pooled human erythrocytes in the absence and presence of various NSAIDs using the previously published high-performance liquid chromatography-UV method. To determine the inhibition type and K(i) value for each compound, we performed kinetic analysis at five different inhibitor concentrations close to the IC(50) value obtained in preliminary experiments. Naproxen (K(i) = 52 microM), mefenamic acid (K(i) = 39 microM), and tolfenamic acid (K(i) = 50 microM) inhibited TPMT activity in a noncompetitive manner. The estimated K(i) values for the inhibition of TPMT by ketoprofen (K(i) = 172 microM) and ibuprofen (K(i) = 1043 microM) indicated that the propionic acid derivatives were relatively weak inhibitors of TPMT. Our results suggest that coadministration of thiopurines and various NSAIDs may lead to drug interactions.

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We searched the Cochrane Menstrual Disorders & Subfertility Group trials register (searched April 2007), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library, Issue 1, 2007), MEDLINE (1966 to April 2007), EMBASE (1985 to April 2007), CINAHL (1982 to April 2007), Current Contents (1993 to April 2007) and reference lists of articles. We also contacted manufacturers and researchers in the field.

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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.

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The effect of prostaglandin synthesis inhibition on the postprandial intestinal hyperemia was examined in the jejunum of anesthetized dogs. Both intravenous and intra-arterial infusion of the cyclooxygenase inhibitors indomethacin and mefenamic acid reduced resting jejunal blood flow and markedly enhanced the food-induced jejunal hyperemia. The jejunal vascular response to food did not change after either intravenous or intra-arterial infusion of the carrier solutions or intra-arterial infusion of angiotensin II. The enhancement of the jejunal hyperemia was associated with an increase in the food-induced increase in jejunal oxygen consumption. Infusion of the cyclooxygenase inhibitors increased the mean amplitude of the monophasic intestinal contractions; however, this did not appear to play a role in the enhancement of the food-induced hyperemia. The study indicates that inhibition of prostaglandin synthesis has a marked effect on the postprandial intestinal hyperemia and that this may be due to its enhancement of the jejunal metabolic response to food. The prostaglandins involved and their mechanism of action are unknown.

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A number of nonsteroidal anti-inflammatory drugs (NSAIDs) are subject to glucuronidation in humans, and UDP-glucuronosyltransferase (UGT) 2B7 is involved in the glucuronidation of many NSAIDs. The objective of this study was to identify a NSAID with potent inhibitory potential against UGT2B7 using liquid chromatography with tandem mass spectrometry (LC-MS/MS).

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Prospective, randomized, controlled, single-blinded, clinical trial.

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GABA(A) receptor (R) positive allosteric modulators that selectively modulate GABA(A)Rs containing beta(2)- and/or beta(3)- over beta(1)-subunits have been reported across diverse chemotypes. Examples include loreclezole, mefenamic acid, tracazolate, and etifoxine. In general,"beta(2/3)-selective" GABA(A)R positive allosteric modulators are nonbenzodiazepines (nonBZs), do not show alpha-subunit isoform selectivity, yet have anxiolytic efficacy with reduced ataxic/sedative effects in animal models and humans. Here, we report on an enantiomeric pair of nonBZ GABA(A)R positive allosteric modulators that demonstrate differential beta-subunit isoform selectivity. We have tested this enantiomeric pair along with a series of other beta(2/3)-subunit selective, alpha-subunit isoform-selective, BZ and nonBZ GABA(A) positive allosteric modulators using electrophysiological, pharmacokinetic, and behavioral assays to test the hypothesis that ataxia may be correlated with the extent of modulation at beta(1)-subunit-containing GABA(A)Rs. Our findings provide an alternative strategy for designing anxioselective allosteric modulators of the GABA(A)R with BZ-like anxiolytic efficacy by reducing or eliminating activity at beta(1)-subunit-containing GABA(A)Rs.

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The pain intensity in the mefenamic and ginger group was 39.01 ± 17.77 and 43.49 ± 19.99, respectively, in the first month, and 33.75 ± 17.71 and 38.19 ± 20.47, respectively, in the second month (p > 0.05). The severity of dysmenorrhea, pain duration, cycle duration and bleeding volume was not significantly different between groups during the study. The menstrual days were more in the ginger group in the first (p = 0.01) and second cycle (p = 0.04). Repeated measurement showed a significant difference in pain intensity within the groups by time, but not between groups.

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Based on the studies carried out so far, the efficacy of aspirin, steroid and NSAIDs (traditional NSAIDs and COX-2 inhibitors) is not proven. Therefore, these drugs cannot be recommended for the treatment of AD.

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A swelling-activated, background K(+) current in the corneal epithelium is characteristically activated by fenamates and inhibited by diltiazem. Fatty acids also stimulate this current, indicating that its origin is a lipid-sensitive mechano-gated 2P domain K(+) channel. In the present study, modulation of TREK-1, TREK-2, and TRAAK channels by fenamates and diltiazem was examined. TREK-1, TREK-2, and TRAAK currents transiently expressed in COS-7 cells were recorded by the perforated-patch configuration. As previously reported, arachidonic acid (20 microM) stimulated all of these channels, and a volatile anesthetic, halothane (1 mM) augmented TREK-1 and TREK-2 but not TRAAK. Flufenamic acid (FA, 100 microM), niflumic acid (NA, 100 microM), and mefenamic acid (MA, 100 microM) markedly stimulated TREK-1, TREK-2, and TRAAK. The potency sequence for the activation of TREK-1 and TREK-2 was FA > NA = MA, and the potency sequence for the activation of TRAAK was FA = NA > MA. Diltiazem (1 mM) inhibited TREK-1 and TREK-2, but not TRAAK. In conclusion, fenamates are openers of the lipid-sensitive mechano-gated 2P domain K(+) channels, and diltiazem may be a specific blocker for TREK. These novel findings could help to further understand channel functions of the mechano-gated 2P domain K(+) channels.

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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.

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All the commonly used non-steriodal anti-inflammatory drugs (NSAIDs), except mefenamic acid, when extracted from the pharmaceutical dosage forms or the urines of users, and derivatized by silylation and then analysed by GC/MS, gave the mono- or the di-trimethylsilyl derivatives (depending on the number of derivatized groups in the drug) as the sole products. Mefenamic acid gave a mixture of products. When extracted from pharmaceutical dosage froms or from the urines of users, and analysed by GC/MS without derivatization, some of the NSAIDs were separated and detected as the unchanged molecules as the sole products, while others were separated and detected in altered forms as sole products or mixtures, depending on: (a) the solvent in which the extract was dissolved for injection into GC/MS, (b) the chemical structure of the drug, and (c) specifically for diflunisal, the presence or absence of potential methylating and/or acetylating agents on the GC column and/or septum. The main thermally-induced reactions of the underivatized NSAIDs included (i) methyl ester formation at the COOH group when the extract was dissolved in methanol, (ii) decarboxylation (i.e., loss of CO2), (iii) dehydration (i.e., loss of H2O) when the chemical structure permitted, such as for diclofenac, and (iv) cleavage at a carbon-heterocyclic nitrogen bond when one is present in an NSAID. Heating the urine in approximately 2 M HCl at 100 degrees C for 30 min, has been found to be a satisfactory means for effecting hydrolysis of the NSAIDs glucuronide conjugates. No metabolites, resulting from aromatic-ring hydroxylation, have been detected in urine for any of the NSAIDs studied.

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Ginger was as effective as mefenamic acid and ibuprofen in relieving pain in women with primary dysmenorrhea. Further studies regarding the effects of ginger on other symptoms associated with dysmenorrhea and efficacy and safety of various doses and treatment durations of ginger are warranted.

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ponstel s medicine 2015-08-04

Tranexamic acid (Transamin), Cyklokapron, Exacyl, Cyklo-f) is a synthetic lysine derivative that exerts its antifibrinolytic effect by reversibly blocking lysine binding sites on plasminogen and thus preventing fibrin degradation. In a number of small clinical studies in women with idiopathic menorrhagia, tranexamic acid 2-4.5 g/day for 4-7 days reduced menstrual blood loss by 34-59% over 2-3 cycles, significantly more so than placebo, mefenamic acid, flurbiprofen, etamsylate and oral luteal phase norethisterone at clinically relevant dosages. Intrauterine administration of levonorgestrel 20 microg/day, however, produced the greatest reduction (96% after 12 months) in blood loss; 44% of patients treated with levonorgestrel developed amenorrhoea. Tranexamic acid 1.5 g three times daily for 5 days also significantly reduced menstrual blood loss in women with intrauterine contraceptive device-associated menorrhagia compared with diclofenac sodium (150 mg in three divided doses on day 1 followed by 25 mg three times daily on days 2-5) or placebo. Tranexamic acid, mefenamic acid, etamsylate, flurbiprofen or diclofenac sodium had no effect on the duration of menses in the studies that reported such data. In a large noncomparative, nonblind, quality-of-life study, 81% of women were satisfied with tranexamic acid 3-6 g/day for 3-4 days/cycle for three cycles, and 94% judged their menstrual blood loss to be 'decreased' or 'strongly decreased' compared with untreated menstruations. The most commonly reported drug-related adverse events are gastrointestinal in nature. The total incidence of nausea, vomiting, diarrhoea and dyspepsia in a double-blind study was 12% in patients who received tranexamic acid 1g four times daily for 4 days for two cycles (not significantly different to the incidence in placebo recipients). In conclusion, the oral antifibrinolytic drug tranexamic acid is an effective and well tolerated treatment for idiopathic menorrhagia. In clinical trials, tranexamic acid was more effective at reducing menstrual blood loss than mefenamic acid, flurbiprofen, etamsylate and oral luteal phase norethisterone. Although it was not as effective as intrauterine administration of levonorgestrel, the high incidence of amenorrhoea and adverse events such as intermenstrual bleeding resulting from such treatment may be unacceptable to some patients. Comparative studies of tranexamic acid with epsilon - aminocaproic acid, danazol and combined oral contraceptives, as well as long-term tolerability studies, would help to further define the place of the drug in the treatment of menorrhagia. Nevertheless, tranexamic acid may be considered as a first-line treatment for the initial management of idiopathic menorrhagia, especially for patients in whom hormonal treatment is either buy ponstel not recommended or not wanted.

ponstel tablets 2015-03-05

Adenomyosis is the major cause of menorrhagia, dysmenorrhea, and an enlarged uterus, which causes great distress to the patient. Surgical hysterectomy has been used in the past as a treatment option for adenomyosis, but acceptability of this intervention is minimal due to an increased risk in morbidity and mortality. This article presents the successful medical treatment of an enlarged adenomyotic uterus with the levonorgestrel-releasing intrauterine system (LNG-IUS) using a case report of a 42-year-old woman with adenomyosis who received the LNG-IUS as a long-term therapy for menorrhagia and dysmenorrhea. Regular menstruation without pain was reported after 3 months of treatment with a 27% decrease in uterine size after 9 months. The effectiveness of the LNG-IUS was hypothesized to be due to two factors: 1) decidualization and subsequent marked atrophy of the endometrium; 2) direct action of the hormone on the foci of the adenomyosis. A reported side effect of the LNG-IUS is the irregularity of bleeding during the initial treatment. The study suggests that use of the LNG-IUS is a viable option and buy ponstel could greatly advance the treatment of adenomyosis.

ponstel syrup 2016-10-27

The current study simultaneously monitored the pharmacokinetic and pharmacodynamic interactions in a single animal. Four groups of Sprague-Dawley rats (n=7 each) received oral doses of a standardized SR extract (300mg/kg, twice daily), MEF (40mg/kg, daily), combination of SR extract and MEF, and vehicle control, respectively, for 5 days. On Day 5, blood samples were collected after first dose over 24h for the determination of (1) plasma concentrations of SR bioactive components, MEF and its metabolites by LC-MS/MS, and (2) prostaglandin E2 (PGE2) production and cyclooxygenase-2 (COX-2) gene expression by ex vivo buy ponstel analyses using LPS-stimulated RAW264.7 macrophage cells, ELISA and real time-PCR. After the rats were sacrificed, stomachs were isolated to assess their gross mucosal damage. Statistical comparisons were conducted using ANOVA and t-test.

ponstel dosing 2017-06-23

Blood mononuclear cell suspensions from patients with a severe form of periodontal disease failed to respond by in vitro stimulation to a sonicate from the oral bacterium, Veillonella alcalescens. The proliferative response could be restored by the depletion of TG cells by rosetting with IgG-coated ox erythrocytes and by reconstitution of the cell suspension with 10% plastic-adherent monocytes. Small but statistically significant restoration of the Veillonella response was also achieved by the addition of indomethacin or mefenamic acid to unfractionated cell cultures, indicating only a minor role of prostaglandin (PG) synthesis in the expression of suppressor cells. Since the in vitro response to an unrelated antigen buy ponstel PPD had been found unimpaired, the described TG-cell-mediated suppression of the Veillonella response is apparently antigen-specific.

ponstel pills 2016-10-27

In this study, electrospun nanofibers were used as solid-phase microextraction (SPME) fiber coatings after substituting the water-soluble sheath of the emulsion electrospun polystyrene (PS)@Plurinic F-127 core-sheath nanofibers with biocompatible and water-stable buy ponstel polydopamine (PDA) and subsequently being appropriately cross-linked with glutaraldehyde (GA) to enhance the strength of the electrospun architecture. The novel custom-made PS@PDA-GA coating was wettable in aqueous solutions and thus exhibited much higher extraction efficiency than the nonsheathed PS nanofiber coating and the thicker polydimethylsiloxane (PDMS) coating. The novel coating also possessed excellent stability (relative standard deviations (RSDs) less than 7.3% for six sampling-desorption cycles), interfiber reproducibility (RSDs less than 14.3%), and antibiofouling ability, which were beneficial for in vivo sampling. The PS@PDA-GA fiber was used to monitor pharmaceuticals in dorsal-epaxial muscle of living fish, and satisfactory sensitivities with the limits of detection in the range of 1.1 (mefenamic acid) to 8.9 (fluoxetine) ng·g(-1) and comparable accuracies to liquid extraction were achieved. In general, this study explored a convenient and effective method to sheath nanofibers for high-efficient in vivo SPME of analytes of interest in semisolid tissues.

ponstel generic cost 2016-08-18

Most patients with bacterial infections suffer from fever and various pains that require complex treatments with antibiotics, antipyretics, and analgaesics. The most common drugs used to relieve these symptoms are non-steroidal anti-inflammatory drugs (NSAIDs), which are not typically considered antibiotics. Here, we investigate the effects of NSAIDs buy ponstel on bacterial susceptibility to antibiotics and the modulation of bacterial efflux pumps.

ponstel medication 2016-06-08

Antifibrinolytic therapy causes a greater reduction in objective measurements of heavy menstrual bleeding when compared to placebo or other medical therapies (NSAIDS, oral luteal phase progestagens and ethamsylate). This treatment is not associated with an increase in side effects compared to placebo, NSAIDS, oral luteal phase progestagens or ethamsylate. Flooding and leakage and sex life is significantly improved after tranexamic acid therapy when compared with oral luteal progestogens but no other measures of quality of life were assessed. No buy ponstel study has used resource cost as an outcome. There are no data available within randomised controlled trials which record the frequency of thromboembolic events.

ponstel 250 mg 2017-05-11

Many idiosyncratic non-steroidal anti-inflammatory drugs (NSAIDs) cause GI, liver and bone marrow toxicity in some patients which results in GI bleeding/ulceration/fulminant hepatic failure/hepatitis or agranulocytosis/aplastic anemia. The toxic mechanisms proposed have been reviewed. Evidence is presented showing that idiosyncratic NSAID drugs form prooxidant buy ponstel radicals when metabolised by peroxidases known to be present in these tissues. Thus GSH, NADH and/or ascorbate were cooxidised by catalytic amounts of NSAIDs and hydrogen peroxide in the presence of peroxidase. During GSH and NADH cooxidation, oxygen uptake and activation occurred. Furthermore the formation of NSAID oxidation products was prevented during the cooxidation indicating that the cooxidation involved redox cycling of the first formed NSAID radical product. The order of prooxidant catalytic effectiveness of fenamate and arylacetic acid NSAIDs was mefenamic acid>tolfenamic acid>flufenamic acid, meclofenamic acid or diclofenac. Diphenylamine, a common moiety to all of these NSAIDs was a more active prooxidant for NADH and ascorbate cooxidation than these NSAIDs which suggests that oxidation of the NSAID diphenylamine moiety to a cation and/or nitroxide radical was responsible for the NSAID prooxidant activity. The order of catalytic effectiveness found for sulfonamide derivatives was sulfaphenazole>sulfisoxazolez.Gt;dapsone>sulfanilic acid>procainamide>sulfamethoxazole>sulfadiazine>sulfadimethoxine whereas sulfanilamide, sulfapyridine or nimesulide had no prooxidant activity. Although indomethacin had little prooxidant activity, its major in vivo metabolite, N-deschlorobenzoyl indomethacin had significant prooxidant activity. Aminoantipyrine the major in vivo metabolite of aminopyrine or dipyrone was also more prooxidant than the parent drugs. It is hypothesized that the NSAID radicals and/or the resulting oxidative stress initiates the cytotoxic processes leading to idiosyncratic toxicity.

ponstel generic price 2016-10-07

The European Union regulated the use of non-steroidal anti-inflammatory drugs (NSAIDs) in animal production and set the official analytical controls to detect their residues in plasma, serum, and milk within the frame of national monitoring programs in each member state. In this work, a multi-residue reversed-phase high-performance liquid chromatography with diode array detector (DAD) method is described for buy ponstel the simultaneous determination of 13 NSAIDs in serum and plasma of farm animals. Chromatographic separation by a C12 stationary phase column with a linear gradient is able to resolve all the compounds considered: salicylic acid, ketoprofen, flurbiprofen, phenylbutazone and its metabolite (oxyphenbutazone), carprofen, ibuprofen, naproxen, niflumic acid, suxibutazone, diclofenac, mefenamic acid, and tolfenamic acid. These compounds are chosen as the most representative of the different NSAID chemical sub-classes. The DAD analysis allows the confirmation of all drugs on the basis of their own UV-vis spectrum, according to the requirements of the European Council Decision 2002/657/EC. Moreover, the method is in-house validated, evaluating mean recoveries, specificity, repeatability, and within-laboratory reproducibility as the performance parameters required by the Decision. The results of this study indicate the method is specific and repeatable, with the mean percentage recoveries of the drugs ranging between 72.5% and 104.5%. Only salicylic acid has poor recovery, with results ranging between 36.3% and 54.9%.

ponstel user reviews 2017-11-19

To assess the efficacy of single dose oral mefenamic acid in acute postoperative pain, and any buy ponstel associated adverse events.

ponstel dosage 2016-07-24

Cyclooxygenase enzymes (COX-1 and COX-2) catalyze the conversion of arachidonic acid to prostaglandin G2. The inhibitory activity of rapid, reversible COX inhibitors (ibuprofen, naproxen, mefenamic acid, and lumiracoxib) demonstrated a significant increase in potency and time dependence of inhibition against double tryptophan murine COX-2 mutants at the 89/90 and 89/119 positions. In contrast, the slow, time-dependent COX inhibitors (diclofenac, indomethacin, and flurbiprofen) were unaffected by those mutations. Further mutagenesis studies suggested that mutation at position 89 was principally responsible buy ponstel for the changes in inhibitory potency of rapid, reversible inhibitors, whereas mutation at position 90 may exert some effect on the potency of COX-2-selective diarylheterocycle inhibitors; no effect was observed with mutation at position 119. Several crystal structures with or without NSAIDs indicated that placement of a bulky residue at position 89 caused a closure of a gap at the lobby, and alteration of histidine to tryptophan at position 90 changed the electrostatic profile of the side pocket of COX-2. Thus, these two residues, especially Val-89 at the lobby region, are crucial for the entrance and exit of some NSAIDs from the COX active site.

ponstel medication information 2016-04-12

The objective of this study was to enhance the solubility as well as to mask the intensely bitter taste of the poorly soluble drug, Mefenamic acid (MA). The taste masking and solubility of the drug was improved by using Eudragit(®) E PO in different ratios via hot melt extrusion (HME), solid dispersion technology. Differential scanning calorimetry (DSC) studies demonstrated that MA and E PO were completely miscible up to 40% drug loads. Powder X-ray diffraction analysis indicated that MA was converted to its amorphous phase in all of the formulations. Additionally, FT-IR analysis indicated hydrogen bonding between the drug and the carrier up to 25% of drug loading. SEM images indicated aggregation of MA at over 30% of drug loading. Based on the FT-IR, SEM and dissolution results for the extrudates, two optimized formulations (20% and 25% buy ponstel drug loads) were selected to formulate the orally disintegrating tablets (ODTs). ODTs were successfully prepared with excellent friability and rapid disintegration time in addition to having the desired taste-masking effect. All of the extruded formulations and the ODTs were found to be physically and chemically stable over a period of 6 months at 40°C/75% RH and 12 months at 25°C/60% RH, respectively.

ponstel medicine 2017-08-17

Higher surface exposure of polar functional groups correlates with higher tendency to stick to metal surfaces and buy ponstel AFM tips, indicating involvement of specific polar interactions in the adhesion behavior. In addition, an AFM method is identified to prospectively assess the risk of sticking during the early stages of drug development.

ponstel generic name 2015-08-01

The measurement of serum tryptase levels does not appear to be helpful to differentiate mild allergic or nonallergic reactions from 'hysterical' ones. The milder decrease in the group with objective drug reactions might indicate buy ponstel slight mast cell activation in some patients. More severe clinical drug reactions led to stronger mast cell degranulation. Mild reactions did not increase the tryptase levels consistently.

buy ponstel online 2016-02-19

Manual crushing of one blastocyst performed on 181 bicornuate twin pregnancies between Days 24 and 45 has shown that the uncrushed blastocyst can either survive and develop normally to full term or may be rejected and resorbed like its crushed twin, depending mainly on the stage of pregnancy. Crushing, which causes rupture of fetal membranes, results in a rapid fall in the survival rate of the uncrushed blastocyst when performed after Day 31. In some mares rupture is not possible after Day 35 even if extreme pressure is used. Crushed, but unruptured, blastocysts mainly between Days 35 and 45 may (a) resorb as does the uncrushed twin (60%) (b) resorb without loss of the uncrushed twin (20%) or (c) survive, as does the uncrushed twin, even when several attempts on alternate days are made to destroy the blastocyst (20%). At no stage of pregnancy is the uncrushed embryo resorbed unless the crushed twin is destroyed. The rejection and resorption of the uncrushed twin is not due to transference of pressure, but presumably to physiological processes involving prostaglandin. Mefenamic acid appears to increase survival rates especially when crushing is performed after 31 days, Diovan Pill although the twin of apparently successful crushings at this stage may be lost between Days 50 and 70.

ponstel suspension 2016-09-29

The ability of anti-inflammatory agents to modulate cellular sensitivity to anticancer drugs was investigated for pulmonary carcinoma cells in vitro. We examined the drug sensitivity of two pulmonary adenocarcinoma cell lines (76-2, 77-4) in the presence of two drugs, an anticancer drug and an anti-inflammatory agent, for 72 hr by the 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay with 96 well plates. Anticancer drugs used for screening test were cyclophosphamide (CPM), mitomycin C (MMC), adriamycin (ADR), 5-fluorouracil (5FU), vindesine (VDS), cisplatin (CDDP), cytarabine (Ara C), methotrexate (MTX), etoposide (VP-16), and vincristine (VCR). Anti-inflammatory agents examined as modulators to anticancer drugs were aspirin, mefenamic acid, ibuprofen, sulindac, piroxicam, phenacetin, dicrofenac, ketoprofen, tolmetin and indomethacin. Screening tests showed indomethacin to be the most effective modulator, resulting in more than a 3-fold increase in cytotoxicity of VCR as compared with that produced by VCR alone. Study of each of the ten anticancer drugs in combination with indomethacin showed VCR to be the most effective anticancer drug in this combination. In 76-2 cells, the concentration of VCR producing 50% growth inhibition (IC50) for VCR alone and VCR in combination with 2 micrograms/ml indomethacin were 1.58 +/- 0.16 and 0.52 +/- 0.1 ng/ml respectively, which represents a 3-fold decrease. In 77-4 cells, the IC50 for VCR alone and VCR in combination with 2 micrograms/ml indomethacin were 2.86 +/- 0.2 and 0.52 +/- 0.11 ng/ml respectively, which represents a 3.8-fold decrease. Our studies indicate that clinically achievable concentrations of indomethacin may be useful in modulating VCR resistance in human pulmonary adenocarcinoma Suprax Pediatric Dosage cells, so that combined use of VCR and indomethacin may be of potential clinical significance in the treatment of lung cancer.

ponstel syrup children 2016-09-22

New non-steroidal anti-inflammatory agents (NSAIAs) were tested on lens protein-, endotoxin- and interleukin-1-induced ocular inflammation. It was found that most NSAIAs, including REV 5901, mefenamic acid, indomethacin, CK-17 and CK-102, inhibited lens protein-induced inflammation. Endotoxin induced inflammation indirectly through the release of IL-1 which was inhibited by fewer agents, including CK-17, CK-102 and prednisolone. However, the direct effect of IL-1 can only be suppressed by CK-17 and prednisolone. Therefore, CK-17 could become an important NSAIA which acts similarly to corticosteroids yet produces no steroidal side effects. CK-17 was different from most NSAIAs as it Detrol Dosage Info affected little, if any, arachidonate metabolism. Most importantly, CK-17 was found to be 2-fold more potent than prednisolone in inhibiting IL-1-induced uveitis, while no side effects were noted at doses tested to date.

ponstel 250 tablets 2015-08-25

CRP test is a useful indicator Ventolin Nebulizer Dosage for quantitative assessment for comparative evaluation of NSAIDs.

ponstel s dosage 2016-12-21

Flufenamic acid (FFA) is a nonsteroidal anti-inflammatory drug (NSAID). It has anti-inflammatory and antipyretic properties. In addition, it modulates multiple channel activities. Detrol 40 Mg The mechanisms underlying the pharmacological actions of FFA are presently unclear. Given that AMP-activated protein kinase (AMPK) has both anti-inflammatory and channel-regulating functions, we examined whether FFA induces AMPK activation. 1) Exposure of several different types of cells to FFA resulted in an elevation of AMPKα phosphorylation at Thr172. This effect of FFA was reproduced by functionally and structurally similar mefenamic acid, tolfenamic acid, niflumic acid, and meclofenamic acid. 2) FFA-induced activation of AMPK was largely abolished by the treatment of cells with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis(acetoxymethyl ester) (an intracellular Ca(2+) chelator) or depletion of extracellular Ca(2+), whereas it was mimicked by stimulation of cells with the Ca(2+) ionophore 5-(methylamino)-2-({(2R,3R,6S,8S,9R,11R)-3,9,11-trimethyl-8-[(1S)-1-methyl-2-oxo-2-(1H-pyrrol-2-yl)ethyl]-1,7-dioxaspiro[5.5]undec-2-yl}methyl)-1,3-benzoxazole-4-carboxylic acid (A23187) or ionomycin. 3) FFA triggered a rise in intracellular Ca(2+), which was abolished by cyclosporine, a blocker of mitochondrial permeability transition pore. Cyclosporine also abolished FFA-induced activation of AMPK. 4) Inhibition of Ca(2+)/calmodulin-dependent kinase kinase β (CaMKKβ) with 7-oxo-7H-benzimidazo[2,1-a]benz[de]isoquinoline-3-carboxylic acid acetate (STO-609) or down-regulation of CaMKKβ with short interfering RNA largely abrogated FFA-induced activation of AMPK. 5) FFA significantly suppressed nuclear factor-κB activity and inducible nitric-oxide synthase expression triggered by interleukin-1β and tumor necrosis factor α. This suppression was also largely abrogated by STO-609. Taken together, we conclude that FFA induces AMPK activation through the Ca(2+)-CaMKKβ pathway. Activation of AMPK is a presently unrecognized important mechanism underlying the pharmacological effects of FFA.

ponstel medication cost 2016-01-29

An 18-month-old previously healthy child had an ointment applied topically to a diaper rash by his mother, consisting of a single pump of a prescription ointment that her husband received from a compounding pharmacy for neck pain. Approximately 20 minutes later, when the child had been put down for a nap, he had gasping respiration but was otherwise unresponsive. Emergency medical services was called, and the child was unresponsive. In the ED, vital signs were pulse of 57 beats/min, blood pressure 74/35 mm Hg, respiratory rate 21 breaths/min, and O2 saturation 98% on a nonrebreather. Fingerstick glucose was 105 mg/dL. In the ED, physical examination was significant for unresponsiveness, pinpoint pupils, and hyporeflexia. The patient's mental status continued to deteriorate with depressed respirations, and he was intubated. Laboratory results were noncontributory. Electrocardiogram revealed only sinus bradycardia. The patient was transported to a pediatric intensive care unit. He did well over the next several hours with supportive care and had return to Cefixime Dosing Pediatrics normal vital signs over the following 12 hours. He was extubated the following morning without problems. Blood taken at the time of ED presentation had a serum clonidine level of 9.2 ng/mL (reference range, 0.5-4.5 ng/mL) and a norketamine level of 41 ng/mL (reporting limit, >20 ng/mL).

ponstel buy 2015-07-14

1. The effect of the non-steroidal anti-inflammatory drugs naproxen, mefenamic acid, phenylbutazone, piroxicam and tolmetin on the vanadate (0.3 mM)-induced tonic contraction, as well as the modifications of these effects by the G-protein inhibitor pertussis toxin, and the inhibitors of protein kinase A, Rp-cAMPS (Rp-Adenosine 3',5'-cyclic monophosphothioate triethylamine salt) and protein kinase C, H-7 [1(5-isoquinolynilsulfonyl)-2-methyl-piperazine], have been assayed to study the possible nature of intracellular mediators contributing to the inhibitory effects of NSAIDs in rat uterine smooth muscle incubated in medium lacking calcium plus EDTA. The effect of phorbol 12,13-dibutyrate on vanadate contraction and its modification with H-7 has also been examined. 2. Naproxen (6-600 microM), mefenamic acid (6-300 microM), phenylbutazone (6-300 microM), piroxicam (6-600 microM) and tolmetin (6-600 microM) produced concentration-dependent relaxation of vanadate-induced tonic contraction. The potency order, in accordance with their respective IC50 values was: phenylbutazone > or = mefenamic acid > or = naproxen > tolmetin > or Minipress Max Dose = piroxicam. 3. The relaxant effects of naproxen, phenylbutazone, piroxicam and tolmetin were significantly antagonized with pertussis toxin (50 ng ml-1), Rp-cAMPS (100 microM) and H-7 (1 microM). However, the effect of mefenamic acid was unmodified by the three drugs. This suggests that the effect of mefenamic acid and other NSAIDs occur by different mechanisms. 4. Phorbol 12,13-dibutyrate relaxed the vanadate contraction but the maximal relaxation achieved (54.8 +/- 8.3%, n = 4) was lower than those induced with the NSAIDs. On the other hand, H-7 (1 microM) did not modify the relaxant effect of phorbol 12,13-dibutyrate. This suggests that H-7 behaves as a PKA, but not a PKC inhibitor, under the present experimental conditions. 5. The relaxation by naproxen, phenylbutazone, piroxicam and tolmetin is presumably produced by increasing cAMP because the effects of these are antagonized with Rp-cAMPS and H-7, and by pertussis-toxin-sensitive mechanisms.

ponstel pill 2017-01-02

A well controlled double blind prospective trial was undertaken to Paracetamol Drug Study determine the efficacy of mefenamic acid in the treatment of menorrhagia. Eighty patients who had unexplained cyclical menorrhagia with secretory endometrium received mefenamic acid orally in a dose of 500 mg 8 hourly or a placebo tablet thrice daily starting from day-one of the cycle for 5 days or till cessation of menses. Mefenamic acid administration caused a statistically significant reduction in the number of days of bleeding from 9.7 +/- 3.1 days before treatment to 4.1 +/- 0.6 days after treatment. It also brought about significant reduction in the amount of bleeding in terms of number of pads used per day, that is from 15.2 +/- 3.1 before treatment to 6.5 +/- 0.02 after treatment. Eighty-six percent patients in the treatment group had control of menorrhagia with the drug compared to 20% in the control group without drugs and this difference was statistically significant. Mefenamic acid proved to be a potent and efficacious agent in the control of unexplained menorrhagia.

ponstel capsules 2017-02-25

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.

ponstel drug interaction 2015-02-19

Only one study, trial B in the report of Gersony 1983, was found eligible. The trial compared the effect of surgical ligation of PDA versus medical treatment with indomethacin, each used as the primary treatment. No trials comparing surgery to other cyclooxygenase inhibitors (ibuprofen, mefenamic acid) were found. Trial B of Gersony 1983 enrolled 154 infants. The study found no statistically significant difference between surgical closure and indomethacin treatment in mortality during hospital stay, chronic lung disease, other bleeding, necrotizing enterocolitis, sepsis, creatinine level, or intraventricular hemorrhage. There was a statistically significant increase in the surgical group in incidence of pneumothorax [RR 2.68 (95% CI 1.45, 4.93); RD 0.25 (95% CI 0.11, 0.38); NNH 4 (95% CI 3, 9)] and retinopathy of prematurity grade III and IV [RR 3.80 (95% CI 1.12, 12.93); RD 0.11 (95% CI 0.02, 0.20), NNH 9 (95% CI 5, 50] compared to the indomethacin group. There was as expected a statistically significant decrease in failure of ductal closure rate in the surgical group as compared to the indomethacin group: [RR 0.04 (95% CI 0.01, 0.27); RD -0.32 (95% CI -0.43, -0.21), NNT 3 (95% CI 2, 4)].

ponstel 250 reviews 2017-07-07

A high-performance liquid chromatographic method for the quantitation of a new anti-inflammatory agent, 2-(10,11-dihydro-10-oxodibenzo[b,f]thiepin-2-yl)propionic acid (CN-100; I), has been developed. The assay consists in extracting samples containing I and mefenamic acid, the internal standard, under acidic conditions and analysis by reversed-phase chromatography using ultraviolet detection at 330 nm. Preliminary plasma concentration-time and cumulative urinary excretion profiles from a healthy subject following oral administration of the tablet formulation are presented. This method is simple, sensitive and reproducible and is applicable to studies of the pharmacokinetic behaviour of I in humans.

ponstel 250 capsule 2017-02-16

The radioprotective effect of MEF is probably related to anti-inflammatory property of MEF on human lymphocytes.

ponstel capsule 2017-05-26

An eco-friendly sensitive, rapid and less hazardous micellar liquid chromatographic method was developed and validated for the simultaneous analysis of ethamsylate (ETM) and mefenamic acid (MFA) in the presence of hydroquinone (HQ) and 2,3-dimethylaniline (DMA) the main impurities of ETM and MFA, respectively. Good chromatographic separation was attained using Eclipse XDB-C8 column (150 mm × 4.6 mm, 5 μm particle size) adopting UV detection at 300 nm with micellar mobile phase consisting of 0.12 M sodium dodecyl sulfate, 0.3% triethylamine and 15% 2-propanol in 0.02 M orthophosphoric acid (pH 7.0) at 1.0 mL/min. The analytes were well resolved in <6.0 min, ETM (tR = 1.55 min), HQ (tR = 1.95 min), MFA (tR = 4.55 min) and DMA (tR = 5.80 min). Different validation parameters were examined as recommended by international conference on harmonization (ICH) guidelines. The method was linear over the concentration ranges of 0.5-18.0, 0.5-20.0, 0.01-0.5 and 0.02-0.2 µg/mL with limits of detection of 0.118, 0.159, 0.005 and 0.005 µg/mL and limits of quantification of 0.358, 0.482, 0.014 and 0.015 µg/mL for ETM, MFA, HQ and DMA, respectively. The suggested method was successfully applied for the determination of the two drugs in their bulk powder, laboratory-prepared mixtures, single-ingredient and co-formulated tablets. The obtained results were in accordance with those of the comparison method. The method can also detect trace amounts of HQ and DMA as the main impurities of ETM and MFA, respectively, within the BP limit (0.1%) for both impurities. Furthermore, it is a stability-indicating one for the determination of ETM in its pure form, single-component tablet and co-formulated tablets with other drugs.

ponstel drug 2016-12-10

Neither pre- nor postischemic administration of a dose previously shown effective in preventing epileptic neuronal necrosis was found to reduce necrosis in cortex, nor in any subcortical structures.

ponstel dose 2016-09-29

Cotrimoxazole was the most common cause of FDE, whereas FDE with diclofenac sodium, pyrantel pamoate, clindamycin, and albendazole were reported for the first time. FDE may have multiform presentations.