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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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Celebrex, Voltaren, Dolobid, Lodine, Motrin, Indocin, Orudis, Toradol, Naproxen, Ibuprofen, Diclofenac, Voltaren, Aleve, Advil, Celecoxib, Naprosyn, Motrin, Ketoprofen


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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The most common side effects associated with Ponstel are:

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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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Synthesis of 1,3,4-oxadiazole derivatives of diclofenac and mefenamic acid are described. The target compounds 5-[2-(2,6-dichloroanilino)benzyl]-2-aryl-1,3,4-oxadiazole (3a-3e) and 5-[2-(2,3-dimethylanilino)phenyl]-2-(aryl)-1,3,4-oxadiazole (6a-6e) were obtained by treating 2 and 5 with various aromatic acids using POCl(3) as dehydrating agent. They were purified and characterized by IR, (1)H-NMR and elemental analysis. These compounds were further subjected to antiinflammatory, analgesic and acute ulcerogenic activity. Compound 3c and 6d exhibited good antiinflammatory activity and compounds 3c, 3e, 6c, 6d, 6e were found to be non ulcerogenic.

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A method for assessing inflammatory pain response was developed by modification of the formalin test. Formalin (0.5%, 25 microliters) was injected into the hindpaw of the mouse, and the durations spent in licking or biting response were measured as an indicator of pain response. The response curve was biphasic, having two peaks, from 0 to 5 min (first phase) and from 15 to 20 min (second phase). Morphine, ethylketocyclazocine, ketocyclazocine and pentazocine inhibited the response dose-dependently at the first and the second phases. Aspirin, oxyphenbutazone and dexamethasone inhibited only the second phase. Aminopyrine and mefenamic acid which acted at both central and peripheral sites inhibited both phases; however, the inhibition of the second phase was stronger than that of the first phase. Substance P (SP) antagonist inhibited only the first phase. Bradykinin (BK) inhibitor caused a inhibition of both first and second phases, and pretreatment of compound 48/80 and indomethacin inhibited only the second phase. From these facts, it was suggested that SP and BK played a role in the pain response at the first phase, and histamine, BK and PG were involved at the second phase. Naloxone produced hyperalgesia and bestatin produced analgesia at the second phase; then, it seems that the endogenous opioid system is activated by formalin stimulation and modulates the pain perception. Based on these findings, it is presumed that the pain of the first phase is evoked by the direct stimulation of the nerve fibers, and that of the second phase is due to the inflammatory reaction.

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76 women with dysfunctional uterine bleeding.

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A new and simple high-performance liquid chromatography assay was developed and validated for the simultaneous determination of the above-mentioned drugs in small samples of human plasma (0.25 mL). After protein precipitation with acetonitrile, satisfactory separation was achieved on a Hypersil BDS C18 column (250 × 4.6 mm, 5 m) using a mobile phase comprising 20 mmol/L ammonium phosphate buffer (pH = 3) and acetonitrile at a ratio of 35:65, vol/vol; the elution was isocratic at ambient temperature with a flow rate of 1 mL/min. The UV detector was set at 265 nm.

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Primary dysmenorrhoea is characterised by painful menstrual cramps which appear to have no macroscopically identifiable pelvic pathology. 50% of postpubescent females suffer from dysmenorrhoea, and 10% are incapacitated for 1 to 3 days each month. Many of these patients have an increased synthesis of prostaglandins in their endometrial tissue with increased prostaglandin release in the menstrual fluid. The increased amount of prostaglandins induces incoordinate hyperactivity of the uterine muscle resulting in uterine ischaemia and pain. Recent clinical and laboratory studies have shown that many of the non-steroidal anti-inflammatory drugs such as ibuprofen, naproxen, flufenamic acid, mefenamic acid and indomethacin are capable of relieving primary dysmenorrhoea. These drugs are inhibitors of the prostaglandin synthetase enzymes which are necessary for prostaglandin biosynthesis. Thus, with ibuprofen it has been shown that clinical relief of the dysmenorrhoeic symptoms accompanies the reduction of menstrual fluid prostaglandins. With the oral contraceptive pill there is good relief of primary dysmenorrhoea, significant decrease in menstrual fluid prostaglandins, but no reduction in menstrual fluid volume; this suggests that the reduction in prostaglandins is secondary to the inhibition of endometrial growth and development. In some forms of secondary dysmenorrhoea elevated prostaglandin levels have been implicated. However, the evidence is less conclusive for dysmenorrhoea secondary to endometriosis and uterine myomas than for dysmenorrhoea associated with intrauterine devices. With the intrauterine device, prostaglandin synthetase inhibitors such as flufenamic acid, ibuprofen and naproxen are able not only to relieve dysmenorrhoea but also to reduce menstrual blood loss to normal levels. Thus, the use of appropriately selected prostaglandin synthetase inhibitors can offer effective relief from the miseries of some types of dysmenorrhoea with subsequent restoration of normal daily activities.

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The pharmacokinetics of mefenamic acid (MA), 2 mg/kg, were studied in 17 preterm infants with symptomatic patent ductus arteriosus. They were given this dosage orally at 24 h intervals. There were marked inter-individual differences in some of the pharmacokinetic parameters after the first dose; peak plasma concentration (Cmax) varied from 1.2 to 6.1 micrograms/mL with a mean of 3.8 micrograms/mL, time to reach Cmax (tmax) varied from 2 to 18 h with a mean of 7.7 h and plasma half-life (t1/2) varied from 3.8 to 43.6 h with a mean of 18.7 h. The group of infants (10/17) who had ductus closure after the first dose had significantly lower clearance (P < 0.01), longer t1/2 (P < 0.01) and higher 24 h plasma concentration (P < 0.001) compared to the group of infants (7/17) who had no ductus closure after the first dose. It appeared that the plasma concentration of MA had to be above 2.0 micrograms/mL and maintained at this concentration for at least 12 h for MA associated with ductus closure in preterm infants to take effect. In view of the inter-individual variation of plasma MA concentration and the effective plasma concentration, we suggest that measurement of the plasma concentration should be done 24 h after the first dose. This might be useful for safe and effective therapy for infants with ductus closure failure after the first dose.

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This paper investigates the removal of a broad range of pharmaceuticals during nanofiltration (NF) and reverse osmosis (RO) applied in a full-scale drinking water treatment plant (DWTP) using groundwater. Pharmaceutical residues detected in groundwater used as feed water in all five sampling campaigns were analgesics and anti-inflammatory drugs such as ketoprofen, diclofenac, acetaminophen and propyphenazone, beta-blockers sotalol and metoprolol, an antiepileptic drug carbamazepine, the antibiotic sulfamethoxazole, a lipid regulator gemfibrozil and a diuretic hydrochlorothiazide. The highest concentrations in groundwater were recorded for hydrochlorothiazide (58.6-2548ngL(-1)), ketoprofen (85%). Deteriorations in retentions on NF and RO membranes were observed for acetaminophen (44.8-73 %), gemfibrozil (50-70 %) and mefenamic acid (30-50%). Furthermore, since several pharmaceutical residues were detected in the brine stream of NF and RO processes at concentrations of several hundreds nanogram per litre, its disposal to a near-by river can represent a possible risk implication of this type of treatment.

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We studied binding of T4 to the lipid-complexed apolipoproteins (apo) of high density lipoproteins (HDL), the major lipoprotein carrier of thyroid hormones in human plasma, and to lipid-free apoA-I. HDL isolated from fresh normal plasma by ultracentrifugation (density, 1.063-1.210 g/mL) was photoaffinity labeled with [3,5-(125)I]T4 and analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Two bands corresponding to apoA-I (28.3K) and apoC-II or apoC-III (8.6-9.2K) were seen, and their radioactivity decreased by 50-60% when labeled in the presence of 1 mumol/L T4. Photoaffinity labeling of isolated apoA-I also was demonstrated and was decreased 74% by 1 mumol/L T4, suggesting a higher affinity of the lipid-free protein for T4. T4 binding of isolated apoA-I was optimal at pH 7-8, reached a maximum after 1 h at 23 C, and decreased after incubation at 37 C. Scatchard analysis revealed a single T4-binding site with a Ka of 7.5 x 10(7) L/mol at 23 C, pH 8.2. The potency of T4 analogs as inhibitors of T4 binding to isolated apoA-I was L-T4 = D-T4 = triiodothyroacetic acid = L-rT3 much greater than L-T3 much greater than L-thyronine. The binding of T4 to apoA-I was reduced by known inhibitors of T4 binding to serum proteins (diclofenac = mefenamic acid = furosemide = 8-anilinonaphthalene sulfonic acid much greater than dilantin greater than heparin greater than barbital) and by lipids (unsaturated fatty acids greater than cholesterol = cholesterol esters = phospholipids greater than saturated fatty acids = diglycerides = triglycerides). We conclude that the binding of T4 to HDL is mediated by a specific interaction of the hormone with apoA-I and with apoC-II and/or apoC-III. Since the lipid constituents of HDL inhibit T4 binding to apoA-I, the HDL subfraction in plasma that carries most of the HDL-bound T4 should be one with a low lipid content.

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Bovine corneal endothelial cells (BCECs) were treated for 48 hours with 640 compounds from a Food and Drug Administration (FDA)-approved drug library and then challenged with thapsigargin or H2O2 to induce UPR or oxidative stress, respectively. Cell viability was measured using the CellTiter-Glo survival assay. Selected "hits" were subjected to further dose-response testing, and their ability to modulate expression of UPR and oxidative stress markers was assessed by RT-PCR, Western blot, and measurement of protein carbonyl and 8-hydroxydeoxyguanosine (8-OHdG) adducts in immortalized human corneal endothelial cells (iHCECs).

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Menorrhagia affects the lives of many women. The assessment of menstrual flow is highly subjective and gauging the severity of the condition by objective assessment of menstrual blood loss is impractical. In treating menorrhagia, the primary aim should be to improve quality of life. Women are willing to undergo quite invasive treatment in order to achieve this. Drug therapy is the initial treatment of choice and the only option for those who wish to preserve their reproductive function. Despite the availability of a number of drugs, there is a general lack of an evidence-based approach, marked variation in practice and continuing uncertainty regarding the most appropriate therapy. Adverse effects and problems with compliance also undermine the success of medical treatment. This article reviews the available literature to compare the efficacy and tolerability of different medical treatments for menorrhagia. Tranexamic acid and mefenamic acid are among the most effective first-line drugs used to treat menorrhagia. Despite being used extensively in the past, oral luteal phase norethisterone is probably one of the least effective agents. Women requiring contraception have a choice of the combined oral contraceptive pill, levonorgestrel-releasing intrauterine system (LNG-IUS) or long-acting progestogens. Danazol, gestrinone and gonadotropin-releasing hormone analogues are all effective in terms of reducing menstrual blood loss but adverse effects and costs limit their long-term use. They have a role as second-line drugs for a short period of time in women awaiting surgery. While current evidence suggests that the LNG-IUS is an effective treatment, further evaluation, including long-term follow up, is awaited. Meanwhile, the quest continues for the ideal form of medical treatment for menorrhagia--one that is effective, affordable and acceptable.

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Single-channel currents were recorded from the plasma membrane of white adipocytes of 6-8-week-old male Sprague-Dawley rats. In outside-out patches (high K(+), no Ca(2+) in pipette), a voltage-dependent K-channel (delayed rectifier) with a single-channel conductance (gamma) of 16 pS (24 degrees C) in modified Ringer's was active at a density of 0.5/microm(2). It was blocked by TEA (IC(50)=1.5 mM). A Ca(2+)-activated non-selective cation channel (NSC-channel) appeared at a mean density of 1/microm(2) in inside-out patches ([Ca(2+)](i)=1.2 mM). gamma was 28 pS (24 degrees C). The NSC showed weak voltage dependence and was blocked by mefenamic acid and by internal ATP. In the cell-attached mode spontaneous activity could be blocked reversibly by 100 nM insulin. Noradrenaline (NA, 100 nM) induced a flickering activity of the NSC-channels. Isoproterenol (100 nM) caused activity of the NSC-channel as well. After 1 microM propranolol even 1 microM NA did not induce any activity. The alpha-antagonist phentolamine had no effect on isoproterenol- or on NA-induced currents. The beta(3)-agonists BRL 37344 and BRL 35135A induced activity of the NSC-channel at 100 nM as well. We conclude that white adipocytes express ion channels which are comparable to those in brown adipocytes and that beta-receptor activation opens NSC-channels thus allowing for Na(+) entry into white adipocytes.

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

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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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Clonidine is an imidazoline derivative antihypertensive medication that is also used as adjunctive therapy for neuropathic pain disorders via topical administration. Clonidine overdose can manifest both central and peripheral alpha-adrenergic agonist effects.

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We report on three cases of fixed drug eruption, including a non-pigmenting generalized bullous fixed drug eruption, caused by mefenamic acid in its pure form.

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1. Sodium transport across isolated frog skin, as measured by the short-circuit current, was decreased by acetylsalicylic acid, mefenamic acid, paracetamol and phenylbutazone. Indomethacin (6 X 10(-6) M) had a biphasic effect on the short-circuit current: a transient increase followed by a sustained decrease. 2. The release of prostaglandin-like material from the skin was reduced by acetylsalicylic acid and indomethacin. Paracetamol caused a significant reduction in the short-circuit current response of the skin to low doses of arachidonic acid, but the response to the highest dose tested was not significantly altered. 3. Indomethacin (6 X 10(-6) M) increased the sensitivity of the skin to applied prostaglandin E1. The other prostaglandin synthetase inhibitors did not have this effect. Indomethacin (6 X 10(-6) M) also enhanced the effect of antidiuretic hormone on the short-circuit current. 4. Indomethacin (30 X 10(-6) M) increased the short-circuit current and diminished the response to applied prostaglandin E1. 5. In sulphate Ringer, theophylline increased the short-circuit current and diminished the response to prostaglandin E1. 6. Prostaglandin E1 increased the levels of cyclic AMP in frog skin and these increases preceded the increases in short-circuit current. There was a seasonal variation in the level of cyclic AMP in the skin: the levels in winter exceeded those in summer. There was also a seasonal variation in the cyclic AMP response to prostaglandin E1: the winter response was greater than that in summer. 7. Indomethacin (6 X 10(-6) M) had a biphasic effect on cyclic AMP levels in the skin, an initial increase followed by a decrease. Indomethacin also potentiated prostaglandin E1 stimulated cyclic AMP accumulation. 8. Theophylline increased cyclic AMP levels in the skin and potentiated prostaglandin E1 stimulated cyclic AMP accumulation. 9. Pre-treatment of the skin with theophylline reversed the effects of cyclic AMP on the short-circuit current and open-circuit potential. 10. It is concluded that endogenous prostaglandins help to maintain sodium transport across isolated frog skin and that the effects of E-type prostaglandins on the short-circuit current are mediated by increased cyclic AMP levels. The transient increase in short-circuit current and the increased skin sensitivity caused by indomethacin (6 X 10(-6) M) are attributed to inhibition of phosphodiesterase activity. The failure of theophylline to potentiate the short-circuit current response of the skin to prostaglandin E1 is attributed to alteration of cyclic AMP action on the skin by theophylline.

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Mice were dosed intraperitoneally with mefenamic acid either as a single dose (100 or 200 mg/kg in 10% Dimethyl sulfoxide/Palm oil) or as single daily doses for 14 days (50 or 100 mg/kg in 10% Dimethyl sulfoxide/Palm oil per day). Venous blood samples from mice during the dosing period were taken prior to and 14 days post-dosing from cardiac puncture into heparinized vials. Plasma blood urea nitrogen (BUN) and creatinine activities were measured.

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The aim of the present study was to establish whether, in terminal arterioles from the rat cremaster, acetylcholine (ACh) elicits nitric oxide (NO)-independent dilation corresponding to the transient ACh-induced endothelium-dependent hyperpolarization described in arteries. For this purpose, the responses of terminal arterioles [mean diam 15.0 +/- 0.4 (SE) microns] were studied by intravital microscopy in rat cremaster muscle. During 15 min of superfusion by 10(-5) M ACh, the response was characterized by an initial maximal dilation (peak time < 3 min) followed by a more sustained dilation that slightly decreased with time. Inhibition of NO synthesis by 2 x 10(-4) M N omega-nitro-L-arginine (L-NNA) significantly reduced, but did not eliminate, both the peak and sustained responses. Simultaneous administration of 2 x 10(-4) M L-NNA and 2 x 10(-5) M mefenamic acid, an inhibitor of prostaglandin synthesis, did not induce a significantly different response from that observed with L-NNA alone. Procaine (10(-3) M), which is known to inhibit completely ACh-induced hyperpolarization in carotid artery, drastically reduced the initial part of the ACh-induced dilation but not the sustained response. Simultaneous administration of procaine and L-NNA almost completely inhibited the peak response to ACh. Similar results were obtained when L-NNA was combined with a superfusion bath containing 20 mM KCl, a concentration known to reduce hyperpolarization in arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

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A 48-year-old woman was hospitalized with the diagnosis of hepatitis. She presented with symptoms of jaundice, headache, elevated bilirubin, and elevated hepatic enzymes. She related a recent episode of a bronchial infection that was treated during the previous eight days with paracetamol (500mg, 2 doses only), chlorpheniramine, betamethasone and clindamycin. After an initial clinical and laboratorial improvement, she began to complain of pruritus of the palms and soles. Thereafter, vesicles evolving to blisters developed and a deterioration of her general health ensued. Serologies for hepatitis A, B, and C viruses were negative. Intrahepatic cholestasis and Stevens Johnson Syndrome (SJS) were the final diagnosis. The association of the Stevens Johnson Syndrome and intrahepatic cholestasis simultaneously, related to adverse drug reactions, is very rare. The drugs reportedly involved are mainly antibiotics, such as ampicillin, vancomycin, amoxicillin/clavulinic acid and erythromycin. Other drugs involved are non-steroidal anti-inflamatory drugs, such as mefenamic acid, ibuprofen, and sulindac. The reactions can be minor or severe and can even cause death, an outcome that has been reported in patients of all races and ethnic groups, but appears to be more rare in patients of Latin origin. We present a discussion of this case and review the main characteristics of the Stevens Johnson Syndrome.

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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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Mefenamic acid is a common widely prescribed drug with analgesic activity. Authors report two cases of multifocal fixed drug eruption induced by mefenamic acid. Cases were diagnosed on basis of clinical examination and histopathology of skin lesion. Only a few cases have been reported in the literature and these are the first two described in Greece.

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The MMAS total scores improved significantly in both groups at all time points, but were significantly greater for the LNG-IUS than for usual treatment [mean difference over 2 years was 13.4 points, 95% confidence interval (CI) 9.9 to 16.9 points; p < 0.001]. However, this difference between groups was reduced and no longer significant by 5 years (mean difference in scores 3.9 points, 95% CI -0.6 to 8.3 points; p = 0.09). By 5 years, only 47% of women had a LNG-IUS in place and 15% were still taking usual medical treatment. Five-year surgery rates were low, at 20%, and were similar, irrespective of initial treatments. There were no significant differences in serious adverse events between groups. Using the EQ-5D, at 2 years, the relative cost-effectiveness of the LNG-IUS compared with usual medical treatment was £1600 per QALY, which by 5 years was reduced to £114 per QALY. Using the SF-6D, usual medical treatment dominates the LNG-IUS. The qualitative findings show that women's experiences and expectations of medical treatments for HMB vary considerably and change over time. Women had high expectations of a prompt effect from medical treatments.

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Single dose of mefenamic acid induced mild alteration of kidney histology mainly mild glomerular necrosis and tubular atrophy. Interestingly, chronic doses induced a dose dependent glomerular necrosis, massive degeneration, inflammation and tubular atrophy. Plasma blood urea nitrogen was statistically elevated in mice treated with mefenamic acid for 14 days similar to plasma creatinine.

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Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase-1 (COX-1) and COX-2 enzymes. The NLRP3 inflammasome is a multi-protein complex responsible for the processing of the proinflammatory cytokine interleukin-1β and is implicated in many inflammatory diseases. Here we show that several clinically approved and widely used NSAIDs of the fenamate class are effective and selective inhibitors of the NLRP3 inflammasome via inhibition of the volume-regulated anion channel in macrophages, independently of COX enzymes. Flufenamic acid and mefenamic acid are efficacious in NLRP3-dependent rodent models of inflammation in air pouch and peritoneum. We also show therapeutic effects of fenamates using a model of amyloid beta induced memory loss and a transgenic mouse model of Alzheimer's disease. These data suggest that fenamate NSAIDs could be repurposed as NLRP3 inflammasome inhibitors and Alzheimer's disease therapeutics.

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The ester prodrug (MA-NH) was prepared by condensing mefenamic acid with N-hydroxymethylsuccinimide in the presence of Phosphorus oxychloride. The pharmacokinetic profile, including stability and release of mefenamic acid and N-hydroxymethylsuccinimide from the ester prodrug (MA-NH) was studied by RP- HPLC in acidic medium (pH 1.2), basic medium (pH 7.4), 80 % v/v human plasma, 10 % w/v rat intestinal homogenate and 10 % w/v rat liver homogenate (pH 7.4).

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ponstel generic cost 2016-07-11

A 17-year-old schoolboy was admitted to hospital because of one-sided pelvic pain of uncertain aetiology and fever gradually rising over several days. Bacteriological analysis of blood cultures, skeletal scintigraphy and computed tomography revealed sacroiliitis caused by Salmonella cholerae-suis. Specific antibiotic treatment quickly stopped buy ponstel online all symptoms and cured the infection. Radiologically there remained sclerosis of the sacro-iliac joint.

ponstel dosage instructions 2016-03-25

Pharmaceutical substances have been detected in sewage effluents as well as receiving waters in many parts of the world. In this study, the occurrence and removal of a number of drug compounds were studied within a large sewage treatment plant in the south of England. Samples were buy ponstel online processed using solid phase extraction and analysed using gas chromatography-mass spectrometry (GC-MS). The results demonstrate that ibuprofen, paracetamol, salbutamol and mefenamic acid were present in both the influent and effluent of the works while propranolol-HCl was not found above the limit of quantification in any sample. Elimination rates were circa 90% for each compound but several hundred nanograms per litre were still present in the final effluent.

ponstel dosage 2017-10-18

In vivo assays were conducted for the first time in order to assess the LDH-Mef potential. The hemolytic effects decreased for the intercalated Mef as demonstrated by the higher tolerated hemolytic concentration (1.83 mM) compared to mefenamic acid (MefH), 0.48 mM. Pretreatment of animals with MefH or LDH-Mef reduced carrageenan-, dextran sulfate- and PGE2-induced buy ponstel online paw edema. MefH or LDH-Mef also decrease total leucocytes and neutrophil counts of the peritoneal cavity after inflammation induction with carrageenan. In the nociception model, oral pretreatment with LDH-Mef reduced mechanical hypernociception carrageenan-induced after 3-4h and also the number of writhings induced by acetic acid.

ponstel medication dosage 2015-09-23

To reduce costly late-stage compound attrition, there has been an increased focus on assessing compounds in in vitro assays that predict attributes of human safety liabilities, before preclinical in vivo studies are done. Relevant questions when choosing a panel of assays for predicting toxicity are (a) whether there is general concordance in the data among the assays, and (b) whether, in a retrospective analysis, the rank order of toxicity of compounds in the assays correlates with the known safety profile of the drugs in humans. The aim of our study was to answer these questions using nonsteroidal anti-inflammatory drugs (NSAIDs) as a test set since NSAIDs are generally associated with gastrointestinal injury, hepatotoxicity, and/or cardiovascular risk, with mitochondrial impairment and endoplasmic reticulum stress being possible contributing factors. Eleven NSAIDs, flufenamic acid, tolfenamic acid, mefenamic acid, diclofenac, meloxicam, sudoxicam, piroxicam, diflunisal, acetylsalicylic acid, nimesulide, and sulindac (and its two metabolites, sulindac sulfide and sulindac sulfone), were tested for their effects on (a) the respiration of rat liver mitochondria, (b) a panel of mechanistic endpoints in rat hepatocytes, and (c) the viability and organ morphology of zebrafish. We show good concordance for distinguishing among/between NSAID buy ponstel online chemical classes in the observations among the three approaches. Furthermore, the assays were complementary and able to correctly identify "toxic" and "non-toxic" drugs in accordance with their human safety profile, with emphasis on hepatic and gastrointestinal safety. We recommend implementing our multi-assay approach in the drug discovery process to reduce compound attrition.

ponstel syrup children 2017-06-13

Neonatal lupus is a unique clinical entity characterized primarily by cutaneous or cardiac injury. Dermatitis usually resolves without significant residual effects but heart block may be irreversible and life threatening during the neonatal period. SS-A/Ro and/or SS-B/La antibodies of maternal origin are present in the serum of the mother and affected infant and are markers for this syndrome. For many mothers breast feeding is the preferred choice for infant nutrition. With proper guidance, lactating mothers may safely use several antirheumatic medications such as ibuprofen, piroxicam, flurbiprofen, diclofenac, mefenamic acid, prednisone, sulfasalazine, and methotrexate buy ponstel online .

ponstel capsule 2016-03-01

The effect of a TEI enhancer mixed system consisting of triethanolamine (T), ethanol (E) and isopropyl myristate (IPM) on the skin permeation of acidic, basic and neutral drugs were evaluated in vitro using excised hairless rat skin. The binary enhancer system consisting of IPM and ethanol (El) produced marked improvement on the penetration of all the drugs tested. When T was added to the EI system, buy ponstel online a greater enhancing effect was found only on acidic drugs with a carboxyl group, compared with the flux in the EI system. On addition of another amine to the EI system, instead of T, mefenamic acid (MA), which exhibited the highest enhancing effect of the model drugs, showed an approximately 14-180 times greater flux than when delivered by the EI system. On simultaneous application of isosorbide dinitrate (ISDN) with MA in the TEI system, the flux of MA increased on increasing the T concentration in the TEI system, while, the flux of ISDN, a neutral drug, was unaffected by the T concentration. Application of MA in the EI system after pretreatment of the TEI system showed that the residual amount of T in the skin plays an important role in the skin permeation of MA. Furthermore, at a fixed concentration of MA, the flux of MA increased on increasing the T concentration in the TEI system, while the flux of E remained unchanged. Finally, the infrared spectrum of MA with amine in the E solution indicated that the carboxyl group of MA was ionized. These results demonstrated that the formation of an ion pair between MA and T, but not the effect of T on the skin, may be responsible for the enhanced skin permeation of MA using the TEI system.

ponstel 250 tablets 2017-02-16

We studied in vivo interactions of nitric oxide (NO), oxidative stress, and prostanoids derived from the cyclooxygenase pathway in the arterioles studied by intravital microscopy in peripheral muscle. Topical administration of NO synthase (NOS) inhibitor Nomega-nitro-l-arginine (l-NNA) or cyclooxygenase inhibitor mefenamic acid (MA) alone leads to vasoconstriction. We found that l-NNA after MA induced an additional constriction, whereas MA after l-NNA induced a relative dilation. Therefore, an additional constriction was found when MA was administered after l-NNA in the presence of the thromboxane A2 synthase-PGH2 (TP) receptor antagonist SQ-29548. We also found a relative dilation when the TP receptor antagonist was administered after NOS inhibition by l-NNA. In the presence of superoxide dismutase and catalase, l-NNA-induced vasoconstriction is reduced, and buy ponstel online the dilation observed after addition of MA in presence of the reactive oxygen species is no longer present. Taken together, these results showed that NO inhibition induced a shift in the synthesis or in the effects of cyclooxygenase products, in favor of constrictor prostanoids. This effect of NO inhibition disappears when reactive oxygen species are scavenged by superoxide dismutase and catalase.

ponstel dosing 2017-10-20

Two simple, accurate, economical and reproducible spectrophotometric methods for simultaneous estimation of two-component drug mixture of ethamsylate and mefenamic acid in combined tablet dosage form have been developed. The first developed method involves formation and solving of simultaneous equation using 287.6 nm and 313.2 nm as two wavelengths. Second developed method is based on two wavelength buy ponstel online calculation. Two wavelengths selected for estimation of ethamsylate were 274.4 nm and 301.2 nm while that for mefenamic acid were 304.8 nm and 320.4 nm. Both the developed methods obey Beer's law in the concentration ranges employed for the respective methods. The results of analysis were validated statistically and by recovery studies.

ponstel pills 2017-06-06

Baseline characteristics and buy ponstel online biochemical parameters were comparable and homogenous among all groups (P>0.05). The percentage reduction in lower abdominal pain was 66.89%, 66.49%, and 62.88% in A, B and C groups respectively at the end of the treatment. No adverse drug effects were noticed.

ponstel drug interactions 2017-01-17

Pradigastat, a novel diacylglycerol acyltransferase-1 inhibitor, has activity in common metabolic diseases associated with abnormal accumulation of triglycerides. In vitro studies suggest that glucuronidation is the predominant metabolism pathway for elimination of pradigastat in humans and confirmed the role of uridine 5'-diphosphoglucuronosyltransferase (UGT) enzymes, UGT1A1, -1A3, and -2B7. The in vitro studies using atazanavir as a selective inhibitor of UGT1A1 and -1A3 indicated that these enzymes contribute ∼55% toward the overall glucuronidation pathway. Therefore, a clinical study was conducted to assess the potential for drug interaction between pradigastat and probenecid (purported general UGT inhibitor) or atazanavir (selective UGT1A1, -1A3 inhibitor). The study included 2 parallel cohorts, each with 3 sequential treatment periods and 22 healthy subjects per cohort. The 90%CI of the geometric mean ratios for Cmax,ss and AUCτ,ss of pradigastat were within 0.80-1.25 when administered in combination with probenecid. However, the Cmax,ss and AUCτ,ss of pradigastat decreased by 31% (90%CI: 0.62-0.78) and 26% (0.67-0.82), respectively, when administered in combination with atazanavir. This magnitude of decrease in pradigastat steady-state exposure is not considered clinically relevant. Pradigastat buy ponstel online was well tolerated by all subjects, either alone or in combination with atazanavir or probenecid.

ponstel drug 2017-04-25

We present the case of a 71-year old man with acute eosinophilic pneumonia. By buy ponstel online ruling out other common etiologies and by a positive lymphocyte transformation test the non-steroidal anti-inflammatory drug mefenamic acid was identified as the possible causative agent or this potentially life threatening lung disease. The clinical presentation, diagnosis, and treatment of acute eosinophilic pneumonia as a pulmonary manifestation of a drug-induced allergic reaction are discussed.

ponstel 250 reviews 2015-12-12

Equine ChE and rat brain homogenate were incubated with NSAIDs and horseradish peroxidase (HRP) and H(2)O(2) (HRP-H(2)O(2)). ChE activity was measured by using 5,5'- buy ponstel online dithiobis(nitrobenzoic acid). By using electron spin resonance, NSAID radicals induced by reaction with HRP-H(2)O(2) were detected in the presence of spin trap agents.

ponstel drug interaction 2017-09-07

The purpose of this study was to assess if the definition of high solubility as proposed in the FDA Guidance on Biopharmaceutical Classification System (BCS) is too strict for buy ponstel online highly permeable acidic drugs.

ponstel syrup 2017-02-16

2-Substituted derivatives of 5H-benzothieno [3,2-d] [1,3,4]-thiadiazolo [3,2-a]pyrimidin-5-one and of 10H-benzothieno [2,3-d] [1,3,4]-thiadiazolo [3,2-a]pyrimidin-10-one Nexium Generic Name have been synthesized. The analgesic, antiinflammatory and ulcerogenic activities of these derivatives were evaluated. Some derivatives showed an analgesic activity similar to or a little lower than that of indomethacin, and much higher than that of mefenamic acid, acetylsalicyclic acid and phenylbutazone, with a lower acute toxicity and a better gastric tolerance.

ponstel generic 2015-04-25

Alzheimer's disease (AD) is a complex neurological disorder with multiple inter-connected factors playing roles in the onset and progression of the disease. One strategy currently being explored for the development of new therapeutics for AD involves linking tacrine, a known acetylcholinesterase (AChE) inhibitor, to another drug to create bifunctional hybrids. The role and influence on activity of the linker moiety in these hybrids remains ill-defined. In this study, three series of 6-chlorotacrine with linkers varying in terminal functional group and length were Paracetamol 650 Mg synthesized, evaluated for AChE inhibition, and compared to tacrine and 6-chlorotacrine-mefenamic acid hybrids. Out of the compounds with terminal amine, methyl, and hydroxyl moieties tested, several highly potent molecules (low nanomolar IC50 values) comprised of linkers with terminal amines were identified. These 6-chlorotacrine with linkers were significantly more potent than tacrine alone and were often more potent than similar 6-chlorotacrine-mefenamic acid hybrids.

buy ponstel online 2016-02-09

The in vitro release of endogenous and exogenous PgF2 alpha from plasma and serum proteins by aspirin and other analgesic drugs has been studied by RIA and equilibrium-dialysis techniques, respectively. Before aspirin addition, the mean plasma level of PgF2 alpha measured by RIA was significantly lower in aspirin-sensitive asthma (ASA) patients (11.3 +/- 6.5 pg/ml; n = 8) than in aspirin-tolerant asthma (ATA) patients (25.0 +/- 11.4 pg/ml; n = 21). After aspirin addition (50 micrograms/ml) the mean PgF2 alpha level detected in plasma by RIA was higher in ASA patients (97.6 +/- 5.5 pg/ml) than in ATA patients (66.9 +/- 4.5). Imodium Max Dosage The binding of [3H]PgF2 alpha to serum protein was significantly inhibited by NSAIDs but not by paracetamol (0.2-1.0 mM). These results implicate PgF2 alpha and the protein-binding property of analgesic drugs in the pathogenesis of aspirin-sensitive asthma.

ponstel dosage dysmenorrhea 2016-11-22

This study, as a double-blind clinical trial, was conducted on 64 infertile women undergoing hysterosalpingography, who referred Botox Cost Dallas to radiology ward at Comprehensive Women's hospital. To measure anxiety, visual analog anxiety scale was used 90 minutes before starting procedure, individuals in intervention group (n=32) received a single dose (1,500 mg) of 3 Valeric capsules, together with routine prophylaxy, where routine prophylaxis contains Mefenamic acid 250mg capsules in 30 minutes before procedure, and the same capsules were prescribed to placebo group (n=32) with the same instruction. Anxiety severity before and once 90 minutes after intervention in both groups were measured and compared.

ponstel medication 2015-04-25

Genetic and physiological studies have established a link between potassium channel dysfunction and a number of neurological and muscular disorders. Many 'channelopathies' are accounted for by a dominant-lethal suppression of potassium channel function. In the cardiac I(KS) channel complex comprising the alpha and beta subunits, KvLQT1 and IsK, respectively, several mutations lead to a dominant-negative loss of channel function. These defects are responsible for a human cardiovascular disease called long QT (LQT) syndrome. Here we show that binding of I(KS) channel activators, such as stilbenes and fenamates, to an extracellular domain flanking the Luvox 100mg Tablets human IsK transmembrane segment, restores normal I(KS) channel gating in otherwise inactive IsK C-terminal mutants, including the naturally occurring LQT5 mutant, D76N. Our data support a model in which allosteric interactions exist between the extracellular and intracellular boundaries of the IsK transmembrane segment as well as between domains of the alpha and beta subunits. Disruption of this allosteric interplay impedes slow activation gating, decreases current amplitude and restores channel inactivation. Owing to allosteric interactions, stilbene and fenamate compounds can rescue the dominant-negative suppression of I(KS) produced by IsK mutations and thus, may have important therapeutic relevance for LQT syndrome.

ponstel tablets 2017-03-30

The aim of this double-blind, placebo-controlled study was to evaluate the effect of mefenamic acid and placebo on controlling irregular uterine bleeding secondary to Norplant use. A total of 67 Norplant users attending the Family Planning Clinic of Chulalongkorn Hospital all had irregular bleeding. These women were randomly allocated into two groups. A total 34 users received mefenamic acid, 500 mg twice a day for 5 days, and placebos were given to the other 33 in the same manner. The total days of bleeding and spotting Buy Cytoxan Cyclophosphamide and the percentage of women in whom bleeding was stopped were analyzed in weeks 1 and 4. The percentage of subjects in whom bleeding was stopped during week 1 after initial treatment was significantly higher in the mefenamic acid group than the placebo group (76%, 27%; p < 0.001). In the follow-up period (4 weeks after initial treatment), a bleeding-free interval of > 20 days was found in 68% of the subjects treated with mefenamic acid and 33% treated with the placebo; the mean number of bleeding/spotting days was lower with mefenamic acid treatment (11.6 and 17.2 days; p < 0.05). The difference was statistically significant. It is concluded that mefenamic acid was more effective than placebo in short-term control of irregular bleeding and spotting associated with Norplant use.

ponstel 250 mg 2017-01-31

Renal papillary necrosis (RPN) is a significant problem in human beings, especially in England and in Australia where it has been reported to account for 15% to 20% of patients needing renal transplants. Many compounds, including aspirin, phenacetin, phenylbutazone, indomethacin, mefenamic acid, flufenamic acid, fenoprofin, naproxen, and ibuprofen have been linked to renal papillary necrosis in human beings. Although the exact mechanism of RPN is unknown, there are several theories that have good scientific evidence behind them. Study of RPN in animals as models for the disease in human beings Motilium Tablets Uses is limited by several factors, including anatomical differences between human beings and most animal species as well as technical difficulties in studying the renal papilla.

ponstel generic price 2017-08-13

The fates of anti-inflammatory drugs (e.g., ibuprofen, naproxen, mefenamic acid and ketoprofen), which are frequently detected in the discharges of wastewater treatment plants (WWTPs) and river water in Japan, were clarified in two WWTPs. The concentrations of ibuprofen, naproxen, mefenamic acid and ketoprofen were 69-1080, 179-305, 143-1580 and 160-1060 ng/L in the influent, and N.D. (< 40 ng/L), 74-166, 72-265, 64-107 ng/L in Buspar Drug Interactions the effluent, respectively. The concentrations of the anti-inflammatory drugs analyzed were almost equal to or lower than those reported in foreign countries. High removal efficiencies of the drugs, except ibuprofen, were observed in the WWTP that has longer hydraulic retention time than that of the other WWTP. For ibuprofen, high removal efficiencies were observed in both WWTPs (84 to 98%). Disinfection by chlorination was not effective to remove the drugs surveyed. On the other hand, the effective removal of ketoprofen by ultraviolet (UV) radiation for disinfection was demonstrated, although the disinfection by-products were not identified.

ponstel dose 2016-10-14

Emulgels have emerged as a promising drug delivery system for the delivery of hydrophobic drugs. The objective of the study was to prepare emulgel of mefenamic acid, a NSAID, using Carbapol 940 as a gelling agent. Mentha oil and clove oil were used as penetration enhancers. The emulsion was prepared and it was incorporated in gel base. The formulations were evaluated for rheological studies, spreading coefficient studies, bioadhesion strength, skin irritation studies, in vitro release, ex vivo release studies, anti-inflammatory activity and analgesic activity. Formulation F2 and F4 showed comparable analgesic and anti-inflammatory activity when they Inderal Pill compared with marketed diclofenac sodium gel. So, it can be concluded that topical emulgel of mefenamic acid posses an effective anti-inflammatory and analgesic activity.

ponstel buy 2015-09-17

The effects of the nonsteroidal anti-inflammatory drugs (NSAIDs) acetylsalicylic acid, metamizole, phenylbutazone, indometacin, piroxicam, naproxen, tolmetin, diclofenac, and mefenamic acid on methacholine (10 mumol/l), prostaglandin F2 alpha (1 mumol/l), and KCl (60 mmol/l) induced contractions of isolated rat uterus were assayed. All of these cause a concentration-dependent inhibition of methacholine and prostaglandin F2 Celebrex 300 Mg alpha-induced contractions with the exception of acetylsalicylic acid, metamizole, and naproxen. All except acetylsalicylic acid and metamizole relaxed in a concentration-dependent manner the tonic contractions induced by KCl. CaCl2 (0.1-10 mmol/l) totally counteracted the relaxant effects of naproxen and tolmetin, but not those of the other NSAIDs. Bay K8644 did not revert the effect of the NSAIDs. Pertussis toxin (50 micrograms/l) did not modify the effect of indometacin, mefenamic acid, and tolmetin, but partially antagonized the effects of diclofenac and naproxen and increased the effect of phenylbutazone and piroxicam. These results suggest that some of the NSAIDs assayed induce smooth muscle relaxation by mechanisms independent of prostaglandin synthesis inhibition, but related to the inhibition of extracellular calcium influx through mechanisms related or unrelated to pertussis toxin sensible G proteins.

ponstel capsules 2017-10-06

No statistically significant difference in the effectiveness of ibuprofen compared to indomethacin in closing a PDA was found. Ibuprofen compared with indomethacin reduces the risk of oliguria and is associated with lower serum creatinine levels following treatment. Pulmonary hypertension has been observed in three infants after prophylactic use of ibuprofen and one infant receiving ibuprofen for treatment in this review developed pulmonary hypertension. One additional case of pulmonary hypertension following treatment with ibuprofen to close a PDA was identified from the literature. The available data support the use of either drug for the treatment of a PDA. As both drugs are equally effective in closing a PDA, the clinician needs to weigh the potential side effects of one drug vs. the Vermox Single Dose other when making a decision which drug to use. The most urgent research question to be answered is whether ibuprofen compared to indomethacin confers an improved rate of intact survival (survival without impairment) at 18 months corrected age and at the age of school entry.

ponstel pill 2017-03-07

Gastric infection with Helicobacter pylori was excluded in all patients. Of the 16 patients on NSAIDs, four had gastritis, four had erosions or ulceration and eight had a normal examination. Endoscopy was normal in all patients in the control group. The LI% (mean +/- S.E.M.) in the entire NSAID group was 4.09 +/- 0.29 and in the control group 3.57 +/- 0.29. No significant difference was observed. In the NSAID patients with gastritis and erosions or ulceration, the LI% was 4.99 +/- 0.61 and 3.07 +/- 0.32, respectively. There was no significant difference in LI% between the endoscopic subgroups of patients on NSAIDs or between patients on NSAIDs who had normal endoscopy and the control patients.

ponstel s medicine 2015-10-10

Microspheres were formed when a solution of cellulose phthalate was extruded into 30% glacial acetic acid solution. Sulphonamides entrapped in such microspheres leached into the hardening solution because they dissolved freely in the acetic acid solution. This resulted in poor loading efficiency of the sulphonamides in the microspheres. When mixtures of sulphaguanidine and sulphathiazole in various drug ratios were microencapsulated by this method, the observed drug ratios were found to be markedly changed. This was attributed to the difference in solubility of the two sulphonamides in acid such that their extent of diffusion into the hardening solution was not similar. NSAIDS such as ibuprofen and mefenamic acid which are acidic and more hydrophobic in nature are less soluble in acetic acid. These drugs were retained better in the microspheres during the hardening process and the loading efficiency was consequently improved. In cases where mixture of the NSAIDS were encapsulated, the drug ratios showed little deviation from the theoretical values. This study shows that loading of the CAP microspheres is dependent on the solubility of the drugs in acetic acid. When more than one drug is required to be microencapsulated, the drug ratio may change if the drugs have different solubility in acetic acid.

ponstel 250mg capsules 2015-08-17

Diphenylamine is a common structure of nonsteroidal anti-inflammatory drugs (NSAIDs) to uncouple mitochondrial oxidative phosphorylation and to cause a decrease in hepatocellular ATP content and hepatocyte injury. The mechanism for acute cell injury induced by diphenylamine and its structurally related NSAIDs was investigated with rat liver mitochondria and freshly isolated hepatocytes, focusing on the relation to the uncoupling of oxidative phosphorylation. Incubation of mitochondria with diphenylamine as well as mefenamic acid and diclofenac caused pseudoenergetic mitochondrial swelling, indicating that these compounds induce mitochondrial membrane permeability transition. Diphenylamine also caused changes in safranine-binding spectra to mitochondria that was energized by succinate oxidation. This spectral shift indicates the loss of mitochondrial membrane potentials, which is known as one of the characteristics for uncouplers of oxidative phosphorylation, and also was caused by mefenamic acid and diclofenac. Incubation of hepatocytes with mefenamic acid, diclofenac, and diphenylamine diminished cellular ATP content, followed by leakage of lactose dehydrogenase from hepatocytes. Fructose, a low K(m) substrate for glycolysis, partially protected against the ATP depletion and hepatocyte injury induced by these compounds. Further addition of oligomycin, which blocks ATPase, pronounced the protection against cell injury. These results suggested that decreases in cellular ATP content, mainly caused by uncoupling of mitochondrial oxidative phosphorylation, were responsible for acute hepatocyte injury induced by diphenylamine and structurally related NSAIDs.

ponstel medicine 2017-05-20

Recorded daily doses for drugs within the 'Anti-rheumatics, non-steroidal plain' anatomical classification were studied. First prescriptions of a distinct NSAID substance within 13-month time periods in a patient's history were included. To enable grouping and comparison of NSAIDs, doses were analysed as prescribed daily doses (PDDs) relative to the adult defined daily dose, stated as the relative PDD (rPDD) in this study. Multiple regression analysis was performed with the rPDD as the response variable, and age, indication, dosage form, NSAID substance and year of prescription as the explanatory variables.

ponstel medication cost 2016-05-21

The current work investigates the application of low intensity ultrasonic irradiation for improving the cooling crystallization of Mefenamic Acid for the first time. The crystal shape and size has been analyzed with the help of optical microscope and image analysis software respectively. The effect of ultrasonic irradiation on crystal size, particle size distribution (PSD) and yield has been investigated, also establishing the comparison with conventional approach. It has been observed that application of ultrasound not only enhances the yield but also reduces the induction time for crystallization as compared to conventional cooling crystallization technique. In the presence of ultrasound, the maximum yield was obtained at optimum conditions of power dissipation of 30W and ultrasonic irradiation time of 10min. The yield was further improved by application of ultrasound in cycles where the formed crystals are allowed to grow in the absence of ultrasonic irradiation. It was also observed that the desired crystal morphology was obtained for the ultrasound assisted crystallization. The conventionally obtained needle shaped crystals transformed into plate shaped crystals for the ultrasound assisted crystallization. The particle size distribution was analyzed using statistical means on the basis of skewness and kurtosis values. It was observed that the skewness and excess kurtosis value for ultrasound assisted crystallization was significantly lower as compared to the conventional approach. XRD analysis also revealed better crystal properties for the processed mefenamic acid using ultrasound assisted approach. The overall process intensification benefits of mefenamic acid crystallization using the ultrasound assisted approach were reduced particle size, increase in the yield and uniform PSD coupled with desired morphology.