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Non-steroidal anti-inflammatory drugs (NSAIDs) are the most commonly used analgesics and antipyretics, which form an interesting drug group because of their new and alternate functions. The ability of the NSAIDs belonging to the oxicam chemical group to induce membrane fusion at low physiologically relevant concentrations is a new function that has drawn considerable attention. Membrane fusion is dependent on the interplay of physicochemical properties of both drugs and membranes. Here, we have elucidated the effects of different oxicam drugs, Meloxicam, Piroxicam, Tenoxicam, Lornoxicam, and Isoxicam, on an identical membrane-mimetic system. This highlights only the differential effects of the drugs on drug-membrane interactions, which in turn modulate their role as membrane fusogens. The partitioning behavior and the location of the drugs in dimyristoylphosphatidylcholine vesicles have been studied using second-derivative absorption spectroscopy, fluorescence quenching, steady-state fluorescence anisotropy, and time-resolved fluorescence lifetime measurements. Fusion kinetics has been monitored by fluorescence assays and dynamic light scattering was used to provide a snapshot of the vesicle diameter distribution at different time points. The differential perturbing effect of the drugs on the membrane is dependent both on their partitioning and location. Although partitioning governs the extent of fusion, the location modulates the rates of each step.
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Intraperitoneal tenoxicam inhibited the formation of postoperative intra-abdominal adhesions without compromising wound healing in this bacterial peritonitis rat model. Tenoxicam also decreased the oxidative stress during peritonitis.
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In the present study we investigated the influence of several nonsteroidal anti-inflammatory drugs on calcium efflux in isolated rat renal cortex mitochondria in order to assess their potential to disrupt cell calcium homeostasis, as well as aspects of the mechanisms associated with oxidation of mitochondrial pyridine nucleotides (NAD(P)H) and with inhibition of the process by cyclosporin A (CsA). Calcium efflux was estimated with arsenazo III as an indicator and the redox state of NAD(P)H was monitored fluorimetrically at the 366/450 nm excitation/emission wavelength pair. Dipyrone, paracetamol and ibuprofen did not induce calcium efflux even at 1 mM, piroxicam and salicylate were poor inducers, while diclofenac sodium and mefenamic acid were potent inducers releasing calcium even at 20 microM and 10 microM, respectively. In the presence of 10 microM calcium, CsA had no appreciable effect while in the presence of 30 microM calcium it delayed calcium efflux. Oxidation of mitochondrial NAD(P)H, concomitant with calcium efflux and inhibited by CsA, was observed only in the presence of 30 microM calcium. The results suggest that diclofenac sodium and mefenamic acid induce calcium efflux in mitochondria through both a mechanism intrinsic to the mitochondrial membrane permeability transition and a mechanism including the electroneutral Ca2+/nH+ porter.
We hypothesized that the addition of toceranib to metronomic cyclophosphamide/piroxicam therapy would significantly improve disease-free interval (DFI) and overall survival (OS) in dogs with appendicular osteosarcoma (OSA) following amputation and carboplatin chemotherapy.
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Current knowledge on side-effects of non-steroidal anti-inflammatory drugs (NSAIDs) is reviewed. These occur most commonly in the gastro intestinal tract and include peptic ulceration and haemorrhage as well as effects on the small and large bowel. Renal effects with many manifestations are also increasingly described. Photosensitivity is the most common adverse dermatological effect. The role of various NSAIDs in causing asthma is now well recognised. Many less common side-effects occur, the most significant of which is marrow aplasia. Phenylbutazone and indomethacin are rarely but definitely associated with this, but other NSAIDs including ibuprofen are also suspected, but unproven, causes. A strategy for minimising side-effects is outlined. Where there is not a strong indication for use of an NSAID, local physical measures or a pure analgesic can be substituted. If an NSAID is really necessary, it is best to commence with a drug of lesser potency in the first instance, unless the patient is suffering from a severe inflammatory disorder. Indomethacin and piroxicam should be reserved for when other NSAIDs have not been effective. Patients who have a past or present history of peptic ulceration but still need to continue their NSAID therapy, should combine it with an anti-ulcer drug. In the case of younger patients a H2 receptor antagonist is the drug of first choice, whereas in the older patient a mucosal protective agent such as sucralfate is preferred. In the event of ulcer relapse, combination with a prostaglandin analogue is the next step. The growing awareness of side-effects with NSAIDs suggests that monitoring of patients commencing NSAIDs and on long-term treatment, should be increasingly practiced.
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The interaction of tenoxicam with six metal ions, viz. Fe(III), Bi(III), Sb(III), Cr(III), Cd(II) and Al(III) was studied using potentiometric and fluorimetric methods. In the potentiometric method the ionization constant of the ligand and stability constants of the complexes formed have been tabulated at 25+/-0.1 degrees C, ionic strength of NaNO3 in 50% (v/v) aqueous acetonitrile solution was 0.05 mol x dm(-3). Complexes of 1:1 and/or 1:2 and/or 1:3 metal to ligand ratios are formed. The fluorescence of tenoxicam in the presence and absence of the metal ions was studied. The drug can be determined fluorimetrically in 0.5 M HNO3 at an emission wavelength of 450 nm (excitation at 350 nm). The linear range is 0.040-0.2 microg/ml in the absence of Al(III) and 0.016-0.1 microg/ml in the presence of Al(III). Tenoxicam was determined by the proposed method in tablet, suppository and injection. The recovery percent ranged from 98.16 to 102.22%. The effect of 2-aminopyridine on the recovery of tenoxicam was also investigated.
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Inhibition of cyclooxygenase-2 (COX-2) represents a possible avenue for the prevention and/or treatment of some cancers. Our goal was to compare the effect of a selective inhibitor of COX-2, deracoxib, and a COX-1 and -2 inhibitor, piroxicam, on the growth of canine mammary tumours in a murine model. CMT-9 was used to induce xenografts in nude mice. Mice were treated with piroxicam (0.6 mg kg(-1)), deracoxib (6 mg kg(-1)) or a control solution. Tumour volumes between 0 and 24 days post-treatment showed no significant difference between all groups. A second series of experiments was performed with a higher dose of piroxicam (0.9 mg kg(-1)). Tumour volumes between 14 and 21 days post-treatment were significantly smaller in piroxicam-treated mice compared with controls. These results demonstrate that COX inhibition reduced the growth of canine mammary cancer xenografts in mice, suggesting that COX inhibitors could have a positive effect in dogs.
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The doctors questioned chose a limited number of NSAIDs. Major preferences were diclofenac and piroxicam. The main criteria for selection were: efficacy and safety of the drug; previous and/or current gastrointestinal pathology of the patient; the difference between acute and chronic use; and the type of inflammatory process. There were a large number of combinations of routes of administration. The histamine H2 antagonists were the prophylactic drugs which were used most for gastropathy.
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The sequential action of phospholipase A(2) and cyclooxygenase leads to the production of prostaglandins in the brain, an event hypothesised to cause dopaminergic stimulation. To investigate this further, we examined the effect of the nonselective cyclooxygenase inhibitors indomethacin and piroxicam on several indices of dopaminergic function in adult male rats. Both drugs inhibited catalepsy induced by the dopamine D1-like receptor antagonist R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine (SCH23390), the dopamine D2-like receptor antagonist raclopride and by haloperidol, findings in agreement with a dopaminergic effect of cyclooxygenase inhibitors. However, neither cyclooxygenase inhibitor had an effect upon disruption of prepulse inhibition of the auditory startle reflex by amphetamine or on the rate of amphetamine self-administration. Both drugs reduced amphetamine-stimulated locomotor activity. Our data indicate that the mechanism by which cyclooxygenase inhibitors alter motor behaviour is unlikely to be due to a simple direct action at the dopaminergic synapse. Their apparent ability to antagonise hypoactivity without generalised dopaminergic stimulation suggests that other, possibly multiple, neurotransmitter systems may be involved.
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A strong reduction of fibroblasts from nasal polyps in vitro is possible with usual rhinological medicaments but also with unusual substances in this field.
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Administration of Cc significantly reduced gastric lesions induced by different ulcerogenic agents in rodents. This extract administered by oral route significantly increased gastric volume without exerting antisecretory effect. The Cc effect involved an increase of the defense mechanism of the gastrointestinal mucosa such as NO and SH groups that prevent and attenuate the ulcer process. The Cc also has antioxidant property against oxidative stress but does not modify microcirculation response in gastric mucosa.
To develop an efficient topical delivery system for piroxicam using poloxamer gel formulation, physicochemical behavior of piroxicam in poloxamer was studied. The gelling property of poloxamer and the solubility of piroxicam in the poloxamer were investigated. The interaction between piroxicam and poloxamer was studied by x-ray diffractometry (XRD), infrared (IR) spectroscopy and differential thermal analysis (DTA) with a solid dispersion, coprecipitate, or physical mixture. Poloxamer 407 solutions showed the property of a gel when the concentration was higher than 15% (w/w) and poloxamer 407 increased the aqueous solubility of piroxicam by about 11-fold at the concentration of 22.5% (w/w). The results of XRD did not show the crystalline from of piroxicam in the solid dispersion and results of IR spectroscopic analysis showed an association between functional groups of piroxicam and poloxamer.
Two cases of photosensitivity to the nonsteroidal anti-inflammatory agent piroxicam are described. The action spectrum appears to be in the ultraviolet A (UVA) range (320 to 400 nm). Hallmarks of the photosensitivity reaction include an acute eczematous dermatitis with frank vesicle formation clinically and spongiosis and a perivascular mononuclear cell infiltrate histologically. Piroxicam and other nonsteroidal anti-inflammatory drugs are capable of inducing cutaneous photosensitivity.
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Retrospective study of 30 dogs diagnosed with osteosarcoma. All dogs underwent amputation and chemotherapy treatment with one of the two maximal-tolerated dose protocols. Metronomic chemotherapy was administered in conjunction with these protocols, and continued subsequently. The protocols included 0 · 3 mg/kg piroxicam and 10 to 12 mg/M(2) cyclophosphamide with 300 mg/M(2) carboplatin alone, or 300 mg/M(2) carboplatin alternating with 30 mg/M(2) doxorubicin.
Transdermal patches of meloxicam (MX) and lornoxicam (LX) were aimed to be prepared in order to overcome their side effects by oral application. The strategy was formulation of optimized films to prepare transdermal patches by determination of physical properties and investigation of drug-excipient compatibility. As the next step, in vitro drug release, assesment of anti-inflammatory effect on Wistar Albino rats, ex vivo skin penetration and investigation of factors on drug release from transdermal patches were studied. Hydroxypropyl methylcellulose (HPMC) was concluded to be suitable polymer for formulation of MX and LX transdermal films indicating pharmaceutical quality required. MX and LX transdermal patches gave satisfactory results regarding to the edema inhibition in the assessment of anti-inflammatory effect. MX was found out to be more effective compared to LX on relieving of edema and swelling. These results were supported by data obtained from ex vivo penetration experiments of drug through rat skin. Indicative parameters like log P, molecular weight and solubility constraint on penetration rate of drugs also indicated good skin penetration. Transdermal patches of MX and LX can be suggested to be used especially for the immediate treatment of inflammated area since it displays anti-inflammatory effect, soon.
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Administrative data of patients 50 years or older who received a non-steroidal anti-inflammatory drug or acetaminophen prescription between 1998 and 2004 were used.
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A three-month, double-blind, indomethacin-controlled, European multicenter study of isoxicam (Maxicam), a nonsteroidal anti-inflammatory drug, was conducted in 365 patients who had degenerative joint disease of the knee or hip. Patients were randomly assigned to receive one of two treatments: isoxicam, 133 mg per day (Week 1), 166 mg per day (Week 2), and 200 mg per day (Weeks 3 to 12); or indomethacin, 100 mg per day (Week 1), 125 mg per day (Week 2), and 150 mg per day (Weeks 3 to 12). Efficacy measurements included, for patients with knee or hip involvement, intensity of starting pain on motion, pain on walking, night pain, overall assessment by physician and patient, and global assessment at the end of treatment; maximal extension and flexion (knee); extent of pain-free abduction and maximal abduction (hip). The results of the efficacy measurements favor isoxicam over indomethacin, although the differences are not statistically significant. The isoxicam group had significantly fewer adverse reactions than the indomethacin group.
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Two review authors independently assessed trial quality and extracted data. The area under the "pain relief versus time" curve was used to derive the proportion of participants with tenoxicam experiencing least 50% pain relief over 4 to 6 hours, using validated equations. The number needed to treat to benefit (NNT) was calculated using 95% confidence intervals (CI). The proportion of participants using rescue analgesia over a specified time period, and time to use of rescue analgesia, were sought as additional measures of efficacy. Information on adverse events and withdrawals was also collected.
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Of 793 retrieved citations, 120 contained original reports on 186 interactions. The weighted kappa statistic was 0.67, representing substantial agreement. Of 86 different drugs and foods appraised, 43 had level 1 evidence. Of these, 26 drugs and foods did interact with warfarin. Warfarin's anticoagulant effect was potentiated by 6 antibiotics (cotrimoxazole, erythromycin, fluconazole, isoniazid, metronidazole, and miconazole); 5 cardiac drugs (amiodarone, clofibrate, propafenone, propranolol, and sulfinpyrazone); phenylbutazone; piroxicam; alcohol (only with concomitant liver disease); cimetidine; and omeprazole. Three patients had a hemorrhage at the time of a potentiating interaction (caused by alcohol, isoniazid, and phenylbutazone). Warfarin's anticoagulant effect was inhibited by 3 antibiotics (griseofulvin, rifampin, and nafcillin); 3 drugs active on the central nervous system (barbiturates, carbamazepine, and chlordiazepoxide); cholestyramine; sucralfate; foods high in vitamin K; and large amounts of avocado.
Randomized, prospective, double-blind, controlled study.
A positively charged submicron emulsion with zeta potential values ranging from 35 to 45 mV and mean droplet size around 150-250 nm has recently been developed and characterized. This formulation is based on three surface-active agents, an egg yolk phospholipid mixture, poloxamer 188, and stearylamine, a cationic lipid with a pKa of 10.6. The emulsion toxicity was evaluated in three animal studies. The results of the ocular tolerance study in the rabbit eye indicated that hourly administration of one droplet of the positively charged emulsion vehicle was well tolerated without any toxic or inflammatory response to the ocular surface during the five days of the study. No marked acute toxicity was observed when 0.6 mL of positively charged emulsion was injected intravenously to BALB/c mice. Furthermore, no difference was noted between this group of animals and the group injected with the marketed and clinically well accepted negatively charged Intralipid emulsion. These observations were further confirmed in a four week toxicity study following intravenous administration to rats of 1 mL/kg of the positively charged emulsion as compared to Intralipid. No toxic effect was noted in any of the various organs examined, whereas the results of the hematological and blood chemistry tests remained in the normal range for both emulsions, confirming the preliminary safety study findings. In addition, it was demonstrated by means of a non-invasive technique that alpha-tocopherol positively charged emulsions prevented oxidative damage in rat skin subjected to UVA irradiation. The intrinsic ability of positively charged emulsified oil droplets to protect against reactive oxygen species cannot be excluded, and could act synergistically with the antioxidant alpha-tocopherol itself. The effect of blank and piroxicam positively charged emulsions on rabbit eye following alkali burn was also evaluated. The blank emulsion showed a very rapid healing rate during the first three days with a breakdown in day 14. Complete re-epithelialization was observed in day 28. The same behavior (albeit less pronounced), was noted in piroxicam emulsion, although piroxicam is known to inhibit the epithelial healing process. It can therefore be deduced that the positively charged emulsion vehicle prevented piroxicam from interfering with the epithelial healing process due to the intrinsic free radical scavenger ability of the positively charged submicron emulsion previously demonstrated. Finally, the efficacy of this promising emulsion vehicle containing effective cosmetic ingredients in preventing skin damage and aging following oxidative stress is evaluated.
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The anti-inflammatory and analgesic activity of the beta-cyclodextrin-piroxicam (beta CDP) complex was assessed in a randomized single-blind controlled parallel study vs nabumetone (NAB). Forty patients, 18 men and 22 women aged 18 to 65 and suffering from chronic osteoarthritis, were treated. Both drugs were orally administered, once a day in the morning, for 4 consecutive weeks. PI and SPID, evaluated for 24 hours following the first drug administration, showed a quicker onset of the analgesic action of beta CDP, with statistically significant differences between treatments (p less than 0.05). In the medium-term treatment, beta CDP proved to be more effective on joint swelling, spontaneous pain, pain on passive movement and functional limitation. Both treatments were well tolerated but a higher gastro-intestinal side-effect incidence was recorded in NAB group.
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Piroxicam beta-cyclodextrin has recently been observed to be equal to, or even possibly to be superior to, indomethacin (mainly with regard to side effects) in a single case of hemicrania continue. Piroxicam beta-cyclodextrin, 20 to 40 mg per day, was, accordingly, tried in six patients with chronic paroxysmal hemicrania and six patients with hemicrania continua with a previously proven response to indomethacin. The study was conducted over a period of 3 weeks and in an open fashion. A placebo effect is considered to be negligible in these disorders. In such a comparison, piroxicam beta-cyclodextrin seemed inferior to indomethacin, in particular in chronic paroxysmal hemicrania.
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HC should be considered among the diagnostic hypotheses of patients with continuous headache, with no change in neurological examination and additional tests, regardless the age of onset. The standard treatment with indomethacin (100-150mg.day(-1)) has significant risks associated with both short and long term use and may not be a good choice for continuous use. Recent studies point out possible alternatives: gabapentin, topiramate, cyclooxygenase-2 inhibitors, piroxicam, beta-cyclodextrin, amitriptyline, melatonin. Other drugs were described in different reports as efficient, but most of them were considered inefficient in other HC cases.
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Membranous nephropathy presents clinically as nephrotic syndrome, with subepithelial immune complex deposits seen on biopsy. Historically, in about three-quarters of membranous cases, no obvious etiologic agent or condition can be identified. More recently, serum antibodies to the phospholipase A2 receptor have been discovered in many patients with primary/idiopathic membranous nephropathy. About one-quarter of patients have membranous nephropathy as a manifestation of another systemic disorder, such as autoimmune conditions, infection, malignancy, toxin exposure, or drugs (classically gold or penicillamine). In this report, we present a case of recurrent nephrotic syndrome with biopsy-proven membranous nephropathy closely associated with use of the nonsteroidal anti-inflammatory drugs (NSAIDs) naproxen and piroxicam. Characterization of the immunoglobulin G (IgG) subclass profile of the deposits showed abundant IgG1, weak IgG4, and positive staining for phospholipase A2 receptor. This case serves to highlight membranous nephropathy as an under-recognized renal complication of NSAID use. Other kidney effects of NSAIDs, such as hemodynamic compromise, interstitial nephritis, and minimal change disease, are more broadly recognized.
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The purpose of this study was the isolation and structure elucidation of chemical compounds from the rhizomes of Eremostachys laciniata (L) Bunge (EL), an Iranian traditional medicinal herb with a thick root and pale purple or white flowers as well as the clinical studies on the therapeutic efficacy and safety of topical application of the EL extract in the management of some inflammatory conditions, e.g., arthritis, rheumatoid arthritis and septic arthritis (Riter's syndrome).