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Male Sprague-Dawley rats were left untreated (control), injected with capsaicin, or pretreated with sumatriptan/naproxen, sumatriptan, or naproxen for 1 hour prior to capsaicin. Trigeminal ganglia and the spinal trigeminal nucleus were isolated 2 and 24 hours after capsaicin or drug treatment, and levels of 90 proteins were determined using a RayBio® Label-Based Rat Antibody Array (RayBiotech, Norcross, GA, USA).
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The authors report a case of hypersensitivity angiitis presenting with cutaneous, muscular, articular, and renal signs. They suggest a possible etiological mechanism for such disorders: a circulating immune-complex disease, and criticize the often improper interpretation of the results of lymphoblast transformation tests. Hypersensitivity angiitis, "ground base disease", requires investigation for possible underlying immunity abnormalities or neoplasms.
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The effect on cytotoxicity of combining a range of clinically important non-steroidal anti-inflammatory drugs (NSAIDs) with a variety of chemotherapeutic drugs was examined in the human lung cancer cell lines DLKP, A549, COR L23P and COR L23R and in a human leukaemia line HL60/ADR. A specific group of NSAIDs (indomethacin, sulindac, tolmetin, acemetacin, zomepirac and mefenamic acid) all at non-toxic levels, significantly increased the cytotoxicity of the anthracyclines (doxorubicin, daunorubicin and epirubicin), as well as teniposide, VP-16 and vincristine, but not the other vinca alkaloids vinblastine and vinorelbine. A substantial number of other anticancer drugs, including methotrexate, 5-fluorouracil, cytarabine, hydroxyurea, chlorambucil, cyclophosphamide, cisplatin, carboplatin, mitoxantrone, actinomycin D, bleomycin, paclitaxel and camptothecin, were also tested, but displayed no synergy in combination with the NSAIDs. The synergistic effect was concentration dependent. The effect appears to be independent of the cyclo-oxygenase inhibitory ability of the NSAIDs, as (i) the synergistic combination could not be reversed by the addition of prostaglandins D2 or E2; (ii) sulindac sulphone, a metabolite of sulindac that does not inhibit the cyclooxygenase enzyme, was positive in the combination assay: and (iii) many NSAIDs known to be cyclo-oxygenase inhibitors, e.g. meclofenamic acid, diclofenac, naproxen, fenoprofen, phenylbutazone, flufenamic acid, flurbiprofen, ibuprofen and ketoprofen, were inactive in the combination assay. The enhancement of cytotoxicity was observed in a range of drug sensitive tumour cell lines, but did not occur in P-170-overexpressing multidrug resistant cell lines. However, in the HL60/ADR and COR L23R cell lines, in which multidrug resistance is due to overexpression of the multidrug resistance-associated protein MRP, a significant increase in cytotoxicity was observed in the presence of the active NSAIDs. Subsequent Western blot analysis of the drug sensitive parental cell lines, DLKP and A549, revealed that they also expressed MRP and reverse-transcription-polymerase chain reaction studies demonstrated that mRNA for MRP was present in both cell lines. It was found that the positive NSAIDs were among the more potent inhibitors of [3H]-LTC4 transport into inside-out plasma membrane vesicles prepared from MRP-expressing cells, of doxorubicin efflux from preloaded cells and of glutathione-S-transferase activity. The NSAIDs did not enhance cellular sensitivity to radiation. The combination of specific NSAIDs with anticancer drugs reported here may have potential clinical applications, especially in the circumvention of MRP-mediated multidrug resistance.
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Hyperkalemia is an electrolyte abnormality that can lead to severe consequences. Paralysis induced by hyperkalemia has been described in only a few reports. We describe a 60-year-old man who experienced paralysis presumably due to hyperkalemia. He presented to the emergency department with severe weakness in all extremities. The patient's serum potassium concentration was greater than 8 mEq/L and his serum creatinine concentration was 7 mg/dl. Findings on electrocardiography were abnormal. Of note, his drug therapy included lisinopril and naproxen. After treatment for hyperkalemia, the patient's symptoms resolved; however, he was admitted for further workup for renal failure. The patient was discharged after approximately 1 week with a diagnosis of end-stage renal disease. Use of the Naranjo adverse drug reaction probability scale indicated a probable relationship (score of 5) between the patient's paralysis and hyperkalemia. Although hyperkalemia as a cause of paralysis is extremely rare, clinicians should be aware of this potentially life-threatening, noncardiac toxicity.
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Trichloroethylene (TCE) is a widely used chemical to which humans are frequently exposed. Toxicological interactions with drugs are among factors having the potential to modulate the toxicity of TCE. The aim of this study was to identify metabolic interactions between TCE and 14 widely used drugs in rat suspended hepatocytes and characterize the strongest using microsomal assays (oxidation and/or glucuronidation). The concentrations of TCE and its metabolites, trichloroethanol (TCOH) and trichloroacetate (TCA), were measured by gas chromatography with injection headspace coupled to mass spectrometry (GC-MS). Results in hepatocyte incubations show that selected drugs can be segregated into four groups: group 1: drugs causing no significant interactions (five drugs: amoxicillin, carbamazepine, ibuprofen, mefenamic acid and ranitidine); group 2: increasing both TCE metabolites (two drugs: naproxen and salicylic acid); group 3: decreasing both TCE metabolites (five drugs: acetaminophen, gliclazide, valproic acid, cimetidine and diclofenac) and group 4: affecting only one (two drugs: erythromycin and sulphasalazine). Naproxen and salicylic acid (group 2) and acetaminophen, gliclazide and valproic acid (from group 3) presented the strongest interactions (i.e. drugs changing metabolite levels by 50% or more). For group 2 drugs, characterization in rat microsomes confirmed interaction with naproxen only, which was found to partially competitively inhibit TCOH glucuronidation (K(i) = 211.6 μM). For group 3 selected drugs, confirmation was positive only for gliclazide (K(i) = 58 μM for TCOH formation) and valproic acid (K(i) = 1215.8 μM for TCA formation and K(i) = 932.8 μM for TCOH formation). The inhibition was found to be partial non competitive for both drugs. Our results confirm the existence of interactions between TCE and a variety of widely used drugs. Further efforts are undertaken to determine if these interactions are plausible in humans and if they can impact the risk of toxicity of TCE in medicated population.
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Scirpus validus was grown hydroponically and exposed to the pharmaceuticals, carbamazepine and naproxen at concentrations of 0.5-2.0 mg L(-1) for an exposure duration of up to 21 d. By the end of experiment, carbamazepine elimination from the nutrient solution reached to 74%, while nearly complete removal (>98%) was observed for naproxen. Photodegradation and biodegradation played only minor roles for carbamazepine elimination, while naproxen showed a high potential for both photodegradation and biodegradation. Levels of carbamazepine ranged from 3.3 to19.0 μg g(-1) (fresh weight) in the roots and 0.3-0.7 μg g(-1) (fresh weight) in the shoots, while naproxen concentrations were 0.2-2.4 μg g(-1) (fresh weight) in the roots and 0.2-2.8 μg g(-1) (fresh weight) in the shoots. Bioaccumulation factors (BAFs) for carbamazepine ranged from 5.5 to 13.0 for roots and 0.3-1.0 for shoots, and uptake by S. validus accounted for up to 22% of the total mass loss of carbamazepine in the nutrient solutions. All BAFs for naproxen were less than 4.2 and plant uptake accounted for less than 5% of the total mass loss of naproxen, implying that plant uptake was not significant in naproxen elimination. The rather limited plant uptake of naproxen was not surprising despite the fact that its log K(ow) is close to the optimal range (1.8-3.1) for maximal potential for plant uptake. Apparently, for ionizable compounds such as naproxen, the effects of pK(a) and pH partitioning might be more important than lipophilicity.
Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase (COX) and can thereby reduce renal function, especially with respect to solute excretion and renal perfusion. AZD3582 [4-(nitrooxy)butyl-(2S)-2-(6-methoxy-2-naphthyl)propanoate] is a COX-inhibiting nitric oxide donator. Donation of nitric oxide by AZD3582 could preserve blood flow and thereby counteract the deleterious effects of COX inhibition in the gastrointestinal tract and possibly in other organ systems, including the kidney. The aim of this single-dose study was to assess the hypothesis that AZD3582 would not adversely affect renal function compared with NSAIDs.
1. This study compared the extent, affinity, and kinetics of drug binding to human serum albumin (HSA) and liver fatty acid binding protein (LFABP) using ultrafiltration and surface plasmon resonance (SPR). 2. Binding of basic and neutral drugs to both HSA and LFABP was typically negligible. Binding of acidic drugs ranged from minor (fu > 0.8) to extensive (fu < 0.1). Of the compounds screened, the highest binding to both HSA and LFABP was observed for the acidic drugs torsemide and sulfinpyrazone, and for β-estradiol (a polar, neutral compound). 3. The extent of binding of acidic drugs to HSA was up to 40% greater than binding to LFABP. SPR experiments demonstrated comparable kinetics and affinity for the binding of representative acidic drugs (naproxen, sulfinpyrazone, and torsemide) to HSA and LFABP. 4. Simulations based on in vitro kinetic constants derived from SPR experiments and a rapid equilibrium model were undertaken to examine the impact of binding characteristics on compartmental drug distribution. Simulations provided mechanistic confirmation that equilibration of intracellular unbound drug with the extracellular unbound drug is attained rapidly in the absence of active transport mechanisms for drugs bound moderately or extensively to HSA and LFABP.
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Mesoporous silica material, MCM-41, was utilized for the first time as an adsorbent in solid phase membrane tip extraction (SPMTE) of non-steroidal anti-inflammatory drugs (NSAIDs) in urine prior to high performance liquid chromatography-ultraviolet (HPLC-UV) analysis. The prepared MCM-41 material was enclosed in a polypropylene membrane tip and used as an adsorbent in SPMTE. Four NSAIDs namely ketoprofen, diclofenac, mefenamic acid and naproxen were selected as model analytes. Several important parameters, such as conditioning solvent, sample pH, salting-out effect, sample volume, extraction time, desorption solvent and desorption time were optimized. Under the optimum extraction conditions, the MCM-41-SPMTE method showed good linearity in the range of 0.01-10μg/mL with excellent correlation coefficients (r=0.9977-0.9995), acceptable RSDs (0.4-9.4%, n=3), good limits of detection (5.7-10.6μg/L) and relative recoveries (81.4-108.1%). The developed method showed a good tolerance to biological sample matrices.
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Etoricoxib 120 mg had a significantly greater least squares (LS) mean TOPAR8 score than placebo (20.9 vs 5.4; P < 0.001) and acetaminophen/codeine 600/60 mg (20.9 vs 11.5; P < 0.001), and a similar LS mean TOPAR8 score to naproxen sodium 550 mg (20.9 vs 21.3). All three active treatments had rapid onset of analgesia, median time approximately 30 minutes. The duration of analgesic effect, defined as median time to rescue medication use, was >24 hours for etoricoxib, 20.8 hours for naproxen sodium, 3.6 hours for acetaminophen/codeine, and 1.6 hours for placebo.
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Parturition in rats is associated with an abrupt and marked increase in myometrial oxytocin (OT) receptor concentrations. In this study, we investigated the role of myometrial OT receptors in the initiation and the process of parturition. We produced chronic OT receptor blockade during the last 3 days of gestation by administration of a specific OT antagonist at 100 micrograms/day and 300 micrograms/day. We also suppressed OT receptor formation by inhibiting prostaglandin synthesis with naproxen sodium at 2 mg/day and 5 mg/day. We found that chronic blockade of OT receptors inhibited the uterotonic response to OT in Day 22 and Day 23 pregnant rats in a dose-dependent manner. OT antagonist treatment did not prolong the gestation period. However, the duration of parturition, fetal mortality, and the mortality incidence were increased in rats treated with the high dose of the OT antagonist compared to controls. Naproxen sodium at both dosage levels prolonged gestation by 24 h or longer, doubled the duration of parturition, and markedly increased fetal mortality and mortality incidence. Combined OT antagonist and naproxen treatment produced adverse outcomes similar to that produced by naproxen treatment alone. Myometrial OT receptor concentrations were markedly increased in all rats immediately postpartum, ranging from 210 to 425 fmol/mg protein compared to the 50 to 100 fmol/mg found in Day 21 and Day 22 pregnant rats. Correlation analyses between OT receptor concentrations and various parameters associated with gestation and parturition showed that there was a correlation between low OT receptor concentrations and long gestation period, prolonged parturition, and high fetal mortality rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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Fifty-two patients entered a randomized, double blind study. Patients were randomized to 3 months treatment with either nabumetone, 1000 mg nightly, or naproxen, 250 mg twice daily, followed by an endoscopist-blind 5-year followup study. After the double blind phase, 15 patients in the nabumetone group and 12 in the naproxen group continued in the longterm endoscopist-blind phase. Endoscopic evaluations for gastroduodenal damage and global assessments of arthritis activity and degree of pain for efficacy were measured.
Current and new users of all classes of nonaspirin NSAIDs had elevated relative risk estimates for MI. Although the increased risk estimates may partly reflect unmeasured bias, they indicate the need for further examination of the cardiovascular safety of all nonaspirin NSAIDs.
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White-rot fungi are a group of microorganisms capable of degrading xenobiotic compounds, such as polycyclic aromatic hydrocarbons or synthetic dyes, by means of the action of extracellular oxidative enzymes secreted during secondary metabolism. In this study, the transformation of three anti-inflammatory drugs: diclofenac, ibuprofen and naproxen were carried out by pellets of Phanerochaete chrysosporium in fed-batch bioreactors operating under continuous air supply or periodic pulsation of oxygen. The performance of the fungal reactors was steady over a 30-day treatment and the effect of oxygen pulses on the pellet morphology was evidenced. Complete elimination of diclofenac was achieved in the aerated and the oxygenated reactors, even with a fast oxidation rate in the presence of oxygen (77% after 2 h), reaching a total removal after 23 h. In the case of ibuprofen, this compound was completely oxidized under air and oxygen supply. Finally, naproxen was oxidized in the range of 77 up to 99% under both aeration conditions. These findings demonstrate that the oxidative capability of this microorganism for the anti-inflammatory drugs is not restricted to an oxygen environment, as generally accepted, since the fungal reactor was able to remove these compounds under aerated and oxygenated conditions. This result is very interesting in terms of developing viable reactors for the oxidation of target compounds as the cost of aeration can be significantly reduced.
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Solid dispersions have been used to improve the bioavailability of poorly water-soluble drugs. However, drug solid-state phase, compositional uniformity, and scale-up problems are issues that need to be addressed. To allow for highly controllable products, the drop printing (DP) technique can provide precise dosages and predictable compositional uniformity of active pharmaceutical ingredients in two-/three-dimensional structures when integrated with edible substrates. With different preparation conditions, DP was conducted to fabricate naproxen (NAP)-polyvinylpyrrolidone solid dispersions with chitosan and hydroxypropyl methylcellulose films as the substrate. Scanning electron microscopy, X-ray diffraction, second harmonic generation microscopy, and atomic force microscopy analyses were performed to characterize the microstructure and spatial distribution of NAP in the solid dispersions. The results identified that composition, temperature, and substrate type all had an impact on morphology and crystallization of samples. The surface energy approach was combined with classical nucleation theory to evaluate the affinity between the nucleus of NAP and substrates. Finally, the collective results of the drug were correlated to the release profile of NAP within each sample.
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This article summarizes the guidelines as they apply to adults and children, and proposes future direction for steps toward optimal treatment of migraine in patients in France.
Experimental tubulointerstitial nephritis (TIN), induced in Brown Norway rats, is an autoimmune disorder in which afflicted animals display high levels of serum autoantibodies directed against antigens present on the tubular basement membrane (TBM). Serious functional damage, due to lesions of the kidney cortex, is evident 10 days after disease initiation. In an earlier study, we could show that cyclosporin A (CsA), an immunosuppressive drug, effectively prevented the onset of this illness, although it did not inhibit the formation of TBM autoantibodies. In the present study, the protective effects of CsA in autoimmune TIN was compared to those of drugs currently used to combat inflammatory ailments (i.e. prednisolone, indomethacin, naproxen, azathioprine) and a novel immunomodulating agent, leflunomide (HWA 486). Leflunomide is known to specifically inhibit the formation of T-dependent antibodies and is effective in preventing and curing animal autoimmune diseases, i.e. adjuvant arthritis disease of rats and murine lupus-like disorders. We found that not only could leflunomide inhibit TIN, but the drug-effects seemed to be more effective than those of CsA. Further, leflunomide was extremely effective in inhibiting the formation of autoantibodies to TBM, whereas CsA displayed only partial suppression. Neither prednisolone, indomethacin nor naproxen were effective in reducing the autoantibody titer, and did not offer any protection to the development of this disease. Together with the known effects on other autoimmune diseases we conclude that leflunomide is a novel immunointerventive drug protecting against several types of autoimmunity.
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Nonsteroidal anti-inflammatory drugs (NSAIDs) frequently cause damage to the gastroduodenal mucosa, principally by suppressing mucosal prostaglandin synthesis. However, such acute mucosal injury usually resolves, despite continued NSAID administration, by a process known as adaptation. Newer NSAIDs, such as etodolac, have been developed to minimize effects on prostaglandin synthesis.
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Renal function and excretion of water, salt, and the prostacyclin hydration product (6-keto-PGF1 alpha) were evaluated in 10 furosemide-treated patients with well-controlled congestive heart failure. Four doses of sulindac (200 mg b.i.d.) and naproxen (500 mg b.i.d.) were given every 12 hours in a double-blind crossover design. Naproxen significantly decreased the urinary excretion of water (19%), sodium (26%), chloride (26%), and 6-keto PGF1 alpha (76%) and decreased osmolal clearance (18%). No significant changes in these functions were observed in the patients receiving sulindac. Plasma renin activity, plasma aldosterone, freewater clearance, or clearance of furosemide did not change significantly with either treatment. Although the basal glomerular filtration rate (GFR) and renal plasma flow (RPF) were reduced, these patients with cardiac disease, with normal serum sodium concentration, did not have any further reduction of GFR or RPF despite naproxen-induced inhibition of renal prostacyclin synthesis. It is concluded that renal prostaglandins contribute to the natriuretic effect of oral furosemide in patients with compensated congestive heart failure. In this clinical setting, GFR and RPF are not critically dependent on intact renal PGI2 synthesis. The lack of effect on renal prostaglandin synthesis and the renal response to oral furosemide supports the concept of a renal sparing effect of sulindac.
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Patients randomized to celecoxib 200 mg b.i.d. (n = 198) or naproxen 500 mg b.i.d. (n = 198) for 7 days.
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In this work, an automated system for the study of the interaction of drugs with human serum albumin (HSA) was developed. The methodology was based on the quenching of the intrinsic fluorescence of HSA by binding of the drug to one of its binding sites. The fluorescence quenching assay was implemented in a sequential injection analysis (SIA) system and the optimized assay was applied to ionic liquids based on the association of non-steroidal anti-inflammatory drugs with choline (IL-API). In each cycle, 100 µL of HSA and 100 µL of IL-API (variable concentration) were aspirated at a flow rate of 1 mL min(-1) and then sent through the reaction coil to the detector where the fluorescence intensity was measured. In the optimized conditions the effect of increasing concentrations of choline ketoprofenate and choline naproxenate (and respective starting materials: ketoprofen and naproxen) on the intrinsic fluorescence of HSA was studied and the dissociation constants (Kd) were calculated by means of models of drug-protein binding in the equilibrium. The calculated Kd showed that all the compounds bind strongly to HSA (Kd<100 µmol L(-1)) and that the use of the drugs in the IL format does not affect or can even improve their HSA binding. The obtained results were compared with those provided by a conventional batch assay and the relative errors were lower than 4.5%. The developed SIA methodology showed to be robust and exhibited good repeatability in all the assay conditions (rsd<6.5%).
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Inflammation is a complex process involving numerous mediators. Because prostaglandins (PG) have been implicated as mediators in all stages of inflammation, inhibition of their synthesis provides the basis for the therapeutic effects of nonsteroidal antiinflammatory drugs (NSAID). Treatment with NSAID is usually accompanied by gastric side effects, attributed to interference with the formation of cytoprotective PG in gastric mucosa. An ideal NSAID should inhibit PG synthesis at the site(s) of inflammation but not in gastric mucosa. Experimental and clinical data support the view that this criterion has been met by etodolac, a structurally distinct NSAID. Thus, in rats and humans with rheumatoid arthritis, longterm daily administration of etodolac at effective antiinflammatory dosages (3 mg/kg in rats; 600 mg in humans) had no effect on PGF2 and prostacyclin levels in gastric mucosa. In contrast, significant decreases in gastric PG levels occurred with antiinflammatory doses of aspirin, naproxen, and piroxicam. Cyclooxygenase (COX), the pivotal enzyme in PG biosynthesis, exists in 2 isoforms: constitutive COX-1, which produces the PG required for maintenance of normal cell activity (e.g., gastric cytoprotection), and COX-2, which is induced in restricted tissue-specific fashion (e.g., by inflammatory stimuli). The antiinflammatory action of NSAID may result from inhibition of COX-2, whereas their gastric side effects may result in large part from inhibition of COX-1; thus, a preferred NSAID should inhibit COX-2 but not COX-1. Results show that etodolac has 10-fold selectivity for COX-2 and indicate that etodolac's pharmacotherapeutic efficacy can be explained by its demonstrably selective inhibition of COX-2, amplified by its favorable tissular pharmacokinetics. The sparing of COX-1 activity in gastric mucosa gives rise to etodolac's noted gastric tolerance.
To investigate the individual effects of ibuprofen, diclofenac, naproxen, and piroxicam on pregnancy outcome.