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Children aged between 1 and 10 years attending the emergency department with a temperature of> 38 degrees C were given one dose of ibuprofen (7 mg/kg). Temperature was recorded before and 30, 60, 90, 120, 180 and 240 min after ibuprofen administration. The influence of age, sex, weight, body surface, nosologic entity, previous antipyretic administration, and the association between physical measurements and temperature evolution were assessed.
Subjects who developed an HDR to APs less than 1 h after drug intake were included. Tolerance to aspirin was assessed and challenge was performed with ibuprofen in all cases, and additionally with the culprit drug (if different) in those patients that tolerated ibuprofen. Serum tryptase levels and tryptase immunohistochemical staining in skin biopsies were also assessed in some patients with a positive DPT to ibuprofen.
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Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used, but have risks associated with their use, including significant upper gastrointestinal tract bleeding. Older persons, persons taking anticoagulants, and persons with a history of upper gastrointestinal tract bleeding associated with NSAIDs are at especially high risk. Although aspirin is cardioprotective, other NSAIDs can worsen congestive heart failure, can increase blood pressure, and are related to adverse cardiovascular events, such as myocardial infarction and ischemia. Cyclooxygenase-2 inhibitors have been associated with increased risk of myocardial infarction; however, the only cyclooxygenase-2 inhibitor still available in the United States, celecoxib, seems to be safer in this regard. Hepatic damage from NSAIDs is rare, but these medications should not be used in persons with cirrhotic liver diseases because bleeding problems and renal failure are more likely. Care should be used when prescribing NSAIDs in persons taking anticoagulants and in those with platelet dysfunction, as well as immediately before surgery. Potential central nervous system effects include aseptic meningitis, psychosis, and tinnitus. Asthma may be induced or exacerbated by NSAIDs. Although most NSAIDs are likely safe in pregnancy, they should be avoided in the last six to eight weeks of pregnancy to prevent prolonged gestation from inhibition of prostaglandin synthesis, premature closure of the ductus arteriosus, and maternal and fetal complications from antiplatelet activity. Ibuprofen, indomethacin, and naproxen are safe in breastfeeding women. Care should be taken to prevent accidental NSAID overdose in children by educating parents about correct dosing and storage in childproof containers.
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A total of 356 patients were enrolled (n = 121, 120, and 115 patients in the diclofenac-K, ibuprofen, and placebo groups, respectively). All patients were white except 1 Asian patient in the diclofenac-K group; 55% to 60% of patients in all 3 groups were male; the mean age in each treatment group was approximately 40 years. At baseline, mean oral temperature ranged from 38.65 degrees C in the placebo group to 38.74 degrees C in the diclofenac-K group. Mean oral temperatures in both active groups were significantly lower than that of the placebo group from 30 minutes through 6 hours (P < 0.001), dropping 0.85 degrees C after 4 hours in the diclofenac-K group and 0.76 degrees C in the ibuprofen group versus 0.32 degrees C for placebo. In the end-of-study global treatment assessment, 89.0% of diclofenac-K and 89.1% of ibuprofen patients rated global efficacy as "good" to "excellent" versus only 32.1% for placebo. Diclofenac-K was superior to placebo (P < 0.001) and similar to ibuprofen on all direct assessments of fever and aches and pains. Both active treatments were as well tolerated as was placebo.
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A total of 48 patients undergoing a Bascom cleft lift operation were included over an 8-month period in a day-case set-up. The operation was performed under saddle block. In addition, patients received a standardised multi-modal analgesic regimen consisting of gabapentin, ketorolac, dexamethasone, acetaminophen (paracetamol) and ibuprofen. The intensity of pain was registered preoperatively and at 2, 24, 48 h, and 30 days post-operatively. Nausea, vomiting, dizziness, ability to void, morphine consumption and post-anaesthesia care unit (PACU) time were registered.
3-Aminobenzonitrile and 2-amino-4-phenyl thiazole on condensation with 4-isothiocyanato-4-methyl pentane-2-one gave condensed monocyclic pyrimidine derivatives 1 and 2, 3, respectively. Condensation of 3-aminopropyl imidazole with 3-isothiocyantobutanal gave condensed monocyclic pyrimidine derivative 4. Bicyclic pyrimidine derivatives 5a and 5b have been synthesized by the condensation of diaminomaleonitrile with 4-isothiocyanto-4-methylpentane-2-one and 3-isothiocyanatobutanal, respectively. Condensation of 4-isothiocyanato-4-methyl pentane-2-one with 2,3-diaminopropionic acid hydrochloride yielded another bicyclic compound 7. 4-Isothiocyanato-4-methyl pentane-2-one, 3-isothiocyanatobutanal and 4-isothiocyanatobutan-2-one on condensation with 2-amino-4-nitro phenol gave tricyclic pyrimidine derivatives 8a, 8b and 8c, respectively. Structures of all the synthesized pyrimidine derivatives are supported by correct IR, 1H NMR and mass spectral data. The anti-inflammatory activity evaluation was carried out using carrageenin-induced paw oedema assay, and compounds 1, 3 and 5b exhibited good anti-inflammatory activity, that is, 27.9, 34.5 and 34.3% at 50 mg/kg po, respectively. Analgesic activity evaluation was carried out using phenylquinone writhing assay and compounds 5a, 5b and 8b showed good analgesic activity, that is, 50, 70 and 50% at 50 mg/kg po, respectively.
Adverse events were reported for 43 of 150 patients (29%). The most common adverse events experienced by patients were infusion site pain in 22 of 150 patients (15%) and flatulence (8 of 150 [5%]). Four patients (3%) discontinued the study drug due to infusion-site pain. In the patients experiencing fever, temperature decreased from baseline over 4 hours (mean [SD] reduction of 1.5 [1.25]°F). In patients experiencing pain, patient-reported visual analog scale scores decreased from baseline over 4 hours (mean [SD] reduction of 27.1 [31.29] mm).
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Cisplatin, a platinum-derived chemotherapeutic agent, produces antineoplastic effects coupled with toxic neuropathic pain and impaired general health status. These side-effects complicate long term studies of neuropathy or analgesic interventions in animals. We recently demonstrated that pretreatment with sodium bicarbonate (4% NaHCO3) prior to cisplatin (3 mg/kg i.p. weekly up to 5 weeks) was associated with improved health status (i.e. normal weight gain, body temperature, creatinine and ketone levels, and kidney weight ratio) in rats (Neurosci Lett 544:41-46, 2013). To reduce the nephrotoxic effects of cisplatin treatment in mice, we compared effects of sodium bicarbonate (4% NaHCO3 s.c.), vitamin C (25 mg/kg s.c.), resveratrol (25 mg/kg s.c.) and saline (0.9% NaCl) pretreatment on cisplatin-induced changes in animal health status, neuropathic pain and proinflammatory cytokine levels in spinal cord and kidney.
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Fish in many surface freshwaters are exposed to a range of pharmaceuticals via wastewater treatment works effluent discharges. In mammals the pregnane X receptor (PXR) plays a key role in the regulation of a suite of genes involved in drug biotransformation, but information on the role of this response pathway in fish is limited. Here we investigated the effects of exposure of carp (Cyprinus carpio) primary hepatocytes to the human PXR agonist rifampicin (RIF) on expression of target genes involved in phase I (cyp2k, cyp3a) and phase II (gstα, gstπ) drug metabolism and drug transporters mdr1 and mrp2. RIF induced expression of all target genes measured and the PXR antagonist ketoconazole (KET) inhibited responses of cyp2k and cyp3a. Exposure of the primary carp hepatocytes to the pharmaceuticals ibuprofen (IBU), clotrimazole (CTZ), clofibric acid (CFA) and propranolol (PRP), found responses to IBU and CFA, but not CTZ or PRP. This is in contrast with mammals, where CTZ is a potent PXR-agonist. Collectively our data indicate potential PXR involvement in regulating selected genes involved in drug metabolism in fish, but suggest some divergence in the regulation pathways with those in mammals. The carp primary hepatocyte model serves as a useful system for screening for responses in these target genes involved in drug metabolism.
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Cyclooxygenase (COX) inhibitors-acetaminophen, ibuprofen and acetylsalicylic acid-have endocrine-disruptive properties in the rainbow trout. In humans, aspirin blocks the androgen response to human chorionic gonadotropin (hCG), and, because hCG-stimulated androgen production in utero is crucial for normal testicular descent, exposure to COX inhibitors at vulnerable times during gestation may impair testicular descent. We examined whether prenatal exposure to acetaminophen, ibuprofen, and acetylsalicylic acid was associated with increased occurrence of cryptorchidism.
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Raman spectroscopy revealed that immersion of the pellets in a drug solution and supercritical fluid impregnation allowed the drug to penetrate into the porous structure of the pellets. The amount of drug incorporated depended on the solubility of the drug in the solvent (water or supercritical CO(2)). Drug release from the porous pellets was immediate and primarily controlled by pure diffusion.
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Drugs were determined by direct injection of plasma samples into a biocompatible extraction column. The column is based on particles with a biocompatible external surface and a hydrophobic internal surface. The pores of the particles are small enough to exclude the protein molecules; the drug molecules can penetrate the porous particle and are retained on the hydrophobic internal surface. Biocompatibility of the particles was obtained by reaction of the external surface with the human plasma protein alpha1-acid glycoprotein. The surface within the pores of the particles contains hydrophobic C8 or C18 groups. The biocompatible extraction column was used in a fully automated system for the determination of ibuprofen, naproxen, propranolol, carbamazepine and phenytoin in plasma. No pressure increase was observed during the analysis of several hundred plasma samples. Plasma concentrations of propranolol in the range 4.5-125 ng/ml were determined with a precision (R.S.D.) of 0.75-1.8%. Linear calibration graphs were observed for the five drugs, and correlation coefficients of 1.0000 were obtained for four of the five model compounds.
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A budget impact model, considering a typical health plan of 1 million enrollees, was used to compare patients receiving: (1) single-tablet ibuprofen/famotidine; (2) chronic NSAID treatment plus any GI-protective agent; and (3) chronic NSAID treatment without a GI-protective agent.
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We investigated whether chemical association of phosphatidylcholine (PC) to ibuprofen enhances the anti-inflammatory/analgesic activity of the nonsteroidal anti-inflammatory drug (NSAID) and whether any change in therapeutic action is due to alterations in drug bioavailability and cyclooxygenase (COX) inhibitory activity. Acute/chronic joint inflammation was induced in rats, by injection of Complete Freund's Adjuvant. In the acute study, rats were administered saline, ibuprofen, or PC-ibuprofen (at NSAID doses of 10, 25, and 50 mg/kg), and 2 h later the pain threshold of the affected joint to pressure was measured. PC-ibuprofen increased the pain threshold at all NSAID doses, whereas unmodified ibuprofen demonstrated analgesic activity at only the highest dose. In the chronic study, we investigated the effects of saline, PC-ibuprofen, and ibuprofen (administered at 15 and 25 mg/kg/day) on ankle thickness and pain threshold, and demonstrated that PC-ibuprofen had significantly greater anti-inflammatory and analgesic activity than ibuprofen, over a 30- to 60-day period. PC association resulted in reduced uptake (decreased Cmax), a modest increase in the area under the curve, and a longer t(1/2) of ibuprofen. We also demonstrated that PC-ibuprofen was a comparable or a more effective inhibitor of both 6-keto-prostaglandin F1alpha concentration of fluid collected from tissue in and around the inflamed stifle joint, and COX-2 activity in activated human umbilical vein endothelial cells. In conclusion, we have demonstrated that PC association results in increases in ibuprofen's anti-inflammatory and analgesic activity in rodent models of acute and chronic joint inflammation, and this effect may relate to alterations in drug bioavailability and COX-inhibitory potency.
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This study suggests that Ibuprofen has no preventive effect on progressive dermal ischemia after burning.
Effective management of migraine headache in children and adolescents requires a balanced approach with an individually tailored regimen targeted to treat an acute attack at its onset, blended with bio-behavioral measures, and, in about 1/3 of patients, daily preventive medicines. The key first step is to assess the disability imposed by the recurrent headache pattern, the headache "burden." Once the burden is established decisions can be made toward selecting the most appropriate course of action. All patients will benefit from some basic bio-behavioral suggestions such as regular sleep, exercise, and eating schedule, moderation of caffeine, and identification of triggers. In addition, all patients should have a readily available analgesic to be used at the onset of a migraine attack. A subset of migraineurs will have sufficient headache burden to necessitate use of daily preventative medications. Unfortunately, there is limited controlled data to provide a comprehensive, evidence-based guideline, however, the most rigorously studied agents for acute treatment are ibuprofen, acetaminophen, and "triptan" nasal spray forms of sumatriptan and zolmitriptan; all of these have shown safety and efficacy in controlled trials. For preventive treatment, flunarizine, not available in the U.S., is the only agent that has demonstrated efficacy in placebo controlled trials, but encouraging data is emerging regarding the use of several antiepileptic agents such as topiramate, disodium valproate, and levetiracetam, as well as the antihistamine cyproheptadine and the antidepressant amitriptyline.
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The dose-dependent analgesic effect of aerosolized ibuprofen was studied in comparison with the oral treatment. It was found that the dose for aerosol treatment is three to five orders of magnitude less than that required for oral treatment at the same analgesic effect. Accompanying effects were moderate venous hyperemia and some emphysematous signs.
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Topical non-steroidal anti-inflammatory drugs are effective in relieving pain in acute and chronic conditions.
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Binding sites on human serum albumin (HSA) for anionic drugs and fatty acids have been thermodynamically characterized by microcalorimetry. The binding and the thermodynamic parameters were directly computed from the calorimetric titration data at 37 degrees C in a phosphate buffer (pH 7.4) using one- and two-class binding models. From compensation analyses plotting the molar enthalpy change (delta Hm,i) versus those of the molar free energy (delta Gm,i) and molar entropy (delta Sm,i) for each class of binding sites, HSA binding sites were classified into groups S1, S2, and S3. Group S1 included high-affinity binding sites for site II-bound drugs, such as ibuprofen, flufenamic acid, and ethacrynic acid, and short- or medium-length alkyl-chain fatty acids; group S2 included low-affinity binding sites of site II-bound drugs and long-length alkyl-chain fatty acids; and group S3 contained the high-affinity binding sites for site I-bound drugs, such as phenylbutazone, oxphenbutazone, and warfarin, and long-length alkyl-chain fatty acids. High- and low-affinity bindings sites for salicylic acid and acetylaslicylic acid agreed with the regions of groups S3 and S2, respectively. Groups S1 and S2 were characterized by large negative values of delta Hm,i and delta Sm,i, reflecting van der Waals interaction and hydrogen-bonding formation in low dielectric media, and the main force to stabilize the binding complex in group S3 was a hydrophobic interaction, characterized by a small negative delta Hm,i and minor or positive values of delta Sm,i (entropy-driven).
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The High-Dimensional Propensity Score (hd-PS) algorithm can select and adjust for baseline confounders of treatment-outcome associations in pharmacoepidemiologic studies that use healthcare claims data. How hd-PS performance is affected by aggregating medications or medical diagnoses has not been assessed.