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PubMed2006

The efficacy and safety of aceclofenac versus placebo and naproxen in women with primary dysmenorrhoea.

OBJECTIVE: To determine the analgesic efficacy and safety of a single oral dose of aceclofenac 100 mg and compare that with placebo and naproxen 500 mg in women with primary dysmenorrhoea. STUDY DESIGN: In this double-blind, prospective, multicentre, randomised, three-way, crossover study, women were randomly assigned to receive one of six treatment sequences, comprising single oral doses of aceclofenac 100 mg, naproxen 500 mg or placebo, when menstrual pain reached a predetermined level of severity. A single dose of the assigned study medication was taken on three menstrual periods; a different medication was taken on each treatment day. Analgesic efficacy was determined by self-reported analgesia scoring and participants' and investigators' global evaluation of treatment effectiveness. Measurements also included physical examination and adverse events. RESULTS: Total pain relief scores were not statistically significantly different for aceclofenac and naproxen, and both were statistically significantly more effective than placebo (p = 0.019 and 0.002, respectively). This finding was supported by secondary endpoints including sum of pain intensity differences (SPID/8), peak analgesia (peak pain intensity and peak pain relief), and participants' and investigators' overall evaluation of effectiveness. Both aceclofenac and naproxen were well tolerated. CONCLUSIONS: Aceclofenac (100 mg) and naproxen (500 mg) effectively treated the pain associated with primary dysmenorrhoea, and both were more effective than placebo at easing menstrual pain assessed by various pain relief criteria.

Adolescent↗

PubMed2004

Thermodynamics of solutions III: comparison of the solvation of (+)-naproxen with other NSAIDs.

Naproxen was studied by classical thermoanalytical methods, namely sublimation calorimetry, solution calorimetry and the solubility method. Temperature dependence of a saturated vapor pressure was obtained and the sublimation enthalpy, deltaHsub(0) and entropy, deltaSsub(0) and their relative fraction of the total process were calculated. These parameters yielded for naproxen were compared to the respective data of other naphthalene derivatives. The crystal lattice energy of naproxen was calculated by two force fields (Gavezzotti et al. and Mayo et al.) and compared to the experimental data. Contributions of different motifs of the naproxen molecule to the total packing energy were analyzed. The Gibbs energy of solvation as well as enthalpic and entropic terms thereof in aliphatic alcohols have been studied for naproxen, and compared to model substances and other non-steroid anti-inflammatory drugs (benzoic acid, diflunisal and flurbiprofen). The major driving force of the solvation process is the enthalpy. The respective contributions of the specific and the non-specific solvation interactions in terms of absolute and relative values have been investigated.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2005

Protective effect of astaxanthin on naproxen-induced gastric antral ulceration in rats.

Frequently used for humans as non-steroidal anti-inflammatory drug, naproxen has been known to induce ulcerative gastric lesion. The present study investigated the in vivo protective effect of astaxanthin isolated from Xanthophyllomyces dendrorhous against naproxen-induced gastric antral ulceration in rats. The oral administration of astaxanthin (1, 5, and 25 mg/kg of body weight) showed a significant protection against naproxen (80 mg/kg of body weight)-induced gastric antral ulcer and inhibited elevation of the lipid peroxide level in gastric mucosa. In addition, pretreatment of astaxanthin resulted in a significant increase in the activities of radical scavenging enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. A histologic examination clearly proved that the acute gastric mucosal lesion induced by naproxen nearly disappeared after the pretreatment of astaxanthin. These results suggest that astaxanthin removes the lipid peroxides and free radicals induced by naproxen, and it may offer potential remedy of gastric ulceration.

Adjuvants, Immunologic↗

PubMed2003

Ternary naproxen: beta-cyclodextrin:polyethylene glycol complex formation.

The aim of this study was to investigate the effect of the presence of the water-soluble polymer polyethylene glycol (PEG)-MW=35000 g/mol-on the complexation of the phototoxic anti-inflammatory drug naproxen, in its sodium salt form, with beta-cyclodextrin (beta-CD). The data revealed that the polymer does not interact with the uncomplexed naproxen whereas it does with the beta-CD. The presence of different proportions of PEG, in the 0-1% (w/w) range, systematically lowers K(app) of the formation of the naproxen:beta-CD inclusion complex. The reason for the decrease in the complexed drug is the presence of other competing equilibria, the first one is an interaction of the polymer with the beta-CD, which in turn reduces the amount of free CD available for including the naproxen, and the second is the formation of a naproxen:beta-CD:PEG ternary complex with lower affinity than the binary complex. The binding constant of these processes are K(2)=(4.5+/-1.0) x 10(5) M(-1) and K(3)=870+/-19 M(-1), respectively. In addition the presence of the PEG produces an important change in the driving force of the complex formation. In this case the process is enthalpically unfavoured and entropically favoured; these are typical characteristics of processes governed by hydrophobic interactions.

Cyclodextrins↗

PubMed2004

Effect of binary and ternary polyvinylpyrrolidone and/or hydroxypropyl-beta-cyclodextrin complexes on the photochemical and photosensitizing properties of Naproxen.

The effect of the polyvinylpyrrolidone and/or hydroxypropyl-beta-cyclodextrin on the photo-lability of aqueous solutions of the anti-inflammatory drug Naproxen was studied. Kinetic studies revealed that the presence of all of these additives reduced drug photodegradation. In all cases, the presence of the different additives elicited a change in the photomixture composition, being the alcoholic derivative the major photoproduct formed. Nevertheless, the change in the efficiency of the process and the amount of the photoproducts formed in the different systems were not related with the biodamage produced by the drug. In this sense, the presence of free Naproxen clearly sensitized the photoperoxidation of linoleic acid. The photosensitizing effect decreased as the PVP concentration increased. Different protection provides the binary (Naproxen:HP-beta-CD) and ternary (Naproxen:HP-beta-CD:PVP) complexes. The binary complex formation had not effect on the prevention of photooxidation of linoleic acid sensitized by the drug, whereas the ternary complex formation suppresses the drug effect. The different behaviour observed with beta-CD and HP-beta-CD and the structural differences of both cyclodextrins seem to indicate that in the case of the HP-beta-CD the linoleic binds with the CD and takes contact with the drug. These results confirm that in these systems the prevention of biodamage would be due to a decrease in the contact between the short-lived species generated during Naproxen photodegradation and biological structures, rather than due to the nature or amount of the photoproducts. In addition, the ability of the complex to interact with the biological structure depends on the structure of both interacting species.

2-Hydroxypropyl-beta-cyclodextrin↗

PubMed2004

Differential effects of naproxen and rofecoxib on the development of hypersensitivity following nerve injury in rats.

The present study was undertaken to determine the effects of cyclooxygenase (COX) inhibitors on the development of neuropathic pain in rats following chronic constriction injury (CCI). A single intraperitoneal administration of naproxen, a nonselective COX inhibitor (10 or 30 mg/kg), or rofecoxib, a selective COX-2 inhibitor (3 or 10 mg/kg) 2 h before nerve injury did not attenuate the development of neuropathic state for 28 days. However, the administration of naproxen [10 or 30 mg/kg, intraperitonelly (i.p.)], but not rofecoxib (3 or 10 mg/kg, i.p.), on day 7 attenuated hypersensitivity but did not alter its development for 28 days. Furthermore, naproxen significantly reduced hyperalgesia and allodynia for 4 h, but the efficacy was not observed 24 h after the treatment, whereas rofecoxib failed to modify the hypersensitivity following perineural (p.n.) or intrathecal (i.t.) administration on day 7. Chronic administration of naproxen (3, 10 or 30 mg/kg), but not rofecoxib (1, 3 or 10 mg/kg), 2 h before, daily for 7 days, after nerve injury significantly attenuated and further delayed the development of hypersensitivity for 21 days following nerve injury. These results suggest that the development of hypersensitivity in the CCI model is not COX-2 dependent and that the chronic administration of naproxen started early before peripheral nerve injury could attenuate the development of hypersensitivity.

Animals↗

PubMed2006

Naproxen treatment prevents periprocedural inflammatory response but not myocardial injury after percutaneous coronary intervention.

BACKGROUND AND AIM: Recent studies have documented that elevation of C-reactive protein (CRP) levels after percutaneous coronary intervention (PCI) have been predictive of adverse outcome. This study was performed to test the hypothesis that preprocedural use of naproxen sodium is associated with a reduction in the extent of inflammatory response and myocardial injury after PCI. METHODS: Ninety-seven patients who were scheduled for elective PCI were randomized either for naproxen sodium (500 mg bid) (n:39, 75% male, 59+/-10 years) or control (n:58, 76% male, 60+/-10 years). All patients were troponin negative before the procedure. Blood samples for CRP, Troponin I and CK-MB were collected at baseline and after the procedure. RESULTS: The characteristics were similar between the two groups. After coronary stenting, the rise in CRP levels was significantly higher in controls than those treated with naproxen (DeltaCRP=6.4 mg/L in the controls and 0.43 mg/L in the naproxen group, p<0.0001). The incidence of any troponin I elevation or CK-MB elevation above upper limit of normal was not statistically different between groups. During follow up (12+/-2 months), major cardiac adverse events (death, myocardial infarction, and revascularization of target lesion) was similar between groups. CONCLUSION: Our data show that naproxen pretreatment leads to significant suppression in PCI related CRP elevation. However this improvement in CRP levels was not associated with any significant reduction in post-PCI myonecrosis.

Aged↗

PubMed2003

Identification of the amino acids of human serum albumin involved in the reaction with the naproxen acyl coenzyme A thioester using liquid chromatography combined with fluorescence and mass spectrometric detection.

Xenobiotic carboxylic acids, that via their metabolites covalently modify proteins, have been associated with serious side effects in man. Such reactive metabolites may be acyl glucuronides or alternatively, the corresponding acyl-CoA thioesters. In this study, the reaction of a model xenobiotic acyl-CoA, the naproxen-CoA, with human serum albumin (HSA), was characterized by high-performance liquid chromatography employing fluorescence and mass spectrometric detection. One mM naproxen-CoA was incubated for 6h with HSA (0.45 mM) at 37 degrees C in a 0.1M phosphate buffer (pH 7.4). The tryptic digest of the reduced and alkylated protein was analyzed in order to identify the amino acids in the sequence that were covalently modified with naproxen. Fluorescent peptides, that represented naproxen-modified peptides, were characterized using HPLC-MS-MS and HPLC-MS in zoom scan mode, which provided information on the structure and the charge of the modified peptides. The naproxen-CoA reacted predominantly with lysine 199, lysine 541, and lysine 351, which was in agreement with the binding pattern that has previously been reported for the reactive acyl glucuronides and their reaction with HSA.

Acyl Coenzyme A↗

PubMed2001

Activation of peroxisome proliferator-activated receptor isoforms and inhibition of prostaglandin H(2) synthases by ibuprofen, naproxen, and indomethacin.

A series of nonsteroidal anti-inflammatory drugs (NSAIDs) [S(+)-naproxen, ibuprofen isomers, and indomethacin] were evaluated for their activation of peroxisome proliferator-activated receptor (PPAR) alpha and gamma isoforms in CV-1 cells co-transfected with rat PPAR alpha and gamma, and peroxisome proliferator response element (PPRE)-luciferase reporter gene plasmids, for stimulation of peroxisomal fatty acyl CoA beta-oxidase activity in H4IIEC3 cells, and for comparative inhibition of ovine prostaglandin endoperoxide H synthase (PGHS)-1 and PGHS-2 and arachidonic acid-induced human platelet activation. Each drug produced a concentration-dependent activation of the PPAR isoforms and fatty acid beta-oxidase activity, inhibition of human arachidonic acid-induced platelet aggregation and serotonin secretion, and inhibition of PGHS-1 and PGHS-2 activities. For PPARalpha activation in CV-1 and H4IIEC3 cells, and the stimulation of fatty acyl oxidase activity in H4IIEC3 cells, the rank order of stereoselectivity was S(+)- ibuprofen > R(-)-ibuprofen; S(+)-ibuprofen was more potent than indomethacin and naproxen on these parameters. On PPARgamma, the rank order was S(+)-naproxen > indomethacin > S(+)-ibuprofen > R(-)-ibuprofen. Each drug inhibited PGHS-1 activity and platelet aggregation with the same rank order of indomethacin > S(+)-ibuprofen > S(+)-naproxen > R(-)-ibuprofen. Notably, the S(+)-isomer of ibuprofen was 32-, 41-, and 96-fold more potent than the R(-)-isomer for the inhibition of PGHS-1 activity, human platelet aggregation, and serotonin secretion, respectively. On PGHS-2, the ibuprofen isomers showed no selectivity, and indomethacin, S(+)-ibuprofen, and S(+)-naproxen were 6-, 27-, and 5-fold more potent as inhibitors of PGHS-1 than PGHS-2 activity. These results demonstrate that the mechanisms of action of NSAIDs on these cell systems are different, and we propose that the pharmacological effects of NSAIDs may be related to both their profile of inhibition of PGHS enzymes and the activation of PPARalpha and/or PPARgamma isoforms.

Animals↗

PubMed1979

Determination of naproxen and its desmethyl metabolite in human plasma or serum by high performance liquid chromatography.

1. A liquid chromatographic method has been developed for the simultaneous determination of the anti-inflammatory agent naproxen and its metabolite, 6-0-desmethyl-naproxen, in human plasma or serum. 2. After addition of p-chlorowarfarin as the internal stardard, plasma is acidified and extracted with either chloroform (for assay of naproxen only) or ethyl acetate (for assay of naproxen and desmethyl-naproxen), the organic solvent is evaporated, the residue is dissolved in acetonitrile and injected onto a reverse phase column coupled with an ultra-violet absorbance detector. 3. Drug and metabolite can be detected readily in concentrations above 2 micrograms per ml in 0.5 ml samples. Salicylic acid and its metabolites and a number of other durgs were found not to interfere with the assay.

Chromatography, High Pressure Liquid↗

PubMed2001

Uniformly sized molecularly imprinted polymer for (S)-naproxen retention and molecular recognition properties in aqueous mobile phase.

A uniformly sized molecularly imprinted polymer (MIP) for (S)-naproxen has been prepared by a multi-step swelling and polymerization method using 4-vinylpyridine (4-VPY) and ethylene glycol dimethacrylate (EDMA) as a functional monomer and cross-linker, respectively. We optimized the preparation method of the MIP by changing the molar amounts of the template molecule and functional monomer. Further, we examined the effects of organic modifier type, column temperature and flow-rate on the retentivity and enantioselectivity for naproxen using a mixture of phosphate buffer and organic modifier (acetonitrile, ethanol and 2-propanol) as an eluent. When the amounts of (S)-naproxen, 4-VPY and EDMA used were 4, 6 and 25 mmol, respectively, the enantioselectivity and resolution for naproxen were good despite the shorter retention. When acetonitrile was used as an organic modifier, the highest column efficiency was obtained for the separation of naproxen enantiomers. With regard to the effects of column temperature and flow-rate, the column performance was improved by elevating a column temperature and decreasing a flow-rate.

Methacrylates↗

PubMedDate not supplied

Comparison of lumiracoxib with naproxen and ibuprofen in the Therapeutic Arthritis Research and Gastrointestinal Event Trial (TARGET), cardiovascular outcomes: randomised controlled trial.

BACKGROUND: The potential for cyclo-oxygenase 2 (COX2)-selective inhibitors to increase the risk for myocardial infarction is controversial. The Therapeutic Arthritis Research and Gastrointestinal Event Trial (TARGET) aimed to assess gastrointestinal and cardiovascular safety of the COX2 inhibitor lumiracoxib compared with two non-steroidal anti-inflammatory drugs, naproxen and ibuprofen. METHODS: 18325 patients age 50 years or older with osteoarthritis were randomised to lumiracoxib 400 mg once daily (n=9156), naproxen 500 mg twice daily (4754), or ibuprofen 800 mg three times daily (4415) in two substudies of identical design. Randomisation was stratified for low-dose aspirin use and age. The primary cardiovascular endpoint was the Antiplatelet Trialists' Collaboration endpoint of non-fatal and silent myocardial infarction, stroke, or cardiovascular death. Analysis was by intention to treat. FINDINGS: 81 (0.44%) patients did not start treatment and 7120 (39%) did not complete the study. At 1-year follow-up, incidence of the primary endpoint was low, both with lumiracoxib (59 events [0.65%]) and the non-steroidal anti-inflammatory drugs (50 events [0.55%]; hazard ratio 1.14 [95% CI 0.78-1.66], p=0.5074). Incidence of myocardial infarction (clinical and silent) in the overall population in the individual substudies was 0.38% with lumiracoxib (18 events) versus 0.21% with naproxen (ten) and 0.11% with lumiracoxib (five) versus 0.16% with ibuprofen (seven). In the naproxen substudy, rates of myocardial infarction (clinical and silent) did not differ significantly compared with lumiracoxib in the population not taking low-dose aspirin (hazard ratio 2.37 [95% CI 0.74-7.55], p=0.1454), overall (1.77 [0.82-3.84], p=0.1471), and in patients taking aspirin (1.36 [0.47-3.93], p=0.5658). In the ibuprofen substudy, these rates did not differ between lumiracoxib and ibuprofen in the population not taking low-dose aspirin (0.75 [0.20-2.79], p=0.6669), overall (0.66 [0.21-2.09], p=0.4833), and in patients taking aspirin (0.47 [0.04-5.14], p=0.5328). INTERPRETATION: The primary endpoint, including incidence of myocardial infarction, did not differ between lumiracoxib and either ibuprofen or naproxen, irrespective of aspirin use. This finding suggests that lumiracoxib is an appropriate treatment for patients with osteoarthritis, who are often at high cardiovascular risk and taking low-dose aspirin.

Aged↗

PubMed2001

Upper gastrointestinal safety evaluation of parecoxib sodium, a new parenteral cyclooxygenase-2-specific inhibitor, compared with ketorolac, naproxen, and placebo.

BACKGROUND: Conventional nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with an increased risk of ulcers and upper gastrointestinal (GI) ulcer complications, which has been attributed to the inhibition of cyclooxygenase-1. These risks are usually increased in elderly populations. Parecoxib sodium is an injectable prodrug of the cyclooxygenase-2-specific inhibitor valdecoxib that has exhibited analgesic activity in previous trials. OBJECTIVE: The purpose of this study was to compare the GI safety and tolerability profile of parecoxib sodium with that of ketorolac, naproxen, and placebo in a 7-day endoscopic trial in elderly subjects. METHODS: This was a randomized, double-blind, double-dummy, placebo-controlled, parallel-group study. After a normal baseline endoscopy, healthy elderly subjects aged 66 to 75 years were randomized to receive i.v. parecoxib sodium (10 mg BID), oral naproxen (500 mg BID), or placebo for 7 days, or placebo for 2 days followed by i.v. ketorolac (15 mg QID) for 5 days. Endoscopy was performed again after 7 days. RESULTS: Among the first 17 subjects enrolled, ulcers were observed in all treatment groups except the parecoxib sodium group (ketorolac, 4/4 subjects; naproxen, 2/4 subjects; and placebo, 2/5 subjects). Four subjects in the ketorolac group and 1 subject in the naproxen group had multiple gastric ulcers or combined gastric and duodenal ulcers. Because of the unexpectedly high incidence of gastroduodenal ulcers observed, the study was terminated early and the randomization blind broken. CONCLUSION: These findings suggest that elderly patients may be at risk for GI ulceration even after short-term use of the conventional NSAIDs ketorolac and naproxen.

Aged↗

PubMed1998

Polyorganophosphazene microspheres for drug release: polymer synthesis, microsphere preparation, in vitro and in vivo naproxen release.

Microsphere preparation for naproxen slow release was investigated using two newly prepared biodegradable polyorganophosphazenes, derivatized at the phosphorus atoms with phenylalanine ethyl ester and imidazole at molar ratios of 71/29 and 80/20. The polymers were prepared by substitution of the chloride atoms of polydichlorophosphazene with a phenylalanine ethyl ester-imidazole mixture followed, after 7 or 48 h reaction, by the addition of excess imidazole. Three methods of microsphere preparation have been considered: spray-drying, emulsion/solvent evaporation and emulsion/solvent evaporation-extraction. Microparticles obtained by spray-drying were found to possess a narrow distribution size with a mean diameter of 2-5 microm. Their internal structure consisted of a porous or empty core depending upon the solvent used for the preparation. Furthermore the microspheres prepared with this technique rapidly released the entrapped naproxen independently of the used polymer, the drug loading or the preparation process. On the other hand microspheres prepared by solvent evaporation or solvent evaporation-extraction showed a distribution size ranging between 10 and 100 microm. By the appropriate choice of pH and solvent composition of the external phase, naproxen could be entrapped, in these microspheres, with a yield higher of 80%. The polymer composition dictates the in vitro release rate of naproxen from the particles, which was faster when the microspheres were prepared with the polymer at higher imidazole content. In vivo experiments, carried out by subcutaneous implantation in rats of microspheres prepared by solvent evaporation, demonstrated that a constant level of naproxen in plasma could be maintained up to 400 h at a suitable concentration for antinflammatory activity.

Animals↗

PubMed1994

Cancellous bone behavior in hindlimb immobilized rats during and after naproxen treatment.

Temporary immobilization creates bone loss. The purpose of this investigation was to use an agent to protect the skeleton from bone loss bone during temporary immobilization. Eighty-nine 6-month-old retired breeder Sprague-Dawley female rats were used. Animals were randomly divided into six groups of equal numbers. Four groups were given drinking water from day 0, containing naproxen (100 or 200 mg/l). At day 7, half the animals in all groups had their right hindlimb immobilized. At day 49, half the immobilized rats and non-immobilized controls were sacrificed. The remaining rats were remobilized and the drug was stopped. At day 91, all remaining rats were sacrificed. Gastrocnemius and soleus muscle weights were determined. Right tibiae were analyzed for cancellous bone mass, bone structural and bone dynamic variables. At the close of immobilization, bone mass was lower in the right (immobilized) hindlimb of the immobilized group than in the non-immobilized group. Immobilized rats drinking 100 mg/l naproxen water had significantly higher bone mass in their immobilized limbs than did untreated immobilized rats, but all rats drinking 200 mg/l naproxen water had lower bone mass than controls. After 6 weeks of recovery, bone mass in the immobilized limb of untreated formerly immobilized rats improved, but remained below untreated never-immobilized rats. Formerly immobilized rats that had been treated with 100 mg/l naproxen water had normal bone mass after 6 weeks of recovery. Naproxen, an agent that mildly depresses activation frequency, prevents some of the transient bone mass and structural deterioration during temporary immobilization. Such treatment facilitates a more rapid return to normal bone mass, though not to normal structure. The more rapid recovery occurs because the difference from normal is less, not because of more rapid formation in recovering animals.

Analysis of Variance↗

PubMed1989

Severe metabolic acidosis after acute naproxen sodium ingestion.

Naproxen, a nonsteroidal anti-inflammatory drug (NSAID), is a propionic acid derivative that possesses analgesic and antipyretic properties through inhibition of prostaglandin synthesis. The propionic acids have been considered the least toxic of the NSAIDs, and one, ibuprofen, is currently available as an over-the-counter medication. Though acidosis has been reported with ibuprofen, no such occurrence has been reported for naproxen sodium. We report the case of a 15-year-old girl who presented with severe metabolic acidosis and seizures that rapidly followed naproxen sodium ingestion. Serum bicarbonate levels returned to normal 12 hours after admission and correlated with the known pharmacokinetics of naproxen. The pharmacokinetics of naproxen and treatment of its overdose, and possible mechanisms of metabolic acidosis are reviewed.

Acidosis↗

PubMed2002

Characterization of physicochemical properties of naproxen systems with amorphous beta-cyclodextrin-epichlorohydrin polymers.

Ground mixtures of naproxen with amorphous beta-cyclodextrin-epichlorohydrin soluble (betaCd-EPS) or insoluble cross-linked (betaCd-EPI) polymers were investigated for both solid phase characterization (Differential Scanning Calorimetry, powder X-ray Diffractometry) and dissolution properties (dispersed amount method). The effect of different grinding conditions and of drug-to-carrier ratio was also evaluated. Co-grinding induced a decrease in drug crystallinity to an extent which depended on the grinding time, and was most pronounced for the cross-linked insoluble polymer, particularly in combinations at the lowest drug content. Both cyclodextrin polymers were more effective in improving the naproxen dissolution properties, not only than the parent betaCd but also than hydroxyalkyl-derivatives, and their performance was almost comparable to that of methyl-derivatives, previously found as the best carriers for naproxen. Dissolution efficiencies of naproxen from physical mixtures with betaCd-EPS, thanks to the high water solubility of this Cd-derivative, were up to three times higher than those from the corresponding products with betaCd-EPI. However this difference in their performance became much less evident in co-ground products and tended to progressively diminish with increasing the polymer content in the mixture, according to the better amorphizing power shown by betaCd-EPI during the co-grinding process. The 10/90 (w/w) drug-carrier co-ground products exhibited the best dissolution properties, giving dissolution efficiencies about 30 times higher than that of naproxen alone.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1993

The clinical effect of naproxen sodium after arthroscopy of the knee: a randomized, double-blind, prospective study.

The aim of this study was to examine the clinical effect of naproxen sodium after knee arthroscopy. The design was randomized, prospective, and double-blind, with a placebo control group. Patients with preoperative synovial reaction were excluded. One hundred twenty consecutive arthroscopies were performed in 77 men and 43 women, median age 34 (range 18-65) years. General anesthesia was used. Ninety-one arthroscopies were operative, whereas 29 were diagnostic. Postoperatively the patients received either 550 mg naproxen sodium twice daily or placebo for 10 days. Patients were given 500 mg acetaminophen to use if needed. Clinical examinations were performed 10 and 20 days postoperation. The results were analyzed using the Mann-Whitney test and chi 2 test. No operative complications were registered. All but two patients completed the study. Six patients had slight gastrointestinal symptoms. At 10 days' follow-up, in patients who had undergone operative arthroscopy naproxen sodium demonstrated a statistically significant effect on synovial effusion (p < 0.01), range of motion (p < 0.001), quadriceps strength (p < 0.05), pain (p < 0.001), walking activity (p < 0.05), and use of crutches (p < 0.01). In patients who had undergone diagnostic arthroscopy naproxen sodium demonstrated a beneficial effect on pain (p < 0.01). At 20 days' follow-up, in the operative group naproxen sodium affected synovial effusion (p < 0.05), range of motion (p < 0.01) and pain (p < 0.05), and walking activity (p < 0.05). No effect was seen in the diagnostic group at 20 days' follow-up.

Adolescent↗