Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Naproxen”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1987

The effects of naproxen and sulindac on renal function and their interaction with hydrochlorothiazide and piretanide in man.

We have studied the effect of a single dose challenge of naproxen (500 mg) and sulindac (200 mg) on renal function in five volunteers, and the effect of a single dose challenge of the thiazide, hydrochlorothiazide (100 mg), and loop diuretic, piretanide (6 mg) on renal function when the diuretics were given alone or when superimposed on chronic therapy of either naproxen or sulindac. None of the nonsteroidal anti-inflammatory drug (NSAID) or diuretic exposures significantly influenced glomerular filtration rate, as measured by creatinine clearance. Over the first 4 h of the study, both naproxen and sulindac reduced fractional excretion of sodium by approximately 50%. Sulindac also caused a significant uricosuria whilst naproxen promoted urate retention. Similar changes were observed over 8 h. Superimposition of either hydrochlorothiazide or piretanide on top of chronic sulindac therapy resulted in a blunting of the natriuresis by approximately 30% compared to when these diuretics were given alone: the action of the diuretics was unchanged by naproxen. Sulindac pretreatment did not alter the urinary excretion of either hydrochlorothiazide or piretanide; naproxen did not alter hydrochlorothiazide excretion. On the basis of these findings, it is concluded that NSAIDs exert direct tubular effects that do not necessarily interfere with the delivery of diuretics to their sites of action within the nephron.

Adult↗
PubMed2004

Topical provocation in fixed drug eruption due to metamizol and naproxen.

The aim of this study was to investigate the usefulness of topical provocation in the diagnosis of metamizol- and naproxen-induced fixed drug eruption (FDE). Five patients with metamizol- and four patients with naproxen-induced FDE established by oral provocation were tested with the causative drugs at concentrations of 10%, 20%, and 50% in white petrolatum both on previously involved and uninvolved skin using the occlusive patch test technique. Additionally, four patients with metamizol- and five patients with naproxen-induced FDE, and 20 healthy controls were tested openly with drug preparations in dimethyl sulfoxide (DMSO). Tape-stripping occlusive patch testing in petrolatum remained negative in all. Open testing with drug preparations in DMSO revealed positive results in all four patients tested with metamizol mainly at concentrations of 20%, and in three of five patients tested with naproxen exclusively at concentrations of 50%. No positive reaction was seen on previously uninvolved skin and in healthy controls with any drug concentration and pure DMSO. In conclusion, repeated open testing with concentrations of the drugs up to 50% in DMSO seems to be a reliable test method in metamizol-induced FDE whereas oral provocation is still the most reliable method for naproxen-induced FDE as false negative results were common when testing topically with naproxen.

Adolescent↗
PubMed1994

A comparison of severe gastric damage as a result of pirprofen and naproxen treatment in rheumatoid arthritis: a controlled endoscopic study.

OBJECTIVE: The aim of this controlled endoscopic study was to compare the therapeutic efficacy and the gastric tolerance of two nonsteroidal anti-inflammatory drugs, pirprofen versus naproxen. DESIGN: A randomized endoscopic double-blind double-dummy study. SETTING: The gastrointestinal unit of a teaching hospital. SUBJECTS: Forty patients suffering from rheumatoid arthritis were enrolled. After an initial upper gastrointestinal endoscopy to rule out the presence of gastric mucosal lesions, the patients were randomly allocated in a double-blind, double-dummy manner, to receive either pirprofen (400 mg t.i.d.) or naproxen (500 mg b.i.d.) for 4 weeks; endoscopic control followed this treatment period, or was anticipated in the event of painful dyspepsia. INTERVENTIONS: Endoscopy at the beginning of the study and at 4 weeks, or anticipated in the event of painful dyspepsia. MAIN OUTCOME MEASURES: Primary outcome measure of the study was the possibility that pirprofen was less toxic to the gastric mucosa than naproxen, and at least as effective. RESULTS: Both drugs proved effective in relieving clinical symptoms, without a statistically significant difference. Gastric mucosa lesions were observed in 90% of pirprofen-treated patients and in 60% of those on naproxen (P = 0.03). The most severe lesions (grades 3 and 4) were found in 65% of subjects treated with pirprofen, as opposed to 15% of those treated with naproxen (P = 0.001). CONCLUSIONS: This study shows that pirprofen is at least as active as naproxen in relieving rheumatic symptoms, but its administration results in a significantly severe degree of gastric damage.

Adult↗
PubMed2003

Incidence of outpatient physician claims for upper gastrointestinal symptoms among new users of celecoxib, ibuprofen, and naproxen in an insured population in the United States.

OBJECTIVE: The aim of this study was to compare the risk of outpatient medical claims for UGI symptoms among new users of celecoxib versus ibuprofen, and naproxen. METHODS: The study was conducted using LifeLink, an insurance claims database of approximately 1.8 million employees, dependents, and retirees in the United States. Patients newly treated with a prescription of celecoxib, ibuprofen, or naproxen between June 1, 1999, and June 30, 2001, were included. A patient with an upper GI (UGI) symptom was any individual with an outpatient physician claim for dyspepsia (ICD-9 = 536.8), abdominal pain (789.0), or nausea/vomiting (787.0). Incidence was determined using person-time analysis. Multivariate analyses were conducted using Poisson and Cox regression models. RESULTS: The cohort consisted of patients prescribed celecoxib (n = 68,939), ibuprofen (n = 71,456), or naproxen (n = 50,014). At baseline, celecoxib users were older and more likely to have a history of UGI or cardiovascular conditions. The incidence rate of any UGI symptom was 0.46 per 1,000 patient-days for celecoxib, 0.70 for ibuprofen, and 0.62 for naproxen. After adjusting for confounding factors using Poisson regression, the ibuprofen rate was 48% higher than the celecoxib rate (incidence rate ratio (IRR) = 1.48; 95% CI = 1.39-1.58; p < 0.001), whereas the naproxen rate was 40% higher (IRR = 1.40; 95% CI = 1.31-1.49; p < 0.001). The association between drug use and UGI symptoms was confirmed by Cox regression analysis; the hazard ratios were 1.21 (95% CI = 1.13-1.29; p < 0.001) for ibuprofen and 1.15 (95% CI = 1.07-1.23; p < 0.001) for naproxen relative to celecoxib. Younger age, female sex, medical history of UGI, cardiovascular and renal conditions, and higher baseline average healthcare expenditures for the 12-month period preceding the index prescription were also significantly associated with an increased incidence of UGI symptoms. CONCLUSIONS: Celecoxib use is associated with a significantly decreased risk of outpatient physician claims for UGI symptoms compared with commonly used prescription nonspecific nonsteroidal anti-inflammatory drugs.

Abdominal Pain↗
PubMed1991

Use of digital radiography to demonstrate the potential of naproxen as an adjunct in the treatment of rapidly progressive periodontitis.

The effect of the non-steroidal anti-inflammatory drug, naproxen, in reducing periodontal disease activity was assessed in 15 patients with rapidly progressive periodontitis. All patients in this double-blind study were treated with scaling and root planing. Thereafter, 7 patients receiving 500 mg naproxen b.i.d. for 3 months, and 8 patients received placebo. Disease activity was assessed in three ways. First, alveolar bone height was determined using standardized radiography. Second, alterations in alveolar bone metabolism were assessed using 99m-Tc-methylene diphosphonate uptake prior to dosing and 3 months later. Finally, bone loss or gain was detected using digital subtraction radiography. In this study, conventional subtraction images were processed to isolate the area of change and superimpose the change on the original radiograph. This allowed determination of both the direction and location of osseous changes. There was significantly less bone loss as determined by analysis of bone height during the 3-month study in the naproxen-treated patients when compared to the placebo-treated patients (p less than 0.001). Radiopharmaceutical uptake was significantly reduced in the alveolar bone in patients receiving naproxen (p less than 0.03), whereas no significant change was observed in the placebo-treated patients. Furthermore, the subtraction radiographs showed a significant increase in the proportion of teeth demonstrating bone gain in the naproxen-treated group. These findings indicate that naproxen may be a useful adjunct to scaling and root planing in patients with rapidly progressive periodontitis.

Adolescent↗
PubMed1990

Effect on gastric and duodenal mucosal prostaglandins of repeated intake of therapeutic doses of naproxen and etodolac in rheumatoid arthritis.

The synthesis of gastric and duodenal mucosal prostaglandin E2, prostaglandin I2, and thromboxane B2 during a 60 minute incubation of biopsy specimens, the degree of endoscopic and histological damage, and the anti-inflammatory response were all studied after a four week, double blind study of therapeutic doses of two non-steroidal anti-inflammatory drugs, naproxen and etodolac, received by 27 patients with active rheumatoid arthritis (13 receiving naproxen, 14 etodolac). Prostaglandin values after treatment did not differ from the baseline levels when all the patients were analysed as one group. Subgroup analysis showed that naproxen suppressed gastric prostaglandin E2 from a median of 29 to 9 ng/mg protein, duodenal prostaglandin E2 from 34 to 11 ng/mg, and duodenal prostaglandin I2 from 62 to 15 ng/mg protein. No overall suppression occurred with etodolac. Also, on the second assessment patients receiving naproxen had lower gastric and duodenal prostaglandin E2 and prostaglandin I2, but higher values of duodenal thromboxane B2, than patients receiving etodolac. Both drugs had comparable anti-arthritic activity and caused microscopic gastritis in similar proportions of patients. No correlation was detected between prostaglandin values and the mucosal damage which developed in seven patients receiving naproxen (54%) and three receiving etodolac (21%). These findings indicate that, unlike naproxen, etodolac does not seem to affect gastric or duodenal prostaglandin synthesis; other mechanisms of injury need to be considered.

Adolescent↗
PubMed2001

Selective inhibition of COX-2 in humans is associated with less gastrointestinal injury: a comparison of nimesulide and naproxen.

BACKGROUND: Selective inhibitors of cyclooxygenase (COX)-2 may provoke less gastric damage and platelet inhibition than conventional non-steroidal anti-inflammatory drugs. AIMS: We compared the biochemical and gastrointestinal effects of nimesulide, a potent and selective COX-2 inhibitor, with naproxen which exhibits no selectivity. SUBJECTS: Thirty six healthy volunteers were randomised to nimesulide 100 mg or naproxen 500 mg twice daily for two weeks in a double blind, crossover study with a washout between treatments. METHODS: Gastrointestinal side effects were assessed by endoscopy, and by estimation of small intestinal absorption-permeability and inflammation. Comparisons were made between variables at the end of each treatment phase. RESULTS: Nimesulide caused significantly less gastric injury using the modified Lanza score (p<0.001) as well as reduced duodenum injury (p=0.039). Nimesulide had lower visual analogue scores (VAS) for haemorrhage and erosive lesions in the stomach (p<0.001) and for mucosal injection in the duodenum (p=0.039). Naproxen increased excretion of calprotectin, a marker of intestinal inflammation (5.5 (1.2) to 12.1 (2.1) mg/l) while nimesulide had no effect (treatment difference p=0.03). Naproxen abolished platelet aggregation to arachidonic acid and suppressed serum thromboxane B(2) (TXB(2)) by 98%, indices of COX-1 activity. In contrast, nimesulide had no significant effect on platelet aggregation, although it reduced serum TXB(2) by 29%. Production of prostaglandin E(2) and prostacyclin by gastric biopsies, also COX-1 dependent, was inhibited by naproxen, but not by nimesulide. COX-2 activity, determined as endotoxin induced prostaglandin E(2) formation in plasma, was markedly suppressed by both treatments. INTERPRETATION: Nimesulide has preferential selectivity for COX-2 over COX-1 in vivo at full therapeutic doses and induces less gastrointestinal damage than that seen with naproxen in the short term.

Adolescent↗
PubMed2000

Antihypertensive properties of a nitric oxide-releasing naproxen derivative in two-kidney, one-clip rats.

Nonsteroidal anti-inflammatory drugs have been reported to exacerbate hypertension. In this study, we tested the hypothesis that a nitric oxide-releasing derivative of naproxen would ameliorate hypertension in the rat. Hypertension was induced by partially occluding one renal artery (the "2K,1C" model), and 2 wk later the rats started receiving naproxen, the nitric oxide-releasing derivative HCT-3012, or vehicle each day for 2 wk. Naproxen significantly exacerbated the hypertension. HCT-3012 significantly reduced blood pressure relative to both the naproxen- and vehicle-treated groups. Both naproxen and HCT-3012 markedly suppressed whole blood thromboxane B(2) synthesis. In studies of anesthetized rats, naproxen significantly enhanced the late hypertensive response to endothelin-1 and significantly blunted the early hypotensive response. In contrast, HCT-3102 did not affect either response to endothelin-1. In vitro, HCT-3012 significantly reduced the responsiveness of aortic rings to the contractile effects of phenylephrine. These studies suggest that HCT-3012 reduces blood pressure in hypertensive rats, not simply through the vasodilatory actions of the nitric oxide it releases, but through alterations in the responsiveness of the vasculature to endogenous pressor agents.

Animals↗
PubMed2001

A look at the safety profile of over-the-counter naproxen sodium: a meta-analysis.

As the trend for Americans to self-medicate continues to increase, it becomes important to review the safety of over-the-counter (OTC) medications. This article will review the safety of an OTC analgesic, Aleve (naproxen sodium). The objective of this meta-analysis is to evaluate the frequency of occurrence of all adverse events in subjects taking various doses of OTC naproxen sodium as compared to placebo. These varying doses and dosage regimens were studied individually and consisted of 220 to 880 mg administered in single, multiple, and PRN (as needed) doses of naproxen sodium. This meta-analysis confirmed the favorable safety profile of naproxen sodium at OTC doses and established that the overall occurrence of adverse events with naproxen sodium was comparable and in some cases significantly lower than placebo. These results indicate that treatment with naproxen sodium may be highly beneficial from a clinical and economical perspective and safe when adhering to labeled directions.

Adverse Drug Reaction Reporting Systems↗
PubMed1990

Effect of naproxen and sulindac on blood pressure response to atenolol.

Twenty-eight patients with mild to moderate essential hypertension well controlled by atenolol entered a five-week, double-blind, placebo-controlled trial of the effects of sulindac and naproxen on blood pressure (BP) control. Atenolol alone was administered during weeks 1, 3, and 5. Naproxen or sulindac was administered with atenolol during week 2, with crossover during week 4. Data were analyzed for 27 of the patients (one dropped out after developing a skin rash). Naproxen significantly increased the systolic BP compared with placebo (mean 4.0 mm Hg; 95 percent confidence interval, 1.1-7.0; p less than 0.05). There were no significant differences in systolic BP during sulindac administration compared with placebo or naproxen. No significant effects on diastolic BP were observed. Weight was increased by naproxen and sulindac compared with placebo (mean 0.6-0.8 kg, p less than 0.05), although not to a clinically significant extent. One-week therapy with naproxen has a greater potential than sulindac to increase systolic BP in well-controlled hypertensive patients receiving atenolol; however, the increase is minor and unlikely to be of clinical significance.

Adult↗
PubMed1984

A double-blind, parallel trial of oxaprozin versus naproxen in the treatment of osteoarthritis.

A double-blind trial was carried out in 24 patients with osteoarthritis of the knee or hip to compare the efficacy and tolerance of oxaprozin with that of naproxen. Patients were assigned at random to receive fixed doses of either 1200 mg oxaprozin once daily or 250 mg naproxen 3-times daily over a period of 8 weeks. Assessments made on entry and after 4 and 8 weeks of treatment showed that in the oxaprozin group there were significant mean decreases, indicating improvement in patient's condition, with respect to observer's opinion, patient's opinion, pain intensity and activity impairment at both on-therapy visits. In the naproxen group, there were significant mean decreases with respect to observer's opinion, patient's opinion, pain intensity and time to walk 15 metres. None of the mean differences between the groups was statistically significant. Adverse effects were reported for 3 of the 12 oxaprozin patients and 6 of the 12 naproxen patients. The specific adverse effects noted for more than 1 patient were diarrhoea for oxaprozin and dyspepsia for naproxen. No difference between the groups was statistically significant from this point of view. Laboratory determinations showed no toxicity in either group. It is concluded that once-daily oxaprozin is an effective and well-tolerated form of treatment for osteoarthritis, equivalent to naproxen given 3-times daily.

Adult↗
PubMed1988

Controlled-release naproxen compared with isoxicam in patients with osteoarthritis.

The therapeutic efficacy and tolerability of a new controlled-release 1000 mg tablet of naproxen (naproxen CR) were compared with 200 mg isoxicam in 100 out-patients with osteoarthritis. Medications were administered once daily for 4 weeks in a controlled, randomized, double-blind, parallel trial. Patients were assessed for duration of stiffness, global pain, pain in the worst affected joint, night pain, pain on full passive movement, and pain on selected activity. No statistically significant differences were found between naproxen CR and isoxicam for any of the efficacy variables. Only 3 patients (2 with naproxen CR, 1 with isoxicam) reported adverse events, all mild to moderate; no patient withdrew from the study. At the conclusion of the study, patients and physician evaluated therapeutic response independently; both drugs provided steady improvement as judged by patients and physician. Both physician and patients evaluated naproxen CR as very good or good for 36 (72%) patients, and isoxicam as good or very good for 35 (73%) patients. Naproxen CR and isoxicam proved equally effective and well-tolerated for the treatment of osteoarthritis in this study.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1985

Neoplastic fever responds to the treatment of an adequate dose of naproxen.

Twenty-one patients with neoplastic fever due to malignancy were treated with naproxen. A prompt and complete lysis of fever was obtained in 20 patients within 12 hours when an adequate dose of naproxen was given, and a sustained normal temperature was maintained in all responding patients while receiving naproxen except for one in whom a low grade fever recurred. Lysis of fever usually was followed by excessive sweating and subjective symptomatic improvement. However, when naproxen was discontinued in ten patients, febrile state to the pretreatment level recurred in seven patients within three days. This observation suggests naproxen has a definite and effective antipyretic activity against neoplastic fever although it may recur as the drug is discontinued. Naproxen may be a useful adjunctive agent in patients with neoplastic fever for a short-term symptomatic relief.

Adult↗
PubMed2002

Synthesis and properties of a naproxen polymeric prodrug.

A water-soluble polymeric prodrug containing a naproxen moiety was synthesized. The carboxylic groups of naproxen were condensed with the hydroxyl groups of 2-hydroxyethyl methacrylate (HEMA) to produce a drug-linked monomer, denoted HN. The polymeric prodrug was prepared by copolymerization of HN with methacrylic acid. The molar percentage of HN in the polymeric prodrug was 26 mol%, as determined by 1H NMR. To investigate the pertinence of this polymeric prodrug, the hydrolysis was studied in-vitro with or without esterase or lipase. The kinetics of enzymatic catalysis was calculated from a Lineweaver-Burk plot. The anti-inflammatory activity was evaluated using the carrageenan-induced oedema test. The polymeric prodrug released a major fraction of the free naproxen and a significant fraction of the hydroxyethyl ester derived-naproxen. The maximum hydrolysis rate Vmax, and the Michaelis constant Km were calculated to be 2.16 x 10(-5) equiv. mol L-1 min-1 and 5.11 x 10(-2) equiv. mol L-1. The maximum anti-inflammatory inhibition of free naproxen appeared at 2 h and quickly decreased thereafter. In contrast, the polymeric prodrug showed a maximum at around 2-3 h and then slowly decreased. This indicates that the polymeric prodrug displays greater potency than free naproxen in the inhibition of acute inflammatory processes over long periods.

Animals↗
PubMed1979

Clinical experience of naproxen in the treatment of primary dysmenorrhea.

The effect of naproxen, Naprosyn, Syntex, in treatment of primary dysmenorrhea was studied in a double-blind, randomized, placebo controlled multicenter study. Nintyseven women, aged between 18--40 years, with severe dysmenorrhea, were treated with either naproxen, 48 women, or placebo, 49 women, for two consecutive menstrual cycles. No oral contraceptive was used. The patients were allowed to take supplementary analgesics 4--6 hours after the study drug was taken if adequate relief was not achieved. The recommended dose of naproxen was 1--2 tablets, 250 mg, as needed, with a maximum of 5 tablets daily. Medication was started at first sign of menstrual distress. Improvement was achieved in 70 per cent of the women in the naproxen group (good to excellent relief) but only in 30 per cent in the placebo group. This difference is statistically significant (p less than 0.001). There was much more supplementary medication used in the placebo group compared to the naproxen treated patients (p less than 0.001). Fewer patients had to stay in bed, or stay at home from work or school, in the naproxen group compared to the placebo group. Few side-effects were reported and most of them belonged to the dysmenorrhea symptomatology. No side-effects could be rement according to the patients' own judgement.

Adult↗
PubMed1985

Gastroscopic findings after treatment with enteric-coated and plain naproxen tablets in healthy subjects.

The damaging effect of enteric-coated and plain naproxen tablets on the gastric mucosa was studied in 12 healthy subjects before and after 7 days' treatment in a randomized, double-blind, double-dummy, cross-over trial. Both formulations of the drug caused mucosal lesions, but the extent of the damage was significantly decreased after enteric-coated naproxen as compared with plain tablets. The subjects' preference was significantly in favour of the enteric-coated naproxen tablets. The plasma naproxen concentration was significantly higher after treatment with enteric-coated naproxen than after treatment with plain tablets. In conclusion, the results of the study indicate that naproxen might damage the gastric mucosa by local and systemic effects and that the local effect might be prevented by enteric coating of the tablets.

Adult↗
PubMed1989

Optimal assessment of gastrointestinal side effects induced by non-steroidal anti-inflammatory drugs. Endoscopic lesions, faecal blood loss, and symptoms not necessarily correlated, as observed after naproxen and oxindanac in healthy volunteers.

Gastrointestinal side effects caused by naproxen and oxindanac (a developmental non-steroidal anti-inflammatory drug) were compared by combined endoscopy and determination of faecal blood loss in 16 healthy male volunteers in a randomized, double-blind, crossover study. Individual daily faecal blood loss was determined by means of 51Cr-labelled erythrocytes. Gastroduodenoscopy was performed before and after administration of naproxen, 750 mg/day, and oxindanac, 600 mg/day, for 1 week each. A washout period of at least 3 weeks was inserted between drug periods. Visual analogue scales (VAS) were used for endoscopic assessment of lesions and subjective complaints. Mean faecal blood loss increased from a base line 0.48 ml/24 h to 1.59 ml/24 h with naproxen (p less than 0.01) and from 0.56 ml/24 h to 1.31 ml/24 h with oxindanac (p less than 0.01). VAS scores for gastroduodenal lesions increased significantly with both drugs. Naproxen caused a significantly greater increase than oxindanac (p less than 0.05). There was no correlation between gastrointestinal blood loss and endoscopic findings. Subjective symptoms were correlated to faecal blood loss with naproxen, but not to endoscopic findings. No such correlations were observed for oxindanac. Naproxen caused a significant prolongation of bleeding time (p less than 0.01), whereas the increase caused by oxindanac was not significant (p = 0.09).

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1986

Effects of sulindac and naproxen in patients with chronic glomerular disease.

Eight patients with chronic glomerulonephritis were treated with either naproxen or sulindac in an open randomized study to observe their effects on the urinary excretion of prostaglandins and renal function. Both drugs were given for 7 days. Naproxen caused a decrease (p less than 0.01) of 80% in prostaglandin PGE2 and decrease (p less than 0.01) of 55% in prostaglandin PGF2 alpha. Sulindac caused a decrease (p = 0.01) of 37% in PGE2 and a decrease (p less than 0.05) in PGF2 alpha of 13%. The decrease in urinary excretion of prostaglandins were greater (p less than 0.05) during the naproxen treatment. Naproxen caused a decrease (p less than 0.05) in 24-hour creatinine clearance of 14 ml/min, an increase (p less than 0.05) in plasma urea of 1.0 mmol/l, an increase (p less than 0.05) in plasma potassium of 0.4 mmol/l and a decrease (p less than 0.01) in 24-hour urinary excretion of albumin of 11 mumol. Sulindac did not change any of these parameters significantly. In conclusion, sulindac affects renal prostaglandin synthesis to a significantly minor degree than naproxen and contrary to naproxen it does not influence the renal function in patients with chronic glomerular disease.

Adult↗