Balanced pre-emptive analgesia: does it work? A double-blind, controlled study in bilaterally symmetrical oral surgery. (1/254)

We studied 32 patients undergoing bilateral symmetrical lower third molar surgery under general anaesthesia to determine if the combined effects of pre-emptive local anaesthetic block using 0.5% bupivacaine, together with i.v. tenoxicam and alfentanil had any benefits over postoperative administration. Patients acted as their own controls and were allocated randomly to have surgery start on one side, the second side always being the pre-emptive side. Difference in pain intensity between the two sides was determined using visual analogue scales completed by each individual at 6 h, and at 1, 3 and 6 days after operation. A long-form McGill pain questionnaire was also used to assess difference in pain intensity between the two sides on the morning after surgery. There was no significant difference in pain intensity at any time after surgery. Our findings indicate that the combined use of pre-emptive analgesia from 0.5% bupivacaine, tenoxicam and alfentanil did not reduce postoperative pain intensity in patients undergoing molar exodontia.  (+info)

Tenoxicam and paracetamol-codeine combination after oral surgery: a prospective, randomized, double-blind, placebo-controlled study. (2/254)

We studied 90 adults undergoing surgical removal of at least both lower third molar teeth as day cases under standardized general anaesthesia. Patients were allocated randomly (with stratification for surgeon) to receive tenoxicam 40 mg, tenoxicam 20 mg or placebo i.v. at induction of anaesthesia and orally (effervescent tablets) with food on each of the subsequent 2 days. Panadeine (paracetamol 500 mg-codeine 8 mg) was given before operation and was available as needed for pain thereafter, to a limit of two tablets every 4 h. Nefopam i.v. was also available. Efficacy variables and adverse reactions were assessed over 6 days. Over the 6-day period, patients who received tenoxicam reported less pain on rest (area under the curve; P < 0.05) and less disturbance in sleep (P < 0.01) even though they used fewer Panadeine tablets (P < 0.05). Differences between tenoxicam 40 mg and 20 mg were not significant. There was no significant difference in nefopam requirements or side effects, and no adverse event attributable to the study medication.  (+info)

Evaluation of 5-aminosalicylic acid (5-ASA) for cancer chemoprevention: lack of efficacy against nascent adenomatous polyps in the Apc(Min) mouse. (3/254)

Recent experimental and epidemiological evidence suggests that nonsteroidal anti-inflammatory drugs (NSAIDs) are effective in the prevention of colorectal cancer. However, the toxicity associated with the long-term use of most classical NSAIDs has limited their usefulness for the purpose of cancer chemoprevention. Inflammatory bowel disease (IBD) patients, in particular, are sensitive to the adverse side effects of NSAIDs, and these patients also have an increased risk for the development of intestinal cancer. 5-Aminosalicylic acid (5-ASA) is an anti-inflammatory drug commonly used in the treatment of IBD and may provide protection against the development of colorectal cancer in these patients. To directly evaluate the ability of 5-ASA to suppress intestinal tumors, we studied several formulations of 5-ASA (free acid, sulfasalazine, and Pentasa) at multiple oral dosage levels [500, 2400, 4800, and 9600 parts/million (ppm)] in the adenomatous polyposis coli (Apc) mouse model of multiple intestinal neoplasia (Min). Although the ApcMin mouse is not a model of colitis-associated neoplasia, it is, nonetheless, a useful model for assessing the ability of anti-inflammatory agents to prevent tumor formation in a genetically preinitiated population of cells. We used a study design in which drug was provided ad libitum through the diet beginning at the time of weaning (28 days of age) until 100 days of age. We included 200 ppm of piroxicam and 160 ppm of sulindac as positive controls, and the negative control was AIN-93G diet alone. Treatment with either piroxicam or sulindac produced statistically significant reductions in intestinal tumor multiplicity (95% and 83% reductions in tumor number, respectively; P < 0.001 versus controls). By contrast, none of the 5-ASA drug formulations or dosage levels produced consistent dose-progressive changes in polyp number, distribution, or size, despite high luminal and serum concentrations of 5-ASA and its primary metabolite N-acetyl-5-ASA. Thus, 5-ASA does not seem to possess direct chemosuppressive activity against the development of nascent intestinal adenomas in the ApcMin mouse. However, because intestinal tumor development in the ApcMin mouse is driven by a germline mutation in the Apc gene rather than by chronic inflammation, we caution that these findings do not definitively exclude the possibility that 5-ASA may exert a chemopreventive effect in human IBD patients.  (+info)

Analgesic and anti-inflammatory efficacy of tenoxicam and diclofenac sodium after third molar surgery. (4/254)

Tenoxicam and diclofenac sodium were compared with each other for analgesic efficacy following removal of third molars under general anesthesia. Thirty-five healthy patients between the ages of 18 and 28 yr were randomly allocated to two groups to participate in this study. Patients in Group A (n = 17) received a single intravenous injection of tenoxicam 40 mg at induction of anesthesia, followed by a 20-mg tablet given in the evening of the day of the operation and thereafter, one 20-mg tablet daily from days 2 to 7. Group B (n = 18) received a single intramuscular injection of diclofenac sodium 75 mg at induction of anesthesia, followed by a 50-mg tablet 4 to 6 hr after the operation and again, between 2100 hr and 2200 hr the same day. Thereafter, a 50-mg tablet was taken 3 times daily for the next 6 days. Pain was measured hourly for the first 4 hr postoperatively, then at 21 hr, and thereafter in the morning and the evenings on days 2 to 7. The highest pain scores were obtained 1 hr postoperatively for both trial groups. At 1 and 2 hr postoperatively, no statistical significant differences in pain scores could be shown for both groups. However, at 3 and 4 hr postoperatively, patients in the tenoxicam group experienced significantly (P < or = 0.05) less pain than those in the diclofenac sodium group. On the evening of the third postoperative day, the tenoxicam group of patients experienced significantly less pain (P < or = 0.05) than those in the diclofenac sodium group. This was again the case on the morning of the fourth postoperative day. On the fifth, sixth, and seventh postoperative days, the average pain scores for patients in the tenoxicam group were statistically significantly lower, both mornings and evenings, than those in the diclofenac sodium group of patients (P = 0.05).  (+info)

Ankylosing spondylitis: what is the optimum duration of a clinical study? A one year versus a 6 weeks non-steroidal anti-inflammatory drug trial. (5/254)

OBJECTIVE: To consider the relevance of the duration of a clinical trial in ankylosing spondylitis: long-term (i.e. 1 yr) vs short-term (i.e. 6 weeks) assessment of a non-steroidal anti-inflammatory drug (NSAID)-placebo controlled study. METHODS: The design was a prospective, multicentre, double-blind, placebo-controlled study of 6 weeks duration with a 12 months double-blind extension. Study drugs were placebo (n = 121) or active NSAID (n = 352). A decrease of at least 50% in pain and/or global assessment and/or functional impairment during the study defined the response to treatment. The percentage of patients discontinuing the study drug over time (life table analysis) permitted the evaluation of both the efficacy and toxicity. RESULTS: Among the 473 recruited patients, the percentage of responders was similar at 1 yr and week 6 with a highly statistically significant difference in favour of the active NSAID groups when compared to placebo (at 1 yr, 17% in the placebo group vs 37, 50 and 43% in the piroxicam 20 mg, meloxicam 15 mg and meloxicam 22.5 mg, respectively, for the patient's overall assessment) without any statistically significant difference between the three active groups. However, evaluation of the patients discontinuing the study drug during the 1 yr of the study permitted the detection of a statistically significant difference between the active NSAID groups. A lower percentage of patients taking meloxicam 22.5 mg had to discontinue the study drug when compared to either meloxicam 15 mg or piroxicam 20 mg (37% vs 53% and 53%, respectively, P < 0.05). By 52 weeks, drug-related upper gastrointestinal adverse events occurred in 13, 32, 20 and 18% in the placebo, piroxicam 20 mg, meloxicam 15 mg and meloxicam 22.5 mg groups, respectively. Some of the adverse events occurred only after week 6. CONCLUSION: This study suggests that a 1 yr trial might be of optimum value compared to a 6 week assessment in order to define better the efficacy and tolerability of NSAIDs in ankylosing spondylitis.  (+info)

Transport of ochratoxin A by renal multispecific organic anion transporter 1. (6/254)

In the present study, we investigated the transport of ochratoxin A (OTA) by kidney-specific organic anion transporter 1 (OAT1). When expressed in Xenopus laevis oocytes, OAT1 mediated sodium-independent uptake of OTA (Km = 2.1 microM). Piroxicam, which has been shown to prevent the nephrotoxicity of OTA, inhibited OAT1-mediated uptake of OTA. By contrast, another protective compound, aspartame, did not. Using a cell line derived from the mouse kidney terminal proximal tubule (S3) transfected with OAT1 cDNA, we investigated the transport of OTA and also its effect on cell proliferation and cell viability. S3 cells expressing OAT1 mediated the saturable transport of OTA (Km = 0.57 microM). Cell proliferation was suppressed in S3 cells expressing OAT1 when exposed to 2 and 10 microM OTA. This suppression was rescued by the coaddition of 1 mM p-aminohippurate in the media. The present study indicates that OTA is transported by OAT1 and that the accumulation of OTA via OAT1 in proximal tubular cells is the primary event in the development of OTA nephrotoxicity.  (+info)

Physical activity, body mass index, and prostaglandin E2 levels in rectal mucosa. (7/254)

BACKGROUND: Evidence suggests a relationship between prostaglandin levels in colonic mucosa and risk of colon cancer. Physical inactivity and a higher body mass index (BMI; weight in kilograms divided by [height in meters]2) have been consistently shown to increase risk of this cancer. We investigated whether higher levels of leisure-time physical activity or a lower BMI was associated with lower concentrations of prostaglandin E2 (PGE2) in rectal mucosa. METHODS: This study was conducted in 41 men and 22 women, 42-78 years of age, with a history of polyps, who participated in a randomized clinical trial testing the effects of piroxicam on rectal mucosal PGE2 levels. An [125I]PGE2 radioimmunoassay kit was used to determine PGE2 levels in samples of extracted rectal mucosa collected before randomization. Leisure-time physical activity was assessed through a self-administered questionnaire collected at baseline. The reported time spent at each activity per week was multiplied by its typical energy expenditure, expressed in metabolic equivalents (METs), to yield a MET-hours per week score. A repeated measures model was used to assess the effect of BMI and physical activity as predictors of PGE2 concentration. All statistical tests were two-sided. RESULTS: After adjustment for age, a higher BMI was associated with higher PGE2 levels (P = .001). A higher level of leisure-time physical activity was inversely associated with PGE2 concentration (P<.03). An increase in BMI from 24.2 to 28.8 kg/m2 was associated with a 27% increase in PGE2. An increase in activity level from 5.2 to 27.7 MET-hours per week was associated with a 28% decrease in PGE2. CONCLUSIONS: Physical activity and obesity may alter the risk of colon cancer through their effects on PGE2 synthesis.  (+info)

The elimination profiles of tenoxicam and hydroxytenoxicam in equine urine and serum after a 200-mg oral dose. (8/254)

Tenoxicam (Mobiflex) was administered orally to four standardbred mares at a dose of 200 mg. Elimination profiles of tenoxicam and hydroxytenoxicam were generated based on quantitation of these analytes in urine and serum by liquid chromatography (LC) with ultraviolet detection. Tenoxicam was confirmed by LC-tandem mass spectrometry daughter ion mass spectra in the last postadministration sample in which tenoxicam was detected. The tenoxicam and hydroxytenoxicam urinary elimination profiles had the same shape for the same horse; however, each horse was significantly different from the others. One horse (Horse 15) showed a much broader and flatter elimination profile than the other horses. Each horse had a peak in analyte concentration at different collection times. The latest detection for both tenoxicam and hydroxytenoxicam was 29-31 h for all horses. The urinary tenoxicam limit of detection (LOD) and limit of quantitation (LOQ) were 0.3 and 0.4 microg/mL, respectively. The urinary hydroxytenoxicam LOD and LOQ were 0.6 and 0.8 microg/mL, respectively. Hydroxytenoxicam was found to be completely conjugated and tenoxicam completely unconjugated in equine urine. Serum elimination profiles of tenoxicam were measured to 120 h postadministration. Hydroxytenoxicam was not detected in postadministration serum. The last serum tenoxicam detection was at the 24-h collection time for all horses. The peak average concentration was 434.5 ng/mL at 3 h. The serum tenoxicam LOD and LOQ were 5.7 and 7.3 ng/mL.  (+info)

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