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We searched the Cochrane Renal Group's Specialised Register (to 27 November 2014) through contact with the Trials' Search Co-ordinator using search terms relevant to this review.
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In a double-blind trial, 427 patients older than 18 years, with documented acute symptomatic superficial vein thrombosis of the legs, were randomly assigned to receive subcutaneous enoxaparin sodium, 40 mg; subcutaneous enoxaparin, 1.5 mg/kg; oral tenoxicam; or placebo, once daily for 8 to 12 days. The primary efficacy outcome was deep venous thromboembolism between days 1 and 12, defined as deep vein thrombosis detected by ultrasonography between days 8 and 12 or earlier if clinically indicated, or documented symptomatic pulmonary embolism. For the secondary efficacy outcomes, superficial vein thrombosis recurrence or extension was also considered.
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This study was undertaken to assess the efficacy, acceptability and side-effects of the Norplant (Leiras) contraceptive system during adolescence.
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Interleukin 1 beta plus interleukin 6 suppressed 3H release and caused an increase in tissue prostaglandin E2 but not leukotriene E4. Piroxicam and cycloheximide but not MK886 attenuated the cytokine-induced increase in prostaglandin E2 and the suppression of [3H]norepinephrine release. Ultrastructural analysis showed macrophage-like cells in the plexus, and the cytokine effects were inhibited by cyclosporin A.
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A simple new method has been developed for producing subacute gastric ulcers in rats, and it has been combined with a novel method for the quantitative evaluation of the healing process. Fasted rats of body weight 120-150 g were used. The animals were anaesthesized by ether and then a polyethylene catheter was orally inserted in the stomach with a fine needle inside. After the cannula reached the gastric wall, the needle was pressed gently so as to punch the tastric wall. Drugs under study were administered orally 30 min and 24 hr after the puncture. Food and water were given ad libitum from 2 hr after the intervention until the end (96 hr) of experiments. In order to follow the healing process of subacute ulcer, the so-called tensile strength of the ulcer was determined by inflating and was expressed in mmHg. The healing rate was calculated. The antiulcer drugs, cimetidine, famotidin, pirenzepine, and sucralfate, dose dependently and significantly increased the healing rate of ulcer. Nonsteroidal antiinflammatory drugs, naproxen, piroxicam, indomethacin, and ibuprofen, significantly delayed the healing of ulcer and acetylsalicylic acid showed no significant effect on the healing. Strong HCl (0.5 molar) significantly delayed the healing of ulcer. N-EM given subcutaneously dose dependently delayed the healing of subacute ulcer.
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Nonsteroidal antiinflammatory drugs may reduce postoperative opioid consumption. We evaluated the analgesic efficacy of preoperatively administered tenoxicam in patients undergoing total abdominal hysterectomy. Patients were randomly assigned to receive IV either normal saline 4 mL (Group NS), tenoxicam 20 mg (Group T20), or tenoxicam 40 mg (Group T40) before the induction of anesthesia in a double-blinded fashion. Patient-controlled analgesia with fentanyl was used to assess postoperative opioid requirements. Pain was evaluated by visual analog scale at 2, 4, 6, 8, and 24 h postoperatively. Intraoperative bleeding as assessed by the surgeon, incidence of nausea, and gastrointestinal symptoms were recorded. No statistically significant difference was identified between groups in fentanyl consumption or pain scores. The incidence of nausea was similar in all groups. Two patients in Group T20 and two in Group T40 exhibited mild gastrointestinal symptoms. Intraoperative oozing was noted in two patients in Group T40. We conclude that patients undergoing total abdominal hysterectomy and receiving fentanyl via patient-controlled analgesia postoperatively do not benefit from tenoxicam pretreatment. On the contrary, the drug may be associated with an increased incidence of side effects.
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The aim of this study was to evaluate the analgesic efficacy and time to onset of effect of the lornoxicam quick-release (LNX-QR) tablet compared with the standard-release tablet (LNX-ST).
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Our objective was to determine the effectiveness of intraperitoneal single dose piroxicam and low molecular weight heparin (LMWH) on prevention of adhesion reformation in the rat uterine horn. This study was carried out in the Surgical Research Laboratory, at Erciyes University. A standard lesion was created by unipolar electrocautery in 72 uterine horns of 36 female Wistar-Albino rats. After 2 weeks, adhesion formation scores were determined and adhesiolysis was performed in the second-look laparotomy. Animals were then randomly assigned into three groups. Each group contained 12 animals: group 1 was the control group where no adjuvant was given; in group 2, 1 ml 50 U Axa IC/ml solution LMWH was applied to the horns postoperatively, and in group 3, 1 ml 2 mg/ml piroxicam solution was applied to the horns after adhesiolysis. Two weeks later the rats were killed and adhesion reformation was evaluated. The number of horns with adhesion formation and the cumulative scores were not significantly different among the three groups in the second-look laparotomies, but after third-look laparotomies, the number of horns with adhesion reformation, after calculating the extent, severity and total scores of adhesion reformation, was found to be significantly less in LMWH and piroxicam groups than in the control group. Also, the effectiveness of piroxicam was significantly greater in all scores of adhesion reformation than LMWH was. In conclusion, both LMWH and piroxicam doses reduce adhesion reformation in the rat uterine horn, but the effectiveness of piroxicam is significantly greater than that of LMWH.
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48 eight-week old female Holtzman rats, weights between 100 and 200 grams, were divided into 6 treatment groups as follow: Group A: water; Group B: piroxicam (30 mg/kg); Group C: omeprazole (5 mg/kg) and piroxicam (30 mg/kg); Group D: honey (2.5 g/kg) and piroxicam (30 mg/kg); Group E: honey (5 g/kg) and piroxicam (30 mg/kg); Group F: honey (7.5 g/kg) and piroxicam (30 mg/kg). Macroscopic studies, using Scion Image, and microscopic histological section of gastric mucosa were performed after the interventions.
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We examined the role of cyclooxygenase (CO)-derived metabolites of arachidonic acid (AA) in the regulation of interleukin 1 (IL 1) production by lipopolysaccharide (LPS)-stimulated murine resident peritoneal macrophages. The use of LPS proved to be an efficacious probe, because it stimulated both IL 1 production and AA metabolism via only the CO pathway. The production of the CO metabolites prostaglandin E2 (PGE2) and prostaglandin I2 (PGI2; measured as its stable metabolite 6-Keto prostaglandin F1 alpha) by LPS-stimulated macrophages was demonstrated by high pressure liquid chromatography and radioimmunoassay. The addition of exogenous PGE2 or PGI2 resulted in a dose-dependent suppression of macrophage IL 1 production. Inhibitors of the CO pathway (indomethacin, piroxicam, and ibuprofen) caused a dose-dependent augmentation in the LPS-induced IL 1 response. This augmentation directly correlated with the efficacy of the compounds as CO inhibitors. Similar results were found when macrophage-derived fibroblast growth factor was assessed. The addition of exogenous IL 1 to macrophage cultures caused an increase in the levels of PGE2, over a narrow dose range (0.05 to 0.6 IL 1 units). These studies provide detailed evidence that AA metabolites synthesized via the CO pathway can modulate the production of growth factors by LPS-stimulated macrophages. In addition, our data support the concept that IL 1, as with classical hormones, can regulate its own production through a self-induced inhibitor, PGE2.
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Ampiroxicam is a nonacidic ether carbonate prodrug of piroxicam. Our results demonstrate that, in contrast to piroxicam, ampiroxicam does not possess detectable prostaglandin synthesis inhibitory activity in vitro. Ampiroxicam, however, has similar in vivo potency to piroxicam in suppressing paw swelling in rat adjuvant arthritis. In an acute model of paw inflammation in rats, ampiroxicam is less potent than piroxicam itself: the ED50's of ampiroxicam are 9- and 3.5-fold higher than those of piroxicam following a single or multiple (5) daily oral doses, respectively. Using the phenylbenzoquinone stretching test as a method of evaluating acute analgetic activity, the ED50 for ampiroxicam is about 3-fold higher than that of piroxicam. These tests of activity share the property of being partially prostaglandin-dependent. Ampiroxicam itself is not observed in plasma after oral dosing to man, nor in the rat, dog, and monkey as reported here. Bioavailability studies show that conversion to piroxicam is about 100%, 90%, 70%, and 50% in these four species, respectively. These results indicate that ampiroxicam's anti-inflammatory activity is produced in vivo by conversion to piroxicam and support its credentials as an efficacious prodrug of piroxicam.
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Pre-operatively administered tenoxicam provides superior post-operative analgesia than tenoxicam administered after surgical incision in patients undergoing breast biopsy.
Female hamsters in groups of six per treatment were used.
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Fifty dogs with TCC without azotemia.
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Lysophosphatidylcholine (lysoPC) (0.01 100 ng/ml) as well as PLA2 (0.01-100 mU/ml) dose-dependently increased the cell migration. Lysophosphatidic acid (10 ng/ml) also increased the migration, but no significant increase in migration was observed when stimulated by lysophosphatidylethanolamine (10 ng/ml) or lysophosphatidylserine (10 ng/ml). Addition of 4-bromophenacyl bromide (BPB), a PLA2 inhibitor, completely blocked the effect of PLA2. However, addition of piroxicam (a cyclooxygenase inhibitor) or nordihydroguaiaretic acid (a lipoxygenase inhibitor) had no significant effect. Combination of PLA2 (10 mU/ml) with lysoPC (10 ng/ml) had no additive effect on migration. Moreover, lysoPC levels were increased in the cells after incubation with PLA2 (10 mU/ml). After pretreatment of RGM-1 cells with replication-inhibiting doses of mitomycin C. PLA2 and lysoPC still increased the cell migration.
We report the case of a 25 year-old man presenting Reiter's syndrome (urethritis, conjunctivitis and oligoarthritis). This clinical triad is a particular expression of reactive arthritis. A genital or enteric infection can be responsible for the onset. Presence of HLA B27 histocompatibility antigen is a genetic factor favoring the development of Reiter's syndrome. Many organs or systems can be affected. In addition to eradication of the initiating infection, treatment is mainly symptomatic and management is multidisciplinary.
We concluded a randomized, controlled trial to compare once-daily 20 mg piroxicam versus once-daily 20 mg tenoxicam in ankylosing spondylitis. We recorded patients' dosing histories with electronic monitors for an average of 225 days (range 55-379) in 34 recipients of piroxicam and 31 recipients of tenoxicam. Dosing histories with the two agents were similar and are combined. Patients took 81% of prescribed doses; 78% once daily (as prescribed) and 3% as two or more daily doses. On 19% of all monitored days, there was no record of a dose being taken; 68% were single no-dose days, the rest (32%) being 2 to >10 consecutive no-dose days. In 3% of monitored days, extra doses were evidently taken, 88% as twice daily and 12% as three or more doses. Only 22% of all patients (14/65) strictly complied with the regimen: one dose daily every day. The remainder alternated between no-dose days and extra-dose days. We found no correlation between patient compliance and improvement in reported pain or morning stiffness.
Droxicam showed high antiinflammatory activity in carrageenin-induced edema in rat. At doses of 0.25 and 0.5 mg/kg, droxicam was as active as piroxicam and more active than phenylbutazone given at 2.5 and 5 mg/kg. Against nystatin-induced edema, droxicam (ED50, p.o., 5, 6, 7, 8 h: 7.5, 12.9, 4.8, 8.4 mg/kg) was 4-11 times more active than phenylbutazone and more than 12 times more active than isoxicam. In cotton pellet-induced granuloma in rats, title compound was as active as suprofen. In U.V. light-induced erythema in guinea pigs, droxicam (ED50, p.o., 1, 2, 3, 4 h: 0.51, 0.94, 1.56, 4.88 mg/kg) was 5-9 times more active than phenylbutazone. At doses of 0.1, 0.33 and 1.0 mg/kg/day, droxicam, similar to piroxicam, showed good antiarthritic activity in rats injected with Mycobacterium butyricum against primary and secondary lesions. Droxicam demonstrated strong analgesic activity in protecting against writhings: induced by phenylbenzoquinone in mice: ED50: droxicam = 5.3, phenylbutazone = 61.5, acetylsalicylic acid = 90.7, dipyrone = 83.6, isoxicam = 88.3 mg/kg, p.o.; induced by acetylcholine bromide in mice: ED50: droxicam = 1.1, phenylbutazone = 32.1, acetylsalicylic acid = 32.2, isoxicam = 32.7 mg/kg, p.o.; induced by acetic acid in rat: ED50: droxicam = 0.94, acetylsalicylic acid = 8.72, isoxicam = 4.70 mg/kg, p.o. Antipyretic activity of title compound was demonstrated in rats with pyresis induced by brewer's yeast, being 4-13 times more active than dipyrone. In pyresis induced by Salmonella typhi, droxicam was more active than acetylsalicylic acid and 4-aminoantipyrine at all times and doses. In a study of protection against diarrhea induced by castor oil in rats, droxicam and piroxicam showed equal activity (ED50 = 0.081 and 0.079 mg/kg, p.o., respectively) and were 3.9 and 15.6 times more active than isoxicam and phenylbutazone, respectively. Droxicam significantly inhibited peritoneal capillary permeability in mice at a dose of 5 mg/kg, p.o., while isoxicam and phenylbutazone required 100 and 200 mg/kg, p.o., respectively. Droxicam did not exhibit uricosuric activity in rats. It did not show cardiovascular or respiratory effects in anesthetized cats, nor modify their response to administration of acetylcholine, norepinephrine and histamine. In the Irwin's test, droxicam did not alter rat behavior (80 mg/kg, i.p.) nor that of mice (160 mg/kg, p.o.). Induction of gastrointestinal injuries in rats by droxicam was 10 times less than by piroxicam (UD50: droxicam, 57 mg/kg, p.o.; piroxicam, 5.6 mg/kg, p.o.). The potentiation of gastric injuries induced by stress through cold in rats was also studied.(ABSTRACT TRUNCATED AT 400 WORDS)
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Piroxicam, a new non-steroidal anti-inflammatory drug, possesses analgesic, antipyretic, and anti-inflammatory properties and inhibits platelet aggregation in animal models. Its elimination half-life is 38 hours, and hepatic metabolism to inactive metabolites is the primary route of elimination. Less than 10% of a dose appears unchanged in the urine. Clinical studies demonstrate that piroxicam's analgesic and anti-inflammatory properties are useful in the management of rheumatoid arthritis and osteoarthritis. Limited clinical studies suggest that piroxicam may be useful in the management of acute gouty arthritis, ankylosing spondylitis, acute musculoskeletal disorders, and as an analgesic. The gastrointestinal system is the major site of adverse effects. Piroxicam is currently marketed in 20 mg capsules and once daily dosing has proven effective for many patients.
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A new series of thienothiazine derivatives were evaluated as a means of clarifying whether the changed chemical structure would have a different effect on carrageenin edema, scalded hyperalgesia and ulcerogenicity in rats and also have a different effect on PGE2 biosynthesis in vitro. The introduction of a Cl or CF3 group, but not an OH group, into position 6 of the thiophene ring resulted in an apparent increase in antiinflammatory and analgesic activity. A derivative with an OH or ester substituent in position 4 of the thiazine ring had a high pharmacological potential, but the introduction of other substituents such as ether and amide led to a significant loss in the activity. The pharmacological potential of two 5-hydroxy-2-aminopyridyl derivatives was less than what was achieved with various 2-aminopyridyl derivatives. Good correlations were observed between the lessening of the carrageenin edema and scalded hyperalgesia and inhibition of PGE2 biosynthesis. There was no statistically significant correlation between the ulcerogenicity and anti-inflammation or the ulcerogenicity and analgesia. As to the safety, tenoxicam, IIIc and IIIh showed relatively higher indices than those of others; and especially, tenoxicam was found to be a potent antiinflammatory drug with the highest safety index.