Disease relevance of Feldene

• Fatal pemphigus vulgaris in a patient taking piroxicam [1].
• Other reactions to nonsteroidal anti-inflammatory drugs not previously recognized include serum sickness, exfoliative erythroderma, and photosensitivity associated with sulindac; toxic epidermal necrolysis was reported with tolmetin, zomepirac sodium, and piroxicam [2].
• This is the first case report in the United States of severe liver toxicity associated with piroxicam [3].
• Severe cholestatic jaundice associated with piroxicam [3].
• Piroxicam-induced renal failure and hyperkalemia [4].

Psychiatry related information on Feldene

• However, inhibition of circulating PG by piroxicam did not block the reductions in appetite, crossover, and rears induced by rIL-1 alpha; it restored normal drinking behavior and only partially restored body weight [5].
• Subsequent treatment with either intramuscular or oral piroxicam further improved these symptoms and most patients recovered their normal physical activity within a week [6].
• CONCLUSIONS: These results suggest that piroxicam is as effective as diclofenac sodium in preventing inflammation after cataract surgery with IOL implantation, and its better tolerance and safety can provide higher patient compliance [7].

High impact information on Feldene

• We had 20 patients with rheumatoid arthritis stop taking NSAIAs for two weeks and then take piroxicam, a new NSAIA, for an additional ten weeks to assess the in vivo effects of NSAIAs on cellular immunity and rheumatoid factor levels [8].
• Unlike its effect on anion secretion, phorbol 12,13-dibutyrate inhibition of sodium uptake by sodium-hydrogen exchange in isolated mature villus enterocytes is not inhibited by piroxicam [9].
• However, the response to atrial natriuretic peptide was not influenced by pretreatment with amiloride (10(-4) M to mucosal and serosal surfaces) or piroxicam (10(-5) M serosally) [10].
• The effects of azodisalicylate in ileum were not inhibited with piroxicam (an inhibitor of cyclooxygenase) [11].
• Piroxicam and pancreatitis [12].

Chemical compound and disease context of Feldene

• Mom1 showed no influence on the development of desmoid fibromas, whereas the combination of piroxicam and difluoromethylornithine exerted a moderate effect [13].
• Synergistic aggregation was inhibited by calmidazolium (10 microM), piroxicam (20-100 microM), and pertussis toxin (20 micrograms/ml) [14].
• Pretreatment of rats with NS-398 or piroxicam (3 mg/kg of body weight, i.p.), which are said, respectively, to possess high and relative specificity for the COX-2 enzyme, also blocked the SWS-promoting effect of IL-1 [15].
• In contrast to the significant toxicity of piroxicam, which caused ulcers complicated by perforation and bleeding, celecoxib caused no gastrointestinal side effects and did not inhibit platelet thromboxane B2 at plasma drug levels similar to those obtained in early clinical trials in humans [16].
• After only 6 weeks of treatment, intestinal adenomas and aberrant crypt foci were counted, and serum levels of piroxicam and thromboxane B2 were quantitated [17].

Biological context of Feldene

• Effects of the cyclooxygenase inhibitor, piroxicam, on tumor response, apoptosis, and angiogenesis in a canine model of human invasive urinary bladder cancer [18].
• Experiments with piroxicam, nordihydroguaiaretic acid, and esculetin, other inhibitors of eicosanoid biosynthesis with varying selectivity for enzymes of the prostaglandin and leukotriene pathways, indicated that MDA-MB-231 cell growth was dependent on leukotriene rather than prostaglandin production [19].
• Piroxicam at levels of 25, 75, and 150 ppm and DFMO at concentrations of 400, 1000, and 4000 ppm (20, 50, and 80% maximum tolerated dose) in AIN-76 diet were tested individually and in combinations [20].
• UVB significantly increased AP-1 activity in Cox-2(-/-) fibroblasts transfected with an AP-1 luciferase reporter gene, and this increase was blocked by NS-389 or piroxicam [21].
• Of additional interest is the relationship between piroxicam pharmacokinetics (particularly steady-state plasma levels) and adverse effects [22].

Anatomical context of Feldene

• In contrast, none of the doses of piroxicam alone decreased tumor multiplicity in the proximal portion of the intestine (duodenum) [23].
• Piroxicam at 12, 25, and 50 ppm in the diet caused dose-dependent decreases in the number of tumors in the middle and distal portions of the small intestine [23].
• In addition, we evaluated the ability of piroxicam, a potent COX inhibitor, to prevent postinitiation events of NMBA-induced tumorigenesis in the rat esophagus [24].
• Furthermore, piroxicam significantly decreased the amount of L-selectin shed by cytokine-treated neutrophils, whereas it did not exert this effect on PMA- or A23187-treated neutrophils [25].
• Moreover, in chemokine-treated T lymphocytes, the expression of activation epitopes on beta 1 integrins was also diminished by piroxicam [25].

Associations of Feldene with other chemical compounds

• Chemoprevention of colon carcinogenesis by concurrent administration of piroxicam, a nonsteroidal antiinflammatory drug with D,L-alpha-difluoromethylornithine, an ornithine decarboxylase inhibitor, in diet [20].
• The MTD levels of piroxicam, DFMO, DHEA analogue, and EA were determined in male F344 rats and found to be 500, 5,000, 500, and 10,000 ppm, respectively, in modified AIN-76A diet [26].
• The effect of other risk factors was also considered, and the adjusted odds ratios were 4.1 for all NSAIDs, 6.4 (95% CI 2.8-15.0) for piroxicam, and 3.3 (95% CI 2.0-5.5) for diclofenac, ketoprofen, and sulindac combined [27].
• NS-398 and piroxicam suppress UVB-induced activator protein 1 activity by mechanisms independent of cyclooxygenase-2 [21].
• Exposure of these cells to celecoxib induces characteristic features of apoptosis, including morphological changes, DNA laddering, and caspase-3 activation, whereas piroxicam, a COX-1-specific inhibitor, displays no appreciable effect on either cancer cell line even after prolonged exposure [28].

Gene context of Feldene

• The genetic modifier Mom1 and the pharmacological agents piroxicam and difluoromethylornithine each reduced intestinal adenoma multiplicity in the absence of p53 function [13].
• Apc(min)/+ progeny of pregnant dams treated with piroxicam and/or DFMO were reduced in number and their ratio to Apc+/+ progeny was decreased to approximately 0.28:1 [23].
• Rheumatoid arthritis treated with tenidap and piroxicam. Clinical associations with cytokine modulation by tenidap [29].
• Among common NSAIDs tested, indomethacin, sulindac sulfide, and piroxicam preferentially inhibited PGH synthase-1; ibuprofen, flurbiprofen, and meclofenamate inhibited both enzymes with comparable potencies; and 6-methoxy-2-naphthylacetic acid preferentially inhibited PGH synthase-2 [30].
• The median within-patient treatment differences (after tenidap minus after piroxicam) in the CRP, ESR, SAA, and IL-6 values were -1.7 mg/dl, -10.0 mm/hour, -22.0 micrograms/ml, and -3.7 pg/ml, respectively, and represent -60.4%, -17.7%, -35.5%, and -26.1% of the respective baseline levels [29].

Analytical, diagnostic and therapeutic context of Feldene

• Rats treated with sulfone at 1000 and 2000 ppm, sulindac, and piroxicam had significantly fewer colonic adenomas and carcinomas compared with rats fed control diet as measured by tumor incidence, multiplicity, and tumor burden [31].
• A double-blind, randomized, multicenter study in which patients with active RA were treated with tenidap 120 mg/day, hydroxychloroquine 400 mg/day and piroxicam 20 mg/day, or piroxicam alone 20 mg/day, for 24 weeks [32].
• The foreign studies suggest that piroxicam at 20-mg doses produces analgesia in patients with postoperative dental pain [33].
• Despite having had poor or no response with other drug therapies, in the majority of cases in which piroxicam was used half of the patients (15 of 30) reported feeling very good or good at their last visit, 13 said they felt fair, and only two reported feeling poor or very poor in terms of their sense of well-being [34].
• Piroxicam in recent epidemiologic studies [35].

References