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Subject NSAIDs

The first two selective COX-2 inhibitors to be marketed and subjected to in depth clinical trials were celecoxib and rofecoxib. Both compounds are as effective as standard NSAIDs in rheumatoid arthritis, osteoarthritis and for pain following orthopaedic or dental surgery. Gastrointestinal side effects were far fewer than with comparator diugs and in fact were no... [Pg.406]

The term refers to a distinct clinical syndrome characterized by aggressive and continuous inflammatory disease of the airways with chronic eosinophilic rhinosinus-itis, asthma and often nasal polyposis [6-8]. Aspirin and other NSAIDs that inhibit COX-1 exacerbate the condition, precipitating violent asthmatics attacks. This is a hallmark of the syndrome. The prevalence of aspirin hypersensitivity in the general population ranges from 0.6 to 2.5%, but is much more frequent in adult asthmatic subjects where it reaches 10-15%, although it is often underdiagnosed. [Pg.173]

Assess the patient s subjective complaints and objective information for adverse effects. For NSAID therapy, be alert for new-onset epigastric pain, dark or tarry stools, blood in vomitus, dizziness or light-headedness, development of edema, decreased urine output by more than 50% over a 24-hour period, or shortness of breath. For colchicine, monitor for nausea or vomiting, diarrhea, easy bruising, cold or flulike symptoms, light-headedness, muscle weakness, or pain. Counsel the patient to inform you of any new medications started or stopped while taking colchicine. [Pg.897]

A recent trend in the pharmaceutical industry has been to harness the intrinsic tissue-protective properties of NO for improving the gastric tolerance of nonsteroidal antiinflammatory drugs (NS AIDs). This trend has led to the synthesis of hybrid, chimeric molecules containing an NSAID or aspirin moiety and a NO-donor functionality [153, 154]. One such hybrid is a NO-releasing derivative of aspirin, NCX-4016. In a doubleblind, randomized, placebo-controlled gastrointestinal safety assessment in healthy subjects, NCX-4016 (400 or 800 mg twice daily for 7 days) acted like aspirin as an inhibitor of arachidonic acid-induced platelet aggregation in vitro [155]. Whether... [Pg.319]

Piateiet aggregation NSAIDs can inhibit platelet aggregation the effect is quantitatively less and of shorter duration than that seen with aspirin. These agents prolong bleeding time (within normal range) in healthy subjects. [Pg.939]

Veld et al. (2001) followed a sample of almost 7000 subjects aged 55 years and older and not suffering from dementia at baseline, i.e. in 1991. Within an average follow-up period of 6.8 years, 394 of the study participants developed dementia (293 AD, 56 vascular dementia, 45 other types of dementia). The observed risk of developing AD then was related to the use of NSAIDs as documented in pharmacy records, resulting in the following relative risks of developing AD ... [Pg.258]

The importance of treatment with glucocorticoids and NSAIDs in the development of sigmoid diverticular abscess perforation has been the subject of a case-control study in 64 patients (38 women), median age 70 years (range 39-91) and 320 age- and sex-matched controls (154). Independently of rheumatic diagnosis glucocorticoid treatment was strongly associated with sigmoid diverticular abscess perforation (OR = 32 95% Cl = 6.4,159). [Pg.21]

Loop diuretics induce renal prostaglandin synthesis, and these prostaglandins participate in the renal actions of these drugs. NSAIDs (eg, indomethacin) can interfere with the actions of the loop diuretics by reducing prostaglandin synthesis in the kidney. This interference is minimal in otherwise normal subjects but may be significant in patients with nephrotic syndrome or hepatic cirrhosis. [Pg.359]

Etodolac distributes well into synovial fluid, the proposed primary site of action of NSAID s. Following multiple doses of 200 mg twice daily for 7 days, the Cmax in synovial fluid was 2.6 pg /mL and the tmax was 3.2 hours [44]. The synovial fluid AUC of total etodolac was about 67% of the serum values [44]. The AUC of the unbound etodolac was 172% of the serum values. After a single 200 mg dose of etodolac, the ratio of (S)-etodolac to (i )-etodolac in six subjects with rheumatoid arthritis was 0.074 in plasma and 0.17 in synovial fluid [45]. [Pg.143]

For any minor injuries sustained during athletic training NSAIDs and corticosteroids (topical, intra-articular) suppress symptoms and allow the training to proceed maximally. Their use is allowed subject to restrictions about route of administration, but strong opioids are disallowed. Similarly, the IOC Medical Code defines acceptable and unacceptable treatments for relief of cough, hay fever, diarrhoea, vomiting, pain and asthma. Doctors should remember that they may get their athlete patients into trouble with sports authorities by inadvertent prescribing of banned substances. ... [Pg.173]

Nonacidic drugs. COXIBs are associated with fewer gastrointestinal adverse effects, but otherwise the general profile of adverse reactions to NSAIDs applies. The possibility that COXIBs may be associated with increased risk of thrombotic cardiovascular events is the subject of pharmacovigilance studies. [Pg.287]

It appears that glucosamine is a safe, effective, and well-tolerated alternative to NSAIDs in the treatment of degenerative joint disease, particularly in the knee, which has been the subject of most trials. However, caution is required as too few long-term studies have been reported to date. [Pg.2436]

Aspirin-sensitive subjects may have attacks induced by other NSAIDs (82). [Pg.23]

In a randomized comparison of celecoxib and diclofenac plus omeprazole, renal adverse events, including hypertension, peripheral edema, and renal insufficiency, were common and similar in the two groups (105). They occurred in the 24% of the patients who took celecoxib and in 31% of those who took diclofenac plus omeprazole. Among patients with renal impairment at baseline, 51% of those who took celecoxib and 41% of those who took diclofenac plus omeprazole had renal adverse events. Careful monitoring of renal function in patients taking COX-2 inhibitors or traditional NSAIDs is mandatory, especially in high-risk subjects (for example those with pre-existing renal disease, diabetes, or heart failure). [Pg.1008]

There have been several reports of impaired renal function in patients taking ketorolac (SEDA-17, 112) (SEDA-18, 105) (SEDA-22, 117). The severity varies from slight to severe forms of renal insufficiency, which may even occur after a single dose of 30 mg. Because recent major surgery is considered a risk factor for renal insufficiency, particularly in elderly patients, the use of ketorolac, or other NSAIDs, for postoperative pain management is warranted only in carefully selected patients. Furthermore, a case report confirmed that oral ketorolac can cause acute renal insufficiency in young subjects without any predisposing factors (SEDA-21,106). [Pg.1979]

Meloxicam may be relatively safe when given to patients with NSAID-induced urticaria/angioedema (14,15). Of 148 NSAID-sensitive subjects with an unequivocal history of urticaria with or without angioe-dema, who were challenged with increasing oral doses of meloxicam (1-7 mg/day) in a single-blind placebo-controlled trial, only two had a positive test (urticaria in one and urticaria/angioedema in the other) both had chronic idiopathic urticaria (16). [Pg.2249]

Another meta-analysis provided more complete and useful results (23). Its primary aim was to produce an estimate of the overall effect of NSAIDs on blood pressure, and its secondary aims were to evaluate the mechanisms by which NSAIDs alter blood pressure and to determine susceptibility factors. Moreover, as NSAIDs have been associated with raised blood pressure in normotensive individuals and in both treated and untreated hypertensive subjects, the authors tried to discover different effects in these subgroups. Finally, they studied whether different NSAIDs alter blood pressure to the same degree. [Pg.2558]

Hemolytic anemia has occasionally been associated with NSAIDs many reports involved mefenamic acid, ibuprofen and sulindac (54). No evidence has been found that any NSAID, except aspirin, constitutes a particular risk for subjects with glucose-6-phosphate dehydrogenase deficiency. [Pg.2561]

The ability of the gastroduodenal mucosa to adapt to repeated exposure to NSAIDs and aspirin is well documented, and some reports have shown the possible involvement of H. pylori in this process (76,81). In one endoscopic study in volunteers, mucosal adaptation to naproxen after 4 weeks of treatment occurred in 53% of H. py/on-positive subjects and in 81% in H. py/on-negative subjects (82). [Pg.2562]

The actual risk of NSAID-associated acute renal dysfunction also continues to be the subject of controversy. There is adequate evidence that underlying renal insufficiency, congestive heart failure, or hepatic cirrhosis are conditions that carry a high risk of NSAID-related renal functional impairment. It is still not known whether old age is a risk factor, whether the risk of renal impairment varies with different NSAIDs, or whether renal function continues to deteriorate, stabilize, or even improve in affected patients with continued use of NSAIDs. Three cases of renal insufficiency caused by topical NSAIDs have been described (SEDA-18,100). [Pg.2567]


See other pages where Subject NSAIDs is mentioned: [Pg.170]    [Pg.177]    [Pg.886]    [Pg.56]    [Pg.331]    [Pg.32]    [Pg.319]    [Pg.330]    [Pg.16]    [Pg.153]    [Pg.128]    [Pg.132]    [Pg.151]    [Pg.41]    [Pg.141]    [Pg.306]    [Pg.89]    [Pg.19]    [Pg.19]    [Pg.22]    [Pg.1003]    [Pg.1007]    [Pg.1008]    [Pg.2557]    [Pg.2558]    [Pg.2558]    [Pg.2561]    [Pg.2561]    [Pg.2565]   
See also in sourсe #XX -- [ Pg.2 , Pg.180 ]




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NSAIDs

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