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Nonsteroidal Anti-inflammatory Drugs NSAIDs

NSAIDs are drugs related to acetyls alley lie acid which inhibit cyclooxygenase (COX), the enzyme in the synthesis of PGs and thromboxanes from arachidonic acid. There are two isoforms of cyclooxygenase, COX-1 and COX-2 [121].The former is constitutively expressed in blood vessels, stomach and kidney, while COX-2 is normally not present at these sites. It can, [Pg.103]

4 Cell Specific Delivery of Anti-Infiammatory Drugs to Hepatic Cells [Pg.104]

Acetyls alley lie acid was shown to prevent cirrhosis under certain experimental conditions [125]. Naproxen and indomethacin partially protected against LPS and D-galactosamine-in-duced hepatotoxicity [126] Acetylsalicylic acid and ibuprofen were also protective in endo-toxic shock [127]. Endotoxaemia is one of the complications in cirrhotic patients [128] and is probably caused by an impaired ability of the liver to take up and detoxify gut-derived LPS [116]. The presence of portosystemic shunts in cirrhotic patients may also contribute to this spill-over of LPS into the systemic circulation [129]. NSAIDs, however, are also reported to provoke deleterious effects on renal function in cirrhosis [130], and can therefore not be used in cirrhotic patients. Cell-specific delivery of NSAIDs to SECs and/or KCs may make application of these drugs in cirrhosis feasible by circumventing the renal side-effects. [Pg.104]

Celecoxib and rofecoxib have also been studied in AD. Randomized double blind, placebo controlled trials failed to demonstrate a therapeutic benefit (Sainetti et al., 2000 Aisen et al., 2003). The rofecoxib trial used naproxen as a control the results were consistent with other studies in which nonselective NSAIDs such as diclofenac, have been ineffective in AD (Scharf et al., 1999). Other NSAIDs including ibuprofen, indomethacin and sulindac sulfide have demonstrated potential efficacy in AD (Rogers et al., 1993 t Veld et al., 2001), but definitive trials have not yet been conducted. [Pg.573]

Beta amyloid immunization was initiated in humans after the successful studies in rodents. Phase I studies were completed without major adverse events and Phase II trials were initiated with AN 1792 (active immunization with amyloid beta 42 and QS-21 adjuvant). The trials were interrupted in 2002 because approximately 6% of those vaccinated developed aseptic meningitis (Orgogozo et al., 2003). Data from the incomplete trial suggest that AD patients who mounted a significant antibody response also showed signs of clinical benefit (Orgogozo et al., 2003 Hock et al., 2003). Autopsy findings from three patients who died approximately 1 year [Pg.573]


Nonnarcotic Analgesics Nonsteroidal Anti-inflammatory Drugs (NSAIDs)... [Pg.159]

The salicylates and nonsteroidal anti-inflammatory drug (NSAIDs) are important in the treatment of arthritic conditions. For example, the salicylates and NSAIDs are used in the treatment of rheumatoid arthritis (a chronic disease characterized by inflammatory changes within the body s connective tissue) and osteoarthritis (a noninflammatory joint disease resulting in degeneration of the articular cartilage and... [Pg.185]

Recognize differences between ulcers induced by Helicobacter pylori (HP) and nonsteroidal anti-inflammatory drugs (NSAIDs) in terms of risk factors, pathogenesis, signs and symptoms, clinical course, and prognosis. [Pg.269]

Nonsteroidal anti-inflammatory drugs (NSAIDs) may be initiated if acetaminophen therapy fails. At equipotent doses, all NSAIDs elicit similar analgesic and anti-inflammatory responses. Selection is based on patient preference, dosing frequency, tolerability, and cost. [Pg.879]

Although generally well tolerated, CSFs may cause bone pain in around 25% of patients. This may be managed with acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs), although attention to the platelet count is warranted with the use of NSAIDs. Sargramostim in particular may result... [Pg.1470]

In addition to their beneficial effects, some medications may actually cause cellular injury and disease. An example of this phenomenon involves nonsteroidal anti-inflammatory drugs (NSAIDS). These drugs include aspirin (a derivative of salicylic acid), ibuprofen (arylpropionic acid, Advil ), and acetaminophen (para-aminophenol derivative, Tylenol ). Because of their beneficial pharmacological effects, consumption of these agents has increased significantly in recent years. NSAIDS have the ability to treat fever, pain, acute inflammation, and chronic inflammatory diseases such as arthritis. They are also used prophylactically to prevent heart disease, stroke, and colon cancer. [Pg.292]

A number of compounds activate TRPA1 without any apparent ability to form covalent adducts, including nonelectrophilic fenamate nonsteroidal anti-inflammatory drugs (NSAIDs), such as flufenamic acid (17, FFA), niflumic acid (18, NFA), and mefenamic acid (19, MFA) [13]. Phenols such as thymol (20) and 2-ferf-butyl-5-methylphenol (21) have been shown to activate human TRPA1 with micromolar EC50 values in stably transfected HEK293 cells [14]. [Pg.39]

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed medicines. Although these compounds represent a very effective class of drugs, their use is associ-... [Pg.55]

Many nonsteroidal anti-inflammatory drugs (NSAIDs) are substituted 2-arylpropionic acids. Most NSAIDs also have a chiral carbon next to the carboxylate and are administered as a racemic mixture of the two enantiomers. In general, the (S)-enantiomcr is responsible for most of the antiinflammatory activity of these agents. It was found that the (/ -enantiomer is converted to the (S)-enantiomer but the reverse does not occur (23). As with amino acid conjugation, the pathway involves reaction with ATP to form an AMP ester, which is, in turn, converted to a Co-A ester, and it is the Co-A ester that undergoes chiral inversion (Fig. 7.14). Substrates include ibuprofen, naproxen, and fenoprofen. [Pg.140]

COX-2 Inhibitor Celecoxib (Celebrex, Pfizer) inhibits the enzyme COX-2, which is involved in pain and inflammation, but it has no effect on the COX-1 enzyme, which helps to maintain stomach lining. It is prescribed for the relief of pain and symptoms of osteoarthritis and rheumatoid arthritis. Previously, nonsteroidal anti-inflammatory drugs (NSAIDs) were used. NSAIDs inhibit both COX-1 and COX-2 enzymes and cause stomach bleeding (see Case Study 2). [Pg.36]


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