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Gastrointestinal NSAIDs

Elucidation of the activities of individual COX isoforms led to the development of drugs that selectively inhibit the inducible form of the enzyme, COX-2. Thus COX-2 inhibitors were expected to minimize NSAID gastrointestinal toxicity and antiplatelet effects (see Fig. 55-3).19 A common misconception is that COX-2 inhibitors are more effective than nonselective NSAIDs in relieving pain and inflammation. In clinical trials, patients experienced similar levels of pain relief with COX-2 inhibitors and nonselective NSAIDs. [Pg.886]

Etodolac This drug has effects similar to those of the other NSAIDs. Gastrointestinal problems may be less common. However, other adverse effects such as fluid retention and abnormal kidney and liver function have been reported. Etodolac may increase the serum levels and thus raise the risk of adverse reactions caused by digoxin, lithium, methotrexate, and enhance the nephrotoxicity of cyclosporine. [Pg.421]

Lonazolac, an arylacetic acid derivative, causes adverse effects like those of other NSAIDs. Gastrointestinal disturbances are followed in frequency by nervous system and skin reactions. The extent of gastrointestinal blood loss is similar to that with diclofenac (1). Cholestatic hepatitis has also been reported (SEDA-8, 106). [Pg.2159]

Salicylates, NSAIDs Gastrointestinal bleeding, hepatic toxicity, renal toxicity, hypertension CBC, creatinine, urinalysis, AST, ALT Dark/black stool, dyspepsia, nausea/vomiting, abdominal pain, shortness of breath, edema CBC yearly, creatinine yearly... [Pg.1587]

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]

Glucocorticoids increase the risk of gastrointestinal complications caused by NSAEDs. Considerable caution is necessary when using NSAIDs in patients with severe liver and kidney damage and they should not be combined with coumarines. Owing to the limited experience obtained, these precautions and contraindications also apply to COX-2-selective inhibitors. [Pg.874]

Indomethacin treatment is associated with a high incidence (30%) of side effects typical for those seen with other NSAIDs (see above). Gastrointestinal side effects, in particular, are more frequently observed after indomethacin than after administration of other NSAIDs. The market share of indomethacin ( 5%) is therefore low compared to that for other non-steroidal anti-rheumatic agents. [Pg.875]

Epidemiological studies have demonstrated that diclofenac causes less serious gastrointestinal complications than indomethacin. However, a rise in plasma liver enzymes occurs more frequently with diclofenac than with other NSAIDs. [Pg.875]

Ibuprofen is the most thoroughly researched 2-ary lpropionic acid. It is a relatively weak, non-selective inhibitor of COX. In epidemiological studies, ibuprofen compared to all other conventional NSAIDs, has the lowest relative risk of causing severe gastrointestinal side effects. Because of this, ibuprofen is the most frequently used OTC ( over the counter , sale available without prescription) analgesic. Ibuprofen is highly bound to plasma proteins and has a relatively short elimination half-life ( 2 h). It is mainly glucuronidated to inactive metabolites that are eliminated via the kidney. [Pg.875]

The indications for these agents are in principle identical to those of the non-selective NSAIDs although the substances have not yet received approval for the whole spectrum of indications of the conventional NSAIDs. Because they lack COX-1-inhibiting properties, COX-2-selective inhibitors show fewer side effects than conventional NSAIDs. However, they are not free of side effects because COX-2 has physiological functions that are blocked by the COX-2 inhibitors. The most frequently observed side effects are infections of the upper respiratory tract, diarrhoea, dyspepsia, abdominal discomfort and headache. Peripheral oedema is as frequent as with conventional NSAIDs. The frequency of gastrointestinal complications is approximately half that observed with conventional NSAIDs. [Pg.875]

The anti-inflammatory effects of the NSAIDs are carried out by inhibition of COX-2. The gastrointestinal adverse reactions are caused by inhibition of COX-1. The newer NSAIDs (celecoxib and rofecoxib) appear to work by specifically inhibiting the COX-2 enzyme, without inhibiting the COX-1 enzyme. Celecoxib and rofecoxib relieve pain and inflammation with less potential for gastrointestinal adverse... [Pg.159]

Before administering an NSAID, it is important for the nurse to determine if the patient has any history of allergy to aspirin or any otiier NSAID. The nurse determines if die patient has a history of gastrointestinal bleeding, hypertension, peptic ulceration, or impaired hepatic or renal function. If so, the nurse notifies the primary health care provider before administering an NSAID. [Pg.163]

Plasma digoxin levels may decrease when the drug is administered with bleomycin. When bleomycin is used witii cisplatin, there is an increased risk of bleomycin toxicity Pulmonary toxicity may occur when bleomycin is administered with other antineoplastic drugs. Plicamycin, mitomycin, mitoxantrone, and dactino-mycin have an additive bone marrow depressant effect when administered with other antineoplastic drugs. In addition, mitomycin, mitoxantrone, and dactinomycin decrease antibody response to live virus vaccines. Dactinomycin potentiates or reactivates skin or gastrointestinal reactions of radiation therapy There is an increased risk of bleeding when plicamycin is administered witii aspirin, warfarin, heparin, and the NSAIDs. [Pg.593]

Determine the appropriate management for a patient taking a non-selective NSAID who is at high risk for ulcer-related gastrointestinal complications or who develops an ulcer. [Pg.269]

Gl, gastrointestinal H. pylori, Helicobacter pylori NSAID, non-steroidal anti-inflammatory drug SRMD, stress-related mucosal damage. [Pg.270]

NSAIDs are one of the most widely used classes of medications in the United States, particularly in the elderly.4 More than 20,000 deaths occur in the United States per year as a direct result of adverse events related to NSAID use. Chronic NSAID ingestion leads to symptoms of nausea and dyspepsia in nearly half of patients. Peptic ulceration occurs in up to 30% of patients who use NSAIDs chronically, with gastrointestinal bleeding or perforation occurring in 1.5% of patients who develop an ulcer. NSAID-related peptic ulcers usually occur in the stomach duodenal ulcers are much less common. [Pg.271]

Previous peptic ulcer disease or upper gastrointestinal bleeding Cardiovascular disease and other comorbid conditions Multiple NSAID use (e.g., low-dose aspirin in conjunction with another NSAID)... [Pg.271]

Two large trials, the Vioxx Gastrointestinal Outcomes Research (VIGOR) study and the Celecoxib Long-term Arthritis Safety Study (CLASS), compared selective COX-2 inhibitors and traditional, non-selective NSAID therapy in terms of their ability to prevent clinical PUD (i.e., symptomatic ulcers and ulcer complications). VIGOR (9-month median follow-up) demonstrated that rofecoxib (50 mg daily) therapy was significantly more efficacious than naproxen.28 The CLASS study (6-month median follow-up) found that high-dose celecoxib (400 mg twice daily) was superior to non-selective NSAID therapy (either ibuprofen 800 mg three times daily or diclofenac 75 mg twice daily).29... [Pg.278]

Patients at increased risk of NSAID-induced gastrointestinal adverse effects (e.g., dyspepsia, peptic ulcer formation, and bleeding) include the elderly, those with peptic ulcer disease, coagulopathy, and patients receiving high doses of concurrent corticosteroids. Nephrotoxicity is more common in the elderly, patients with creatinine clearance values less than 50 mL/minute, and those with volume depletion or on diuretic therapy. NSAIDs should be used with caution in patients with reduced cardiac output due to sodium retention and in patients receiving antihypertensives, warfarin, and lithium. [Pg.494]

NSAIDs Monitor patients for gastrointestinal distress, signs or symptoms of gastrointestinal bleeding, and hypertension and edema that may reflect renal dysfunction. Monitor CBC and serum creatinine as clinically indicated. [Pg.510]


See other pages where Gastrointestinal NSAIDs is mentioned: [Pg.2575]    [Pg.203]    [Pg.2575]    [Pg.203]    [Pg.199]    [Pg.40]    [Pg.153]    [Pg.139]    [Pg.406]    [Pg.872]    [Pg.872]    [Pg.1004]    [Pg.157]    [Pg.162]    [Pg.163]    [Pg.163]    [Pg.164]    [Pg.164]    [Pg.1]    [Pg.80]    [Pg.117]    [Pg.200]    [Pg.269]    [Pg.269]    [Pg.271]    [Pg.277]    [Pg.278]    [Pg.362]    [Pg.494]    [Pg.494]    [Pg.521]    [Pg.730]    [Pg.871]   


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