NSAIDs adverse effects

Fentiazac, a thiazoleacetic acid derivative, has the same adverse reactions profile as other NSAIDs. Adverse effects in as many as 56% of patients (5-56%), are even more frequent than with phenylbutazone (1). 

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. 

Most NSAIDs (e.g., ibuprofen, naproxen, and others) inhibit both COX-1 and COX-2 isoforms. That is, they are nonselective inhibitors of the COX enzyme system. Whereas inhibition of COX-2 is responsible for beneficial effects, inhibition of COX-1 is responsible for the most common and important adverse effects of NSAIDs. COX-2-selective inhibitors have been produced and marketed in attempts to preserve the beneficial effects of COX-2 inhibition while avoiding the deleterious effects associated with inhibition of the COX-1 enzyme. This approach has not been entirely successful, as discussed below. 

In patients taking NSAIDs, monitor for increases in blood pressure, weight gain, edema, skin rash, and central nervous system adverse effects such as headaches and drowsiness. 

Indomethacin was used traditionally, but its relative cyclooxygenase-1 (COX-1) selectivity theoretically increases its gastropathy risk. Thus other generic NSAIDs may be preferred. Adverse effects of NSAIDs include gastropathy (primarily peptic ulcers), renal dysfunction, and fluid retention. NSAIDs generally should be avoided in patients at risk for peptic ulcers, those taking warfarin, and those with renal insufficiency or uncontrolled hypertension or heart failure. 

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. 

Select therapy based on comorbidities and potential for adverse effects. In patients with no other disease states, NSAIDs are the preferred drug class. 

COX-2 inhibitors such as celecoxib are associated with adverse effects such as nephrotoxicity and a potential increased risk of myocardial infarction (see Chaps. 55 and 15 for additional information). Combination of COX-2 inhibitors with alcohol may increase GI adverse effects. All NSAIDs should be used with caution in patients with aspirin-induced asthma.31... 

Evaluate for adverse effects and drug interactions. For patients on topical therapy, evaluate for local adverse effects. For patients on acetaminophen or NSAIDs, inquire about alcohol use. 

Selection of an NSAID depends on prescriber experience, medication cost, patient preference, toxicities, and adherence issues. An individual patient should be given a trial of one drug that is adequate in time (2 to 3 weeks) and dose. If the first NSAID fails, another agent in the same or another chemical class can be tried this process may be repeated until an effective drug is found. Combining two NSAIDs increases adverse effects without providing additional benefit. 

GI complaints are the most common adverse effects of NSAIDs. Minor complaints such as nausea, dyspepsia, anorexia, abdominal pain, flatulence, and diarrhea occur in 10% to 60% of patients. NSAIDs should be taken with food or milk, except for enteric-coated products (milk or antacids may destroy the enteric coating and cause increased GI symptoms in some patients). 

Patients should be asked if they are having adverse effects from their medications. They should also be monitored for any signs of drug-related effects, such as skin rash, headaches, drowsiness, weight gain, or hypertension from NSAIDs. 

Nephrotoxins (N) orototoxins (0) (eg., amphotericin B (N), cisplatin (N/0), cyclosporine (N), furosemide (0), NSAIDs (N), radio contrast (N), vancomycin (N) Additive adverse effects Monitor aminoglycoside SDC and renal function... 

ASA, NSAIDs, food EMS Monitor ECG for hypokalemia (peaked T waves), esp in pts taking K-sparing diuretics may affect glucose (hypoglycemia) concurrent EtOH use can t adverse effects may cause posistent cough OD May cause profound hypotension give IV fluids... 

Altered homeostasis in older persons can lead to important and common adverse drug effects the less robust homeostatic milieu may be stressed by drugs, causing adverse effects. Examples include orthostatic hypotension due to antihypertensives and other agents that cause a-adrenergic blockade (e.g. terazosin, doxazosin, tricyclic antidepressants and phenothiazines) in those with barorecep-tor dysfunction. Diuretics can cause hyponatraemia or hypokalaemia in older patients, whereas ACE inhibitors and NSAIDs can cause hyperkalaemia. 

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