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Cardiovascular Thrombotic Events: Observational studies have indicated that non-selective NSAIDs may be associated with an increased risk of serious cardiovascular events, principally myocardial infarction, which may increase with dose or duration of use. Patients with cardiovascular disease or cardiovascular risk of an adverse cardiovascular event in patient taking NSAID, especially in those with cardiovascular risk factors, the lowest effective dose should be used for the shortest possible duration.
There is no consistent evidence that the concurrent use of aspirin mitigates the possible increased risk of serious cardiovascular thrombotic events associated with NSAID use.
Hypertension: NSAIDs may lead to the onset of new hypertension or worsening the pre-existing hypertension and patients taking antihypertensive with NSAIDs may have an impaired anti-hypertensive response. Caution is advised when prescribing NSAIDs to patients with hypertension. Blood pressure should be monitored closely during initiation of NSAID treatment and at regular intervals thereafter.
Heart Failure: Fluid retention and oedema have been observed in some patients taking NSAIDs, therefore caution is advised in patients with fluid retention or heart failure.
Severe Skin Reactions: NSAIDs may very rarely cause serious cutaneous adverse events such as exfoliative dermatitis, toxic epidermal necrolysis (TEN) and Stevens-Johnson Syndrome (SJS), which can be fatal and occur without warning. These serious adverse events are idiosyncratic and are independent of dose or duration of use. Patients should be advised of the signs and symptoms of serious skin reactions and to consult their doctor at the first appearance of a skin rash or any other sign of hypersensitivity.
Measures such as the use of physical therapy and mild analgesic like paracetamol (when inflammation is not a major factor) should be instituted prior to initiation of therapy with NSAID. NSAIDs should only be used after proper appraisal of potential risks to patients. It should be used with the lowest effective dose for only as long as needed. This drug should not be co-administered with other NSAIDs. Prescribers should inform patients about the signs and/or symptoms of serious GI toxicity and what steps to take if they occur. In considering the use of relatively large doses (within the recommended dosage range), sufficient benefit should offset the potential increased risk of GI toxicity.
Liver function should be monitored periodically during long-term naproxen therapy. Patients who experience sign and/or symptoms suggestive of liver dysfunction or an abnormal liver function test result while receiving naproxen should be evaluated for evidence of the development of a severe hepatic reaction. Severe hepatic reactions, including jaundice and cases of fatal hepatitis, have been reported with this drug as with other NSAIDs. Although such reactions are rare, if abnormal liver test persist or worsen, if clinical signs and symptoms consistent with liver disease develop, or if systemic manifestation occur (e.g. eosinophilia, rash, etc), this drug should be discontinued. Since naproxen can inhibit platelet aggregation, patients who may be adversely affected by a prolongation of bleeding time should be carefully observed during naproxen therapy.
Renal effects: As with other NSAIDs, long term administration of naproxen to animals has resulted in renal papillary necrosis and other abnormal renal pathology. In humans, there have been reports of acute interstitial nephritis with hematuria, proteinuria, and occasionally nephrotic syndrome.
A second form of renal toxicity has been seen in patients with prerenal conditions leading to a reduction in renal blood flow or blood volume, where the renal prostaglandins have a supportive role in the maintenance of renal perfusion. In these patients, administration of a NSAID may cause a dose-dependent reduction in prostaglandin formation and may precipitate overt renal decompensation. Patients at greatest risk of this reaction are those with impaired renal function, heart failure, liver dysfunction, those taking diuretics, and the elderly. Discontinuation of NSAID therapy is typically followed by recovery to the pretreatment state.
Naproxen sodium and its metabolites are eliminated primarily by the kidneys, therefore the drug should be used with great caution in patients with significantly impaired renal function and the monitoring of serum creatinine and/or creatinine clearance is advised in these patients.
Caution should be used if the drug is given to patients with creatinine clearance of less than 20 ml/minute because accumulation of naproxen metabolites has been seen is such patients.
Chronic alcoholic liver disease and probably other forms of cirrhosis reduce the total plasma concentration of naproxen, but the plasma concentration of unbound naproxen is increased. Caution is advised when high doses are required and some adjustment of dosage may be required in these patients. It is prudent to use the lowest effective dose.
Elderly patients are more likely to have age-related renal function impairment, which may increase the risk of NSAID-induced hepatic or renal toxicity. Studies have shown that the unbound (free) fraction of naproxen, but not the total plasma concentration, may be increased in geriatric patients. The steady state concentration of unbound naproxen may be almost doubled in geriatric patients as compared with younger adults.
Some clinicians recommend that geriatric patients, especially those 70 years of age or older be given one-half of the usual adult dose initially. Careful monitoring of the patients is recommended and the lowest effective dose should be used.
550 mg of Naproxen Sodium contain approximately 50 mg of Sodium. This should be considered in patient whose sodium intake is restricted.
Risk Of GI Ulceration, Bleeding and Perforation With NSAIDs: Serious GI Toxicity such as bleeding, ulceration and perforation can occur at any time, with or without warning symptoms, in patient treated with NSAIDs therapy. Although minor upper GI problems (e.g. dyspepsia) are common, usually developing early in therapy, prescribers should remain alert for ulceration and bleeding in patients treated with NSAIDs even in the absence of previous GI tract symptoms.
Studies to date have not identified any subset of patients not at risk of developing peptic ulceration and bleeding. Patients with prior history of serious GI events and other risk factors associated with peptic ulcer disease (e.g. alcoholism, smoking, and corticosteroid therapy) are at increased risk. Elderly or debilitated patients seem to tolerate ulceration or bleeding less than other individuals and account for most spontaneous reports for fatal GI events.
