Sunprox Tablet: Each tablet contains: Naproxen sodium 275 mg equivalent to Naproxen 250 mg.
Sunprox 550 Tablet: Each tablet contains: Naproxen sodium 550 mg equivalent to Naproxen 500 mg.
Pharmacology: Naproxen sodium is a non-steroidal anti-inflammatory drug with analgesic and antipyretic activity. The exact mechanisms of action have not been clearly established, but many of the actions appear to be associated principally with the inhibition of prostaglandin synthesis. Naproxen inhibits the synthesis of prostaglandins in body tissues by inhibiting cyclooxygenase, an enzyme that catalyzes the formation of prostaglandin precursors (endoperoxides) from arachidonic acid. Prostaglandins appear to sensitize pain receptors to mechanical stimulation and to other chemical mediators (e.g. bradykinin, histamine).
Naproxen sodium is rapidly and completely absorbed from the gastrointestinal tract. After administration of naproxen sodium, peak plasma levels of naproxen anion are attained in 1 to 2 hours, with steady state conditions normally achieved after 4 - 5 doses. The mean biological half-life of the anion in humans is approximately 13 hours and at the therapeutic levels it is greater than 99% albumin bound. Approximately 95% of the dose is excreted in the urine, primarily as naproxen, 6-0-desmethylnaproxen or their conjugates. The rate of excretion has been found to coincide closely with the rate of drug disappearance from the plasma.
Naproxen sodium is indicated in the relief of mild to moderate pain and for the treatment of primary dysmenorrhea. It is also indicated for the treatment of rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, tendinitis and bursitis and acute gout.
Oral administration.
In rheumatic disorder, the usual initial dose of naproxen sodium is 275 mg twice daily, adjusted to 1100 mg daily in 2 divided doses. Safety and efficacy of naproxen in children younger than 2 years of age have not been established. There are no adequate efficacy or dose-response data for other pediatric conditions apart from juvenile rheumatoid arthritis. However the dosage form may not be suitable to achieve the required dosage adjustment in children. Therefore it is not recommended for children under 16 years.
In acute gout, an initial dose of 825 mg followed by 275 mg every 8 hours has been suggested. In dysmenorrhoea, 550 mg may be given initially followed by 275 mg every 6 to 8 hours if needed.
Total daily dose should not exceed 1.375 g of naproxen sodium. When patients can tolerate higher dosage well, 1.65 g of naproxen sodium daily may be given for a limited period of time when a greater level of anti-inflammatory and/or analgesic activity is necessary, provided benefit outweighs risk. After assessing the risk/benefit ratio in each individual patient, the lowest effective dose for the shortest possible duration should be used.
Symptoms and treatment for overdosage and antidotes: Studies have indicated that the body can apparently handle doses up to 4 g without saturating any of its eliminating mechanism. One patient who ingested 25 g of naproxen experienced mild nausea and indigestion. Drowsiness, heartburn or vomiting may also occur following overdosage of the drug. One death due to CNS depression has been attributed to naproxen overdosage.
In acute overdosage, the stomach should be emptied immediately by inducing emesis or by gastric lavage. If the patient is comatose, having seizures or lacks the gag reflex, gastric lavage may be performed if an endotracheal tube with cuff inflated is in place to prevent aspiration of gastric contents. Supportive and symptomatic treatment should be initiated. Animal studies indicate that prompt administration of activated charcoal will reduce absorption of the drug. Haemodialysis appears to be of no value in enhancing elimination of naproxen.
Contraindicated in patients with active peptic ulceration. This drug is contraindicated in patients who have had allergic reactions to naproxen sodium. It is also contraindicated in patients in whom aspirin or other NSAID induce the syndrome of asthma, rhinitis and nasal polyps. Both types of reactions have the potential of being fatal.
Therefore, careful questioning of patients for such things as asthma, nasal polyps, urticaria and hypotension associated with nonsteroidal anti-inflammatory drugs before starting therapy is important. In addition, if such symptoms occur during therapy, treatment should be discontinued.
Anaphylactoid reactions to naproxen sodium whether of true allergic type or the pharmacologic idiosyncratic type, usually but not always occur in patients with a known history of such reactions.
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.
The drug should not be used during pregnancy unless clearly needed. It should not be used during late pregnancy due to known effect on the human fetal.
Adverse reactions to naproxen mainly involve the GI tract. Constipation, heartburn, abdominal pain and nausea occur in about 3 - 9% of patients receiving the drug. Less frequently, dyspepsia, diarrhea, stomatitis, vomiting, anorexia and flatulence occur. Naproxen may reactivate latent peptic ulcer and may cause peptic ulcers in patients with no previous history of ulcers. Haemorrhage and perforation of ulcers may occur, occasionally causing fatalities, GI bleeding without obvious ulcer formation and melena have also occurred.
Adverse nervous system effects of naproxen include headache, drowsiness and dizziness, which occur in about 3 - 9% of patients. Vertigo, lightheadedness, inability to concentrate, mental depression, nervousness, irritability, fatigue, malaise, insomnia, sleep disorders and dream abnormalities may also occur.
Patients receiving naproxen have experienced tinnitus and less frequently, hearing or visual disturbances (e.g. hearing impairment). Adverse hematologic effects of naproxen include thrombocytopenia, leukocytopenia, granulocytopenia and eosinophilia. Naproxen can inhibit platelet aggregation and may prolong bleeding time. Pruritus, skin eruptions or rashes and ecchymoses occur frequently during naproxen administration.
Naproxen sodium may cause gastrointestinal bleeding and may inhibit platelet aggregation, thus the drug should be used with caution in patients receiving anticoagulant or thrombolytic agent. The effects of naproxen sodium is substantially potentiated by concomitant administration of probenecid.
Concomitant administration of naproxen sodium and methotrexate can result in severe, sometimes fatal toxicity. Naproxen sodium also interact with prednisolone, furosemide and salicylates.
Lithium: Decreased clearance and increased serum concentration of lithium resulting in toxicity on some occasions have been reported.
Quinolone antibiotics: NSAIDs can increase the central adverse effects leading to convulsions.
Protein-bound drugs: Because naproxen is highly protein bound, it theoretically could be displaced from binding sites by, or it could displace from binding sites, other protein-bound drugs such as oral anticoagulants, hydantoins, salicylates, sulfonamides and sulfonylureas.
Furosemide: The natriuretic effect of furosemide has been reported to be inhibited. It was suggested that NSAIDs not to be used during diuretic therapy for cardiac failure.
Beta-blockers: The antihypertensive effect of propranolol and other beta-blockers can be reduced.
Incompatibilities: Reports of incompatibilities are not available.
Store at or below 30°C. Protect from light.
Shelf-life: 3 years.
M01AE02 - naproxen ; Belongs to the class of propionic acid derivatives of non-steroidal antiinflammatory and antirheumatic products.
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