This dosage information may not include all the information needed to use Oxaprozin safely and effectively. See additional information for Oxaprozin.
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Usual Adult Dose for:
Usual Pediatric Dose for:
Additional dosage information:
Usual Adult Dose for Rheumatoid Arthritis
Initial: 1200 mg orally once a day.
Maintenance: May be increased to 1800 mg in divided doses if necessary.
Usual Adult Dose for Osteoarthritis
Initial: 600 mg orally once a day (mild to moderate).
1200 mg orally once a day (moderate to severe).
Maintenance: May be increased to 1800 mg in divided doses if necessary.
Usual Pediatric Dose for Juvenile Rheumatoid Arthritis
Greater than or equal to 6 years: 10 to 20 mg/kg/day, given in 2 divided doses.
Maximum daily dose: 1200 mg.
Renal Dose Adjustments
For patients with renal impairment and patients undergoing hemodialysis, the initial dose is 600 mg.
Liver Dose Adjustments
Use with caution in patients with severe hepatic impairment.
In cases where a quick onset of action is important, therapy may be started with a one-time loading dose of 1200 to 1800 mg (not to exceed 26 mg/kg). Doses larger than 1200 mg/day should be reserved for patients who weigh >50 kg, have normal renal and hepatic function, are at low risk of peptic ulcer, and whose severity of disease justifies maximal therapy. Individualize dose to the lowest effective dose to minimize adverse effects.
NSAIDs may cause an increased risk of serious cardiovascular (CV) thrombotic events, myocardial infarction, and stroke, which can be fatal. This risk may increase with duration of administration. All NSAIDs, both COX-2 selective and nonselective, may have a similar risk. Patients with known CV disease or risk factors for CV disease may be at greater risk. To minimize the potential risk for an adverse CV event in patients treated with NSAIDs, the lowest effective dose should be used for the shortest duration possible. Prescribers and patients should remain vigilant for the development of such events, even in the absence of previous CV symptoms. Patients should be advised about the signs and/or symptoms of serious CV events and the steps to take if they occur. There is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious CV thrombotic events associated with NSAID use.
Serious gastrointestinal (GI) toxicity, such as bleeding, ulceration, and perforation, can occur at any time with or without warning symptoms, in patients receiving NSAID therapy chronically. These serious adverse events can occur at any time, with or without warning symptoms, in patients treated with NSAIDs. Only one in five patients who develop a serious upper GI adverse event on NSAID therapy is symptomatic. It has been shown that the incidence of symptomatic upper GI ulcers, gross bleeding, or perforation, caused by NSAIDs, increases with duration of use. However, even short-term therapy is not without risk. Patients should be informed about the signs and symptoms of serious GI toxicities and the steps to take if they occur. Great caution should be exercised when using NSAIDs in patients with a prior history of peptic ulcer disease and/or GI bleeding and in patients who may have other comorbid conditions that may increase the risk of GI bleeding. Patients with a prior history of peptic ulcer disease, and/or GI bleeding, and who use NSAIDs have a greater than 10-fold increased risk for developing a GI bleed compared to patients with neither of these risk factors. Other factors that increase the risk for GI bleeding in patients treated with NSAID therapy, smoking, use of alcohol, older age, and poor general health status. Since elderly patients are at greater risk for serious GI events, special care should be taken in treating this population. To minimize the potential risk for an adverse GI event in patients treated with an NSAID, the lowest effective dose should be used for the shortest duration. Patients and physicians should remain alert for signs and symptoms of GI ulceration and bleeding during NSAID therapy and promptly initiate additional evaluation and treatment if a serious GI adverse event is suspected. This should include discontinuation of the NSAID until a serious GI adverse event is ruled out. For high-risk patients, alternate therapies that do not involve NSAIDs should be considered. NSAIDs should be administered with care to patients with a history of inflammatory bowel disease (ulcerative colitis, Crohn's disease) as their condition may be exacerbated.
Oxaprozin is contraindicated for the treatment of perioperative pain in patients undergoing coronary artery bypass graft (CABG) surgery. Patients with a hypersensitivity (angioedema, bronchospasm, urticaria, or rhinitis) to aspirin or other NSAIDs may be cross sensitive to oxaprozin. Patients with the "triad" of asthma, nasal polyps, and aspirin or other NSAID hypersensitivity are at particular risk. The use of oxaprozin is considered contraindicated in these patients.
Renal function may be further compromised by the use of oxaprozin in patients with renal dysfunction, heart failure, hypovolemia, cirrhosis, nephrotic syndrome, or hypoalbuminemia. Renal blood flow in patients with renal dysfunction, edematous disorders, or hypovolemic states is dependent upon renal prostaglandin synthesis. Discontinuation of NSAID therapy is usually followed by recovery to the pretreatment state. Long-term NSAIDs use has resulted in renal papillary necrosis and other renal injury. No information is available from controlled clinical trials regarding the use of oxaprozin in patients with advanced renal disease. Therefore, treatment with oxaprozin is not recommended in patients with advanced renal disease. If oxaprozin must be used, periodic monitoring of renal function is recommended. Oxaprozin should be used with caution in patients with renal dysfunction.
NSAIDs, including oxaprozin, can cause serious skin adverse events such as exfoliative dermatitis, Stevens-Johnson Syndrome (SJS), and toxic epidermal necrolysis (TEN), which can be fatal. These serious events may occur without warning. Patients should be informed about the signs and symptoms of serious skin manifestations and use of the drug should be discontinued at the first appearance of skin rash or any other sign of hypersensitivity.
Borderline increases in one or more liver function test results have been reported in patients treated with NSAIDs, including oxaprozin. These laboratory abnormalities may progress, may remain unchanged, or may be transient with continuing therapy. Clinically important elevations of serum ALT or AST (i.e., 3 times the upper limit of normal) have been reported in patients receiving NSAIDs. In addition, rare cases of severe hepatic reactions, including jaundice, fulminant hepatitis, liver necrosis, and hepatic failure, some of them with fatal outcomes have been reported. Patients with symptoms and/or signs suggesting liver dysfunction, or with abnormal liver test values, should be evaluated for evidence of the development of more severe hepatic reactions while on therapy with oxaprozin. Oxaprozin should be discontinued if patients experience signs or symptoms suggestive of liver dysfunction because severe and sometimes fatal hepatotoxic reactions have occurred. Oxaprozin should be used with caution in patients with hepatic disease.
Anemia has been reported in patients receiving NSAIDs, including oxaprozin. This may due to fluid retention, GI blood loss, or an incompletely described effect upon erythropoiesis. Patients on long-term treatment with NSAIDs, including oxaprozin, should have their hemoglobin or hematocrit checked if they exhibit any signs or symptoms of anemia.
NSAIDs inhibit platelet aggression and have been shown to prolong bleeding time in some patients. Unlike aspirin, their effect on platelet function is quantitatively less, of shorter duration, and reversible. Patients receiving oxaprozin who may be adversely affected by alterations in platelet function, such as those with coagulation disorders, should be carefully monitored.
Patients on long-term treatment with NSAIDs should have their CBC and a chemistry profile checked periodically.
Oxaprozin is not dialyzed because of its high degree of protein binding.