Guest guest Posted July 16, 2004 Report Share Posted July 16, 2004 I went to www.rxlist.com and typed in the med you asked about. Here is the info it listed. I don't know anything about this med personally but I think you should at least call the dr that prescribed it and let him know what your feeling. Good luck with it and below I pasted the info I found. Hope you feel better soon. Hugs Deanna Generic Name: DICLOFENAC SODIUM Drug Class: NONSTEROIDAL ANTIINFLAMMATORY AGENTS INDICATIONS Cataflam Immediate-Release Tablets and Voltaren Delayed-Release Tablets are indicated for the acute and chronic treatment of signs and symptoms of osteoarthritis and rheumatoid arthritis. Voltaren-XR Extended-Release Tablets are indicated for chronic therapy of osteoarthritis and rheumatoid arthritis. In addition, Cataflam Immediate-Release Tablets and Voltaren Delayed-Release Tablets are indicated for the treatment of ankylosing spondylitis. Only Cataflam is indicated for the management of pain and primary dysmenorrhea, when prompt pain relief is desired, because it is formulated to provide earlier plasma concentrations of diclofenac (see CLINICAL PHARMACOLOGY, Pharmacokinetics and Clinical Studies). DOSAGE AND ADMINISTRATION Diclofenac may be administered as 50-mg Cataflam Immediate- ReleaseTablets, as 25-mg, 50-mg, and 75-mg Voltaren Delayed-Release Tablets, or as 1 00-mg Voltaren-XR Extended-Release Tablets. Cataflam Immediate-Release Tablets is the formulation indicated for management of acute pain and primary dysmenorrhea when prompt onset of pain relief is desired because of earlier absorption of diclofenac. For the same reason, Voltaren-XR is not indicated for the management of acute painful conditions and should be used as chronic therapy in patients with osteoarthritis and rheumatoid arthritis. The dosage of diclofenac should be individualized to the lowest effective dose to minimize adverse effects (see CLINICAL PHARMACOLOGY, INDIVIDUALIZATION OF DOSAGE). Osteoarthritis: The recommended dosage is 100 to 150 mg/day: Cataflam or Voltaren Delayed-Release 50 mg b.i.d. or t.i.d.; or Voltaren Delayed-Release 75 mg b.i.d.. The recommended dosage for chronic therapy with Voltaren-XR is 100 mg q.d.. Dosages of Voltaren-XR Extended-Release Tablets of 200 mg daily are not recommended for patients with osteoarthritis. Dosages above 200 mg/day have not been studied in patients with osteoarthritis. Rheumatoid Arthritis: The recommended dosage is 100 to 200 mg/day: Cataflam or Voltaren Delayed-Release 50 mg t.i.d. or q.i.d.; or Voltaren Delayed-Release 75 mg b.i.d.. The recommended dosage for chronic therapy with Voltaren-XR is 100 mg q.d.. In the rare patient where Voltaren-XR 100 mg/day is unsatisfactory, the dose may be increased to 100 mg b.i.d. if the benefits outweigh the clinical risks. Dosages above 225 mg/day are not recommended in patients with rheumatoid arthritis. Ankylosing Spondylitis: The recommended dosage is 100 to 125 mg/day: Voltaren 25 mg q.i.d. with an extra 25-mg dose at bedtime if necessary. Dosages above 125 mg/day have not been studied in patients with ankylosing spondylitis. Analgesia and Primary Dysmenorrhea: The recommended starting dose of Cataflam Immediate-Release Tablets is 50 mg t.i.d.. With experience, physicians may find that in some patients an initial dose of 100 mg of Cataflam, followed by 50-mg doses, will provide better relief. After the first day, when the maximum recommended dose may be 200 mg, the total daily dose should generally not exceed 150 mg. HOW SUPPLIED Cataflam Tablets 50 mg - light brown, round, biconvex (imprinted CATAFLAM on one side and 50 on the other side) Bottles of 100 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . NDC 0028-0151-01 Unit Dose (blister pack) Box of 100 (strips of 10) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . NDC 0028-0151-61 Voltaren Delayed-ReleaseTablets 25 mg - yellow, biconvex, triangular-shaped (imprinted VOLTAREN 25 on one side) Bottles of 60 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . NDC 0028-0258-60 Bottles of 100 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . NDC 0028-0258-01 Unit Dose (blister pack) Box of 100 (strips of 10) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . NDC 0028-0258-61 50 mg - light brown, biconvex, triangular-shaped (imprinted VOLTAREN 50 on one side) Bottles of 60 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . NDC 0028-0262-60 Bottles of 100 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . NDC 0028-0262-01 Bottles of 1000 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . NDC 0028-0262-10 Unit Dose (blister pack) Box of 100 (strips of 10) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . NDC 0028-0262-61 75 mg - light pink, biconvex, triangular-shaped (imprinted VOLTAREN 75 on one side Bottles of 60 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . NDC 0028-0264-60 Bottles of 100 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . NDC 0028-0264-01 Bottles of 1000 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . NDC 0028-0264-10 Unit Dose (blister pack) Box of 100 (strips of 10) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . NDC 0028-0264-61 Voltaren-XR Extended-ReleaseTablets 100 mg - light pink, coated, round, biconvex with beveled edges (imprinted Voltaren-XR on one side and 100 on the other side) Bottles of 100 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . NDC 0028-0205-01 Unit Dose (blister pack) Box of 100 (strips of 10) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . NDC 0028-0205-61 Do not store above 86° F (30° C). Protect from moisture. Dispense in tight container (USP). SIDE EFFECTS Adverse reaction information is derived from blinded, controlled, and open-label clinical trials, as well as worldwide marketing experience. In the description below, rates of more common events represent clinical study results; rarer events are derived principally from marketing experience and publications, and accurate rate estimates are generally not possible. In 718 patients treated for shorter periods, i.e., 2 weeks or less, with Cataflam Immediate-Release Tablets, adverse reactions were reported one-half to one-tenth as frequently as by patients treated for longer periods. In a 6-month, double-blind trial comparing Cataflam Immediate-Release Tablets (N=196) versus Voltaren Delayed- Release Tablets (N=197) versus ibuprofen (N=197), adverse reactions were similar in nature and frequency. In controlled clinical trials, the incidence of adverse reactions for Voltaren Delayed-Release Tablets and Voltaren-XR Extended-Release Tablets at comparable doses were similar. The incidence of common adverse reactions (greater than 1%) is based upon controlled clinical trials in 1,543 patients treated up to 13 weeks with Voltaren Delayed-Release Tablets. By far the most common adverse effects were gastrointestinal symptoms, most of them minor, occurring in about 20%, and leading to discontinuation in about 3%, of patients. Peptic ulcer or G.I. bleeding occurred in clinical trials in 0.6% (95% confidence interval: 0.2% to 1%) of approximately 1,800 patients during their first 3 months of diclofenac treatment and in 1.6% (95% confidence interval: 0.8% to 2.4%) of approximately 800 patients followed for 1 year. Gastrointestinal symptoms were followed in frequency by central nervous system side effects such as headache (7%) and dizziness (3%). Meaningful (exceeding 3 times the Upper Limit of Normal) elevations of ALT (SGPT) or AST (SGOT) occurred at an overall rate of approximately 2% during the first 2 months of Voltaren treatment. Unlike aspirin-related elevations, which occur more frequently in patients with rheumatoid arthritis, these elevations were more frequently observed in patients with osteoarthritis (2.6%) than in patients with rheumatoid arthritis (0.7%). Marked elevations (exceeding 8 times the ULN) were seen in 1% of patients treated for 2- 6 months (see WARNINGS, Hepatic Effects). The following adverse reactions were reported in patients treated with diclofenac: Incidence Greater Than 1% Causal Relationship Probable (All derived from clinical trials.) *Incidence, 3% to 9% (incidence of unmarked reactions is l%-3%). Body as a Whole: Abdominal pain or cramps,* headache,* fluid retention, abdominal distention. Digestive: Diarrhea,* indigestion,* nausea,* constipation,* flatulence, liver test abnormalities,* P.B. i.e., peptic ulcer, with or without bleeding and/or perforation, or bleeding without ulcer (see above and also WARNINGS). Nervous System: Dizziness. Skin and Appendages: Rash, pruritus. Special Senses: Tinnitus. Incidence Less Than 1% - Causal Relationship Probable (Adverse reactions reported only in worldwide marketing experience or in the literature, not seen in clinical trials, are considered rare and are italicized.) Body as a Whole: Malaise, swelling of lips and tongue, photosensitivity, anaphylaxis, anaphylactoid reactions. Cardiovascular: Hypertension, congestive heart failure. Digestive: Vomiting, jaundice, melena, esophageal lesions, aphthous stomatitis, dry mouth and mucous membranes, bloody diarrhea, hepatitis, hepatic necrosis, cirrhosis, hepatorenal syndrome, appetite change, pancreatitis with or without concomitant hepatitis, colitis. Hemic and Lymphatic: Hemoglobin decrease, leukopenia, thrombocytopenia, eosinophilia, hemolytic anemia, aplastic anemia, agranulocytosis, purpura, allergic purpura. Metabolic and Nutritional Disorders: Azotemia. Nervous System: Insomnia, drowsiness, depression, diplopia, anxiety, irritability, aseptic meningitis, convulsions. Respiratory: Epistaxis, asthma, laryngeal edema. Skin and Appendages: Alopecia, urticaria, eczema, dermatitis, bullous eruption, erythema multiforme major, angioedema, s- syndrome. Special Senses: Blurred vision, taste disorder, reversible and irreversible hearing loss, scotoma. Urogenital: Nephrotic syndrome, proteinuria, oliguria, interstitial nephritis, papillary necrosis, acute renal failure. Incidence Less Than 1% - Causal Relationship Unknown (The following reactions have been reported in patients taking diclofenac under circumstances that do not permit a clear attribution of the reaction to diclofenac. These reactions are being included as alerting information to physicians. Adverse reactions reported only in worldwide marketing experience or in the literature, not seen in clinical trials, are considered rare and are italicized.) Body as a Whole: Chest pain. Cadiovascular: Palpitations, flushing, tachycardia, premature ventricular contractions, myocardial infarction, hypotension. Digestive: Intestinal perforation. Hemic and Lymphatic: Bruising. Metabolic and Nutritional Disorders: Hypoglycemia, weight loss. Nervous System: Paresthesia, memory disturbance, nightmares, tremor, tic, abnormal coordination, disorientation, psychotic reaction. Respiratory: Dyspnea, hyperventilation, edema of pharynx. Skin and Appendages: Excess perspiration, exfoliative dermatitis. Special Senses: Vitreous floaters, night blindness, amblyopia. Urogenital: Urinary frequency, nocturia, hematuria, impotence, vaginal bleeding. DRUG INTERACTIONS Aspirin: Concomitant administration of diclofenac and aspirin is not recommended because diclofenac is displaced from its binding sites during the concomitant administration of aspirin, resulting in lower plasma concentrations, peak plasma levels, and AUC values. Anticoagulants: While studies have not shown diclofenac to interact with anticoagulants of the warfarin type, caution should be exercised, nonetheless, since interactions have been seen with other NSAIDs. Because prostaglandins play an important role in hemostasis, and NSAIDs affect platelet function as well, concurrent therapy with all NSAIDs, including diclofenac, and warfarin requires close monitoring of patients to be certain that no change in their anticoagulant dosage is required. Digoxin, Methotrexate, Cyclosporine: Diclofenac, like other NSAIDs, may affect renal prostaglandins and increase the toxicity of certain drugs. Ingestion of diclofenac may increase serum concentrations of digoxin and methotrexate and increase cyclosporine's nephrotoxicity. Patients who begin taking diclofenac or who increase their diclofenac dose or any other NSAID while taking digoxin, methotrexate, or cyclosporine may develop toxicity characteristics for these drugs. They should be observed closely, particularly if renal function is impaired. In the case of digoxin, serum levels should be monitored. Lithium: Diclofenac decreases lithium renal clearance and increases lithium plasma levels. In patients taking diclofenac and lithium concomitantly, lithium toxicity may develop. Oral Hypoglycemics: Diclofenac does not alter glucose metabolism in normal subjects nor does it alter the effects of oral hypoglycemic agents. There are rare reports, however, from marketing experiences, of changes in effects of insulin or oral hypoglycemic agents in the presence of diclofenac that necessitated changes in the doses of such agents. Both hypo- and hyperglycemic effects have been reported. A direct causal relationship has not been established, but physicians should consider the possibility that diclofenac may alter a diabetic patient's response to insulin or oral hypoglycemic agents. Diuretics: Diclofenac and other NSAIDs can inhibit the activity of diuretics. Concomitant treatment with potassium-sparing diuretics may be associated with increased serum potassium levels. Other Drugs: In small groups of patients (7-10/interaction study), the concomitant administration of azathioprine, gold, chloroquine, D- penicillamine, prednisolone, doxycycline, or digitoxin did not significantly affect the peak levels and AUC values of diclofenac. Phenobarbital toxicity has been reported to have occurred in a patient on chronic phenobarbital treatment following the initiation of diclofenac therapy. Protein Binding In vitro, diclofenac interferes minimally or not at all with the protein binding of salicylic acid (20% decrease in binding), tolbutamide, prednisolone (10% decrease in binding), or warfarin. Benzylpenicillin, ampicillin, oxacillin, chlortetracycline, doxycycline, cephalothin, erythromycin, and sulfamethoxazole have no influence in vitro on the protein binding of diclofenac in human serum. Drug/Laboratory Test Interactions Effect on Blood Coagulation: Diclofenac increases platelet aggregation time but does not affect bleeding time, plasma thrombin clotting time, plasma fibrinogen, or factors V and VII to XII. Statistically significant changes in prothrombin and partial thromboplastin times have been reported in normal volunteers. The mean changes were observed to be less than 1 second in both instances, however, and are unlikely to be clinically important. Diclofenac is a prostaglandin synthetase inhibitor, however, and all drugs that inhibit prostaglandin synthesis interfere with platelet function to some degree; therefore, patients who may be adversely affected by such an action should be carefully observed. WARNINGS Gastrointestinal Effects Peptic ulceration and gastrointestinal bleeding have been reported in patients receiving diclofenac. Physicians and patients should therefore remain alert for ulceration and bleeding in patients treated chronically with diclofenac even in the absence of previous G.I. tract symptoms. It is recommended that patients be maintained on the lowest dose of diclofenac possible, consistent with achieving a satisfactory therapeutic response. Risk of G.I. Ulcerations, Bleeding, and Perforation with NSAID Therapy: Serious gastrointestinal toxicity such as bleeding, ulceration, and perforation can occur at any time, with or without warning symptoms, in patients treated chronically with NSAID therapy. Although minor upper gastrointestinal problems, such as dyspepsia, are common, usually developing early in therapy, physicians should remain alert for ulceration and bleeding in patients treated chronically with NSAIDs even in the absence of previous G.I. tract symptoms. In patients observed in clinical trials of several months to 2 years' duration, symptomatic upper G.I. ulcers, gross bleeding, or perforation appear to occur in approximately 1% of patients for 3- 6 months, and in about 2%-4% of patients treated for 1 year. Physicians should inform patients about the signs and/or symptoms of serious G.I. toxicity and what steps to take if they occur. Studies to date have not identified any subset of patients not at risk of developing peptic ulceration and bleeding. Except for a prior history of serious G.I. events and other risk factors known to be associated with peptic ulcer disease, such as alcoholism, smoking, etc., no risk factors (e.g., age, sex) have been associated with increased risk. Elderly or debilitated patients seem to tolerate ulceration or bleeding less well than other individuals, and most spontaneous reports of fatal G.I. events are in this population. Studies to date are inconclusive concerning the relative risk of various NSAIDs in causing such reactions. High doses of any NSAID probably carry a greater risk of these reactions, although controlled clinical trials showing this do not exist in most cases. In considering the use of relatively large doses (within the recommended dosage range), sufficient benefit should be anticipated to offset the potential increased risk of G.I. toxicity. Hepatic Effects Elevations of one or more liver tests may occur during diclofenac therapy. These laboratory abnormalities may progress, may remain unchanged, or may be transient with continued therapy. Borderline elevations (i.e., less than 3 times the ULN [=the Upper Limit of the Normal range]), or greater elevations of transaminases occurred in about 15% of diclofenac-treated patients. Of the hepatic enzymes, ALT (SGPT) is the one recommended for the monitoring of liver injury. In clinical trials, meaningful elevations (i.e., more than 3 times the ULN) of AST (SGOT) (ALT was not measured in all studies) occurred in about 2% of approximately 5,700 patients at some time during Voltaren treatment. In a large, open, controlled trial, meaningful elevations of ALT and/or AST occurred in about 4% of 3,700 patients treated for 2-6 months, including marked elevations (i.e., more than 8 times the ULN) in about 1 % of the 3,700 patients. In that open- label study, a higher incidence of borderline (less than 3 times the ULN), moderate (3-8 times the ULN), and marked (>8 times the ULN) elevations of ALT or AST was observed in patients receiving diclofenac when compared to other NSAIDs. Transaminase elevations were seen more frequently in patients with osteoarthritis than in those with rheumatoid arthritis (see ADVERSE REACTIONS). In addition to enzyme elevations seen in clinical trials, postmarketing surveillance has found rare cases of severe hepatic reactions, including liver necrosis, jaundice, and fulminant fatal hepatitis with and without jaundice. Some of these rare reported cases underwent liver transplantation. Physicians should measure transaminases periodically in patients receiving long-term therapy with diclofenac, because severe hepatotoxicity may develop without a prodrome of distinguishing symptoms. The optimum times for making the first and subsequent transaminase measurements are not known. In the largest U.S. trial (open-label) that involved 3,700 patients monitored first at 8 weeks and 1,200 patients monitored again at 24 weeks, almost all meaningful elevations in transaminases were detected before patients became symptomatic. In 42 of the 51 patients in all trials who developed marked transaminase elevations, abnormal tests occurred during the first 2 months of therapy with diclofenac. Postmarketing experience has shown severe hepatic reactions can occur at any time during treatment with diclofenac. Cases of drug-induced hepatotoxicity have been reported in the first month, and in some cases, the first two months of therapy. Based on these experiences, transaminases should be monitored within 4 to 8 weeks after initiating treatment with diclofenac (see PRECAUTIONS -Laboratory Tests). As with other NSAIDs, if abnormal liver tests persist or worsen, if clinical signs and/or symptoms consistent with liver disease develop, or if systemic manifestations occur (e.g., eosinophilia, rash, etc.), diclofenac should be discontinued immediately. To minimize the possibility that hepatic injury will become severe between transaminase measurements, physicians should inform patients of the warning signs and symptoms of hepatotoxicity (e.g., nausea, fatigue, lethargy, pruritus, jaundice, right upper quadrant tenderness, and " flu-like " symptoms), and the appropriate action patients should take if these signs and symptoms appear. Anaphylactoid REACTIONS As with other NSAIDs, anaphylactoid reactions may occur in patients without prior exposure to diclofenac. Diclofenac should not be given to patients with the aspirin t.i.d. The triad typically occurs in asthmatic patients who experience rhinitis with or without nasal polyps, or who exhibit severe, potentially fatal bronchospasm after taking aspirin or other nonsteroidal anti-inflammatory drugs. Fatal reactions have been reported in such patients (see CONTRAINDICATIONS, and PRECAUTIONS -Preexisting Asthma). Emergency help should be sought in cases where an anaphylactoid reaction occurs. Advanced Renal Disease In cases with advanced kidney disease, treatment with diclofenac, as with other NSAIDs, should only be initiated with close monitoring of the patient's kidney functions (see PRECAUTIONS -Renal Effects). Pregnancy In late pregnancy, diclofenac should, as with other NSAIDs, be avoided because it will cause premature closure of the ductus arteriosus (see PRECAUTIONS - Pregnancy, Teratogenic Effects, Pregnancy Category 5, and Labor and Delivery). PRECAUTIONS General Cataflam Immediate-Release Tablets, Voltaren Delayed-Release Tablets, and Voltaren-XR Extended-Release Tablets should not be used concomitantly with other didofenac-containing products since they do circulate in plasma as the diclofenac anion. Fluid Retention and Edema: Fluid retention and edema have been observed in some patients taking diclofenac. Therefore, as with other NSAIDs, diclofenac should be used with caution in patients with a history of cardiac decompensation, hypertension, or other conditions predisposing to fluid retention. Hematologic Effects: Anemia is sometimes seen in patients receiving diclofenac or other NSAIDs. This may be due to fluid retention, G.I. blood loss, or an incompletely described effect upon erythropoiesis. Renal Effects: As a class, NSAIDs have been associated with renal papillary necrosis and other abnormal renal pathology in long-term administration to animals. In oral diclofenac studies in animals, some evidence of renal toxicity was noted. Isolated incidents of papillary necrosis were observed in a few animals at high doses (20- 120 mg/kg) in several baboon subacute studies. In patients treated with diclofenac, rare cases of interstitial nephritis and papillary necrosis have been reported (see ADVERSE REACTIONS). A second form of renal toxicity, generally associated with NSAIDs, is seen in patients with conditions leading to a reduction in renal blood flow or blood volume, where renal prostaglandins have a supportive role in the maintenance of renal perfusion. In these patients, administration of an NSAID results in a dose-dependent decrease in prostaglandin synthesis and, secondarily, in a reduction of renal blood flow, which may precipitate overt renal failure. 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. Cases of significant renal failure in patients receiving diclofenac have been reported from marketing experience, but were not observed in over 4,000 patients in clinical trials during which serum creatinine and BUN values were followed serially. There were only 11 patients (0.3%) whose serum creatinine and concurrent serum BUN values were greater than 2.0 mg/dL and 40 mg/dL, respectively, while on diclofenac (mean rise in the 11 patients: creatinine 2.3 mg/dL and BUN 28.4 mg/dL). Since diclofenac metabolites are eliminated primarily by the kidneys, patients with significantly impaired renal function should be more closely monitored than subjects with normal renal function. Porphyria: The use of diclofenac in patients with hepatic porphyria should be avoided. To date, 1 patient has been described in whom diclofenac probably triggered a clinical attack of porphyria. The postulated mechanism, demonstrated in rats, for causing such attacks by diclofenac, as well as some other NSAIDs, is through stimulation of the porphyrin precursor delta-aminolevulinic acid (ALA). Aseptic Meningitis: As with other NSAIDs, aseptic meningitis with fever and coma has been observed on rare occasions in patients on diclofenac therapy. Although it is probably more likely to occur in patients with systemic lupus erythematosus and related connective tissue diseases, it has been reported in patients who do not have an underlying chronic disease. If signs or symptoms of meningitis develop in a patient on diclofenac, the possibility of its being related to diclofenac should be considered. Preexisting Asthma: About 10% of patients with asthma may have aspirin-sensitive asthma. The use of aspirin in patients with aspirin- sensitive asthma has been associated with severe bronchospasm which can be fatal. Since cross-reactivity, including bronchospasm, between aspirin and other nonsteroidal anti-inflammatory drugs has been reported in such aspirin-sensitive patients, diclofenac should not be administered to patients with this form of aspirin sensitivity and should be used with caution in all patients with preexisting asthma. Other Precautions: The pharmacologic activity of diclofenac may reduce fever and inflammation, thus diminishing their utility as diagnostic signs in detecting underlying conditions. In order to avoid exacerbation of manifestations of adrenal insufficiency, patients who have been on prolonged corticosteroid treatment should have their therapy tapered slowly rather than discontinued abruptly when diclofenac is added to the treatment program. Blurred and/or diminished vision, scotomata, and/or changes in color vision have been reported. If a patient develops such complaints while receiving diclofenac, the drug should be discontinued and the patient should have an ophthalmologic examination which includes central visual fields and color vision testing. Information for Patients See PATIENT INFORMATION section. Laboratory Tests Hepatic Effects: Transaminases and other hepatic enzymes should be monitored in patients treated with NSAIDs. For patients on diclofenac therapy, it is recommended that a determination be made within 4 weeks of initiating therapy and at intervals thereafter. If clinical signs and symptoms consistent with liver disease develop, or if systemic manifestations occur (e.g. eosinophilia, rash, etc.) and abnormal liver tests are detected, persist or worsen, diclofenac should be discontinued immediately. Hematologic Effects: Patients on long-term treatment with NSAIDs, including diclofenac, should have their hemoglobin or hematocrit checked periodically for signs or symptoms of anemia. Appropriate measures should be taken in case such signs of anemia occur. Drug Interactions See DRUG INTERACTIONS section. Protein Binding In vitro, diclofenac interferes minimally or not at all with the protein binding of salicylic acid (20% decrease in binding), tolbutamide, prednisolone (10% decrease in binding), or warfarin. Benzylpenicillin, ampicillin, oxacillin, chlortetracycline, doxycycline, cephalothin, erythromycin, and sulfamethoxazole have no influence in vitro on the protein binding of diclofenac in human serum. Drug/Laboratory Test Interactions Effect on Blood Coagulation: Diclofenac increases platelet aggregation time but does not affect bleeding time, plasma thrombin clotting time, plasma fibrinogen, or factors V and VII to XII. Statistically significant changes in prothrombin and partial thromboplastin times have been reported in normal volunteers. The mean changes were observed to be less than 1 second in both instances, however, and are unlikely to be clinically important. Diclofenac is a prostaglandin synthetase inhibitor, however, and all drugs that inhibit prostaglandin synthesis interfere with platelet function to some degree; therefore, patients who may be adversely affected by such an action should be carefully observed. Carcinogenesis, Mutagenesis, Impairment of Fertility Long-term carcinogenicity studies in rats given diclofenac sodium up to 2 mg/kg/day (or 12 mg/m2/day, approximately the human dose) have revealed no significant increases in tumor incidence. There was a slight increase in benign mammary fibroadenomas in mid-dose-treated (0.5 mg/kg/day or 3 mg/m2/day) female rats (high-dose females had excessive mortality), but the increase was not significant for this common rat tumor. A 2-year carcinogenicity study conducted in mice employing diclofenac sodium at doses up to 0.3 mg/kg/day (0.9 mg/m2/day) in males and 1 mg/kg/day (3 mg/m2/day) in females did not reveal any oncogenic potential. Diclofenac sodium did not show mutagenic activity in in vitro point mutation assays in mammalian (mouse lymphoma) and microbial (yeast, Ames) test systems and was nonmutagenic in several mammalian in vitro and in vivo tests, including dominant lethal and male germinal epithelial chromosomal studies in mice, and nucleus anomaly and chromosomal aberration studies in Chinese hamsters. Diclofenac sodium administered to male and female rats at 4 mg/kg/day (24 mg/m2/day) did not affect fertility. Pregnancy Teratogenic Effects, Pregnancy Category B: Reproduction studies have been performed in mice given diclofenac sodium (up to 20 mg/kg/day or 60 mg/m2/day) and in rats and rabbits given diclofenac sodium (up to 10 mg/kg/day or 60 mg/m2/day for rats, and 80 mg/m2/day for rabbits), and have revealed no evidence of teratogenicity despite the induction of maternal toxicity and fetal toxicity. In rats, maternally toxic doses were associated with dystocia, prolonged gestation, reduced fetal weights and growth, and reduced fetal survival. Diclofenac has been shown to cross the placental barrier in mice and rats. There are, however, no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should not be used during pregnancy unless the benefits to the mother justify the potential risk to the fetus. Because of the risk to the fetus resulting in premature closure of the ductus arteriosus, diclofenac should be avoided in late pregnancy. Labor and Delivery The effects of diclofenac on labor and delivery in pregnant women are unknown. Because of the known effects of prostaglandin-inhibiting drugs on the fetal cardiovascular system (closure of ductus arteriosus), use of diclofenac during late pregnancy should be avoided and as with other nonsteroidal anti-inflammatory drugs, it is possible that diclofenac may inhibit uterine contractions and delay parturition. Nursing Mothers Because of the potential for serious adverse reactions in nursing infants from diclofenac, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother. Pediatric Use Safety and effectiveness of diclofenac in pediatric patients have not been established. Geriatric Use Of the more than 6,000 patients treated with diclofenac in U.S. trials, 31% were older than 65 years of age. No overall difference was observed between efficacy, adverse event, or pharmacokinetic profiles of older and younger patients. As with any NSAIDs the elderly are likely to tolerate adverse reactions less well than younger patients. PATIENT INFORMATION Diclofenac, like other drugs of its class, is not free of side effects. The side effects of these drugs can cause discomfort and rarely, more serious side effects, such as gastrointestinal bleeding, and more rarely, liver toxicity {see WARNINGS, Hepatic Effects), which may result in hospitalization and even fatal outcomes. NSAIDs are often essential agents in the management of arthritis and have a major role in the management of pain, but they also may be commonly employed for conditions that are less serious. Physicians may w.s. to discuss with their patients the potential risks (see WARNINGS, PRECAUTIONS, and ADVERSE REACTIONS) and likely benefits of NSAID treatment, particularly when the drugs are used for less serious conditions where treatment without NSAIDs may represent an acceptable alternative to both the patient and physician. Because serious G.I. tract ulceration and bleeding can occur without warning symptoms, physicians should follow chronically treated patients for the signs and symptoms of ulceration and bleeding and should inform them of the importance of this follow-up (see WARNINGS, Gastrointestinal Effects, Risk of G.I. Ulcerations, Bleeding, and Perforation with NSAID Therapy). If diclofenac is used chronically, patients should also be instructed to report any signs and symptoms that might be due to hepatotoxicity of dictofenac; these symptoms may become evident between visits when periodic liver laboratory tests are performed (see WARNINGS, Hepatic Effects, and PRECAUTIONS- Laboratory Tests). Quote Link to comment Share on other sites More sharing options...
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