|
||
G Nac Dosage |
||
Carefully consider the potential benefits and risks of G Nac extended-release tablets, and other treatment options before deciding to use G Nac extended-release tablets. Use the lowest effective dose for the shortest duration consistent with individual patient treatment goals.
After observing the response to initial therapy with G Nac extended-release tablets the dose and frequency should be adjusted to suit an individual patient’s needs.
For the relief of osteoarthritis, the recommended dosage is 100 mg daily.
For the relief of rheumatoid arthritis, the recommended dosage is 100 mg daily. In the rare patient where G Nac extended-release tablets 100 mg/day is unsatisfactory, the dose may be increased to 100 mg twice a day if the benefits outweigh the clinical risks of increased side effects.
Different formulations of G Nac (G Nac enteric-coated tablets; G Nac extended-release tablets; G Nac potassium immediate-release tablets) are not necessarily bioequivalent even if the milligram strength is the same.
Ask your doctor before using G Nac if you take an antidepressant such as citalopram, escitalopram, fluoxetine (Prozac), fluvoxamine, paroxetine, sertraline (Zoloft), trazodone, or vilazodone. Taking any of these medicines with an NSAID may cause you to bruise or bleed easily.
Tell your doctor about all your current medicines and any you start or stop using, especially:
cyclosporine;
lithium;
methotrexate;
rifampin;
antifungal medicine;
a blood thinner (warfarin, Coumadin, Jantoven);
heart or blood pressure medication, including a diuretic or "water pill";
other forms of G Nac (Flector, Pennsaid, Solaraze, Voltaren Gel);
other NSAIDs - aspirin, ibuprofen (Advil, Motrin), naproxen (Aleve), celecoxib (Celebrex), indomethacin, meloxicam, and others; or
steroid medicine (prednisone and others).
This list is not complete. Other drugs may interact with G Nac, including prescription and over-the-counter medicines, vitamins, and herbal products. Not all possible interactions are listed in this medication guide.
Aspirin: Concomitant administration of G Nac and aspirin is not recommended because G Nac 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 G Nac 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 G Nac, and warfarin requires close monitoring of patients to be certain that no change in their anticoagulant dosage is required.
Digoxin, Methotrexate, Cyclosporine: G Nac, like other NSAIDs, may affect renal prostaglandins and increase the toxicity of certain drugs. Ingestion of G Nac may increase serum concentrations of digoxin and methotrexate and increase cyclosporineís nephrotoxicity. Patients who begin taking G Nac or who increase their G Nac 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: G Nac decreases lithium renal clearance and increases lithium plasma levels. In patients taking G Nac and lithium concomitantly, lithium toxicity may develop.
Diuretics: G Nac 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 G Nac. Phenobarbital toxicity has been reported to have occurred in a patient on chronic phenobarbital treatment following the initiation of G Nac therapy.
Protein Binding
In vitro, G Nac 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 G Nac in human serum.
Drug/Laboratory Test Interactions
Effect on Blood Coagulation: G Nac 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. G Nac 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.
There are no reviews yet. Be the first to write one! |
Information checked by Dr. Sachin Kumar, MD Pharmacology
|