Consists of etodolac, thiocolchicoside
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Etodolac/thiocolchicoside Dosage |
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Consists of etodolac, thiocolchicoside
Generic name: etodolac
Dosage form: Capsules and Tablets
The information at Drugs.com is not a substitute for medical advice. Always consult your doctor or pharmacist.
Carefully consider the potential benefits and risks of Etodolac and other treatment options before deciding to use Etodolac. Use the lowest effective dose for the shortest duration consistent with individual patient treatment goals.
After observing the response to initial therapy with Etodolac, the dose and frequency should be adjusted to suit an individual patient's needs. As with other NSAIDs, the lowest dose and longest dosing interval should be sought for each patient. Therefore, after observing the response to initial therapy with Etodolac, the dose and frequency should be adjusted to suit an individual patient's needs.
Dosage adjustment of Etodolac is generally not required in patients with mild to moderate renal impairment. Etodolac should be used with caution in such patients, because, as with other NSAIDs, it may further decrease renal function in some patients with impaired renal function.
The recommended total daily dose of Etodolac for acute pain is up to 1000 mg, given as 200-400 mg every 6 to 8 hours. Doses of etodolac greater than 1000 mg/day have not been adequately evaluated in well-controlled clinical trials.
The recommended starting dose of Etodolac for the management of the signs and symptoms of osteoarthritis or rheumatoid arthritis is: 300 mg b.i.d., t.i.d., or 400 mg b.i.d., or 500 mg b.i.d. A lower dose of 600 mg/day may suffice for long-term administration. Physicians should be aware that doses above 1000 mg/day have not been adequately evaluated in well-controlled clinical trials.
In chronic conditions, a therapeutic response to therapy with Etodolac is sometimes seen within one week of therapy, but most often is observed by two weeks. After a satisfactory response has been achieved, the patient's dose should be reviewed and adjusted as required.
Tell your doctor if you are taking an antidepressant such as citalopram (Celexa), duloxetine (Cymbalta), escitalopram (Lexapro), fluoxetine (Prozac, Sarafem, Symbyax), fluvoxamine (Luvox), paroxetine (Paxil), sertraline (Zoloft), or venlafaxine (Effexor). Taking any of these drugs with etodolac may cause you to bruise or bleed easily.
Before taking etodolac, tell your doctor if you are taking any of the following drugs:
This list is not complete and there may be other drugs that can interact with etodolac. Tell your doctor about all the prescription and over-the-counter medications you use. This includes vitamins, minerals, herbal products, and drugs prescribed by other doctors. Do not start using a new medication without telling your doctor.
Reports suggest that NSAIDs may diminish the antihypertensive effect of ACE-inhibitors. This interaction should be given consideration in patients taking NSAIDs concomitantly with ACE-inhibitors.
The concomitant administration of antacids has no apparent effect on the extent of absorption of etodolac. However, antacids can decrease the peak concentration reached by 15% to 20% but have no detectable effect on the time-to-peak.
When etodolac is administered with aspirin, its protein binding is reduced, although the clearance of free etodolac is not altered. The clinical significance of this interaction is not known; however, as with other NSAIDs, concomitant administration of etodolac and aspirin is not generally recommended because of the potential of increased adverse effects.
Etodolac, like other NSAIDs, through effects on renal prostaglandins, may cause changes in the elimination of these drugs leading to elevated serum levels of cyclosporine, digoxin, methotrexate, and increase toxicity. Nephrotoxicity associated with cyclosporine may also be enhanced. Patients receiving these drugs who are given etodolac, or any other NSAID, and particularly those patients with altered renal function, should be observed for the development of the specific toxicities of these drugs. NSAIDs have been reported to competitively inhibit methotrexate accumulation in rabbit kidney slices. This may indicate that they could enhance the toxicity of methotrexate. Caution should be used when NSAIDs are administered concomitantly with methotrexate.
Etodolac has no apparent pharmacokinetic interaction when administered with furosemide or hydrochlorothiazide. Nevertheless, clinical studies, as well as post marketing observations have shown that etodolac can reduce the natriuretic effect of furosemide and thiazides in some patients. This response has been attributed to inhibition of renal prostaglandin synthesis. During concomitant therapy with NSAIDs, the patient should be observed closely for sings of renal failure, as well as to assure diuretic efficacy.
Etodolac has no apparent pharmacokinetic interaction when administered with glyburide.
NSAIDs have produced an elevation of plasma lithium levels and a reduction in renal lithium clearance. The mean minimum lithium concentration increased 15% and the renal clearance was decreased by approximately 20%. These effects have been attributed to inhibition of renal prostaglandin synthesis by the NSAID. Thus, when NSAIDs and lithium are administered concurrently, subjects should be observed carefully for signs of lithium toxicity.
Phenylbutazone causes increase (by about 80%) in the free fraction of etodolac. Although in vivo studies have not been done to see if etodolac clearance is changed by coadministration of phylbutazone, it is not recommended that they be coadministered.
Etodolac has no apparent pharmacokinetic interaction when administered with phenytoin.
The effects of warfarin and NSAIDs on GI bleeding are synergistic, such that users of both drugs together have a risk of serious GI bleeding higher than that of users of either drug alone. Short-term pharmacokinetic studies have demonstrated that concomitant administration of warfarin and etodolac results in reduced protein binding of warfarin, but there was no change in the clearance of free warfarin. There was no significant difference in the pharmacodynamic effect of warfarin administered alone and warfarin administered with etodolac as measured by prothrombin time. Thus, concomitant therapy with warfarin and etodolac should not require dosage adjustment of either drug. However, caution should be exercised because there have been a few spontaneous reports of prolonged prothrombin times, with or without bleeding, in etodolac-treated patients receiving concomitant warfarin therapy.
The urine of patients who take etodolac can give a false-positive reaction for urinary bilirubin (urobilin) due to the presence of phenolic metabolites of etodolac. Diagnostic dip-stick methodology, used to detect ketone bodies in urine, has resulted in false-positive findings in some patients treated with etodolac. Generally, this phenomenon has not been associated with other clinically significant events. No dose relationship has been observed.
Etodolac treatment is associated with a small decrease in serum uric acid levels. In clinical trials, mean decreases of 1 to 2 mg/dL were observed in arthritic patients receiving etodolac (600 mg to 1000 mg/day) after 4 weeks of therapy. These levels then remained stable for up to 1 year of therapy.
Muscle spasms
Adult: Initially, 16 mg daily.
Muscle spasms
Adult: Up to 8 mg daily.
LEXOTAN undergoes hepatic microsomal oxidation via the cytochrome P450 liver enzymes.
Therefore, caution should be taken in patients taking medicines that inhibit the P450 liver enzymes (e.g. azole antifungals, macrolide antibiotics, HIV protease inhibitors, calcium channel blocking agents).
LEXOTAN undergoes oxidative metabolism and, consequently, may interact with disulfiram or cimetidine resulting in increased plasma levels of LEXOTAN. Patients should be observed closely for evidence of enhanced benzodiazepine response during concomitant treatment with either disulfiram or cimetidine; some patients may require a reduction in benzodiazepine dosage.
The benzodiazepines, including LEXOTAN, produce additive CNS depressant effects when coadministered with other medications which themselves produce CNS depression e.g. barbiturates, alcohol, sedatives, antidepressants, hypnotics, anxiolytics, phenothiazines and other antipsychotics,
skeletal muscle relaxants, antihistamines, narcotic analgesics and anaesthetics.
Alcohol should be avoided in patients receiving LEXOTAN.
In the case of narcotic analgesics enhancement of euphoria may also occur, leading to an increase in psychic drug dependence.
The anticholinergic effects of atropine and similar medicines, antihistamines and antidepressants may be potentiated.
Interactions have been reported between some benzodiazepines and anticonvulsants, with changes in the serum concentration of the benzodiazepine or anticonvulsant. It is recommended that patients be observed for altered responses when benzodiazepines and anticonvulsants are prescribed together and that serum level monitoring of the anticonvulsant be performed more frequently.
Interference with Clinical, Laboratory or Other Tests:
Minor EEG changes, usually low voltage fast activity, of no known clinical significance, has been
reported with benzodiazepine administration.
Users | % | ||
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Once in a day | 1 | 100.0% |
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Information checked by Dr. Sachin Kumar, MD Pharmacology
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