Brands, Medical Use, Clinical Data
- Tocolytic Agents
- Cardiovascular Agents
- Anti-inflammatory Agents
- Nonsteroidal Antiinflammatory Agents (NSAIDs)
Brands / Synonyms
Amuno; Apo-Indomethacin; Argun; Arthrexin; Artracin; Artrinovo; Artrivia; Bonidin; Bonidon; Bonidon Gel; Catlep; Chibro-Amuno; Chrono-Indicid; Chrono-Indocid; Confortid; Dolcidium; Dolcidium Pl; Dolovin; Durametacin; Elmetacin; Flexin Continus; Hicin; Idomethine; Imbrilon; IMN; Inacid; Indacin; Indameth; Indmethacine; Indo-Lemmon; Indo-Phlogont; Indo-Rectolmin; Indo-Spray; Indo-Tablinen; Indocid; Indocid Pda; Indocid Sr; Indocin; Indocin I.V; Indocin I.V.; Indocin Sr; Indolar Sr; Indomecol; Indomed; Indomee; Indometacin; Indometacine; Indometacyna; Indomethacine; Indomethacinum; Indomethancin; Indomethazine; Indomethegan; Indomethine; Indometicina; Indomo; Indomod; Indoptic; Indoptol; Indorektal; Indoxen; Inflazon; Infrocin; Inteban Sp; Lausit; Liometacen [As Meglumine Salt]; Metacen; Metartril; Methazine; Metindol; Mezlin; Mezlocillin; Mezolin; Miametan; Mikametan; Mobilan; Novo-Methacin; Novomethacin; Nu-Indo; Reumacide; Rhemacin La; Rheumacin La; Sadoreum; Tannex; USAN; Vonum
For moderate to severe rheumatoid arthritis including acute flares of chronic disease, ankylosing spondylitis, osteoarthritis, acute painful shoulder (bursitis and/or tendinitis) and acute gouty arthritis.
Indomethacin, a nonsteroidal antiinflammatory drug (NSAID) with analgesic and antipyretic properties, is used to treat osteoarthritis and control acute pain.
Mechanism of Action
Antiinflammatory effects of Indomethacin are believed to be due to inhibition of cylooxygenase in platelets which leads to the blockage of prostaglandin synthesis. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation.
Biotrnasformation / Drug Metabolism
Indomethacin should not be used in:
-Patients who are hypersensitive to this product.
-Patients in whom acute asthmatic attacks, urticaria, or rhinitis are precipitated by aspirin or other
nonsteroidal anti- inflammatory agents.
-Suppositories INDOCIN are contraindicated in patients with a history of proctitis or recent rectal
In normal volunteers receiving indomethacin, the administration of diflunisal decreased the renal clearance and
significantly increased the plasma levels of indomethacin. In some patients, combined use of INDOCIN and diflunisal
has been associated with fatal gastrointestinal hemorrhage. Therefore, diflunisal and INDOCIN should not be used
In a study in normal volunteers, it was found that chronic concurrent administration of 3.6 g of aspirin per day
decreases indomethacin blood levels approximately 20%.
The concomitant use of INDOCIN with other NSAIDs is not recommended due to the increased possibility of
gastrointestinal toxicity, with little or no increase in efficacy.
Clinical studies have shown that INDOCIN does not influence the hypoprothrombinemia produced by anticoagulants.
However, when any additional drug, including INDOCIN, is added to the treatment of patients on anticoagulant therapy,
the patients should be observed for alterations of the prothrombin time. In post-marketing experience, bleeding has
been reported in patients on concomitant treatment with anticoagulants and INDOCIN. Caution should be exercised when
INDOCIN and anticoagulants are administered concomitantly.
When INDOCIN is given to patients receiving probenecid, the plasma levels of indomethacin are likely to be
increased. Therefore, a lower total daily dosage of INDOCIN may produce a satisfactory therapeutic effect. When
increases in the dose of INDOCIN are made, they should be made carefully and in small increments.
Caution should be used if INDOCIN is administered simultaneously with methotrexate. INDOCIN has been reported to
decrease the tubular secretion of methotrexate and to potentiate its toxicity.
Administration of non-steroidal anti-inflammatory drugs concomitantly with cyclosporine has been associated with
an increase in cyclosporine-induced toxicity, possibly due to decreased synthesis of renal prostacyclin. NSAIDs
should be used with caution in patients taking cyclosporine, and renal function should be carefully monitored.
Capsules INDOCIN 50 mg t.i.d. produced a clinically relevant elevation of plasma lithium and reduction in renal
lithium clearance in psychiatric patients and normal subjects with steady state plasma lithium concentrations. This
effect has been attributed to inhibition of prostaglandin synthesis. As a consequence, when INDOCIN and lithium are
given concomitantly, the patient should be carefully observed for signs of lithium toxicity. (Read circulars for
lithium preparations before use of such concomitant therapy.) In addition, the frequency of monitoring serum lithium
concentration should be increased at the outset of such combination drug treatment.
INDOCIN given concomitantly with digoxin has been reported to increase the serum concentration and prolong the
half-life of digoxin. Therefore, when INDOCIN and digoxin are used concomitantly, serum digoxin levels should be
In some patients, the administration of INDOCIN can reduce the diuretic, natriuretic, and antihypertensive effects
of loop, potassium-sparing, and thiazide diuretics. Therefore, when INDOCIN and INDOCIN. (Indomethacin) diuretics are
used concomitantly, the patient should be observed closely to determine if the desired effect of the diuretic is
INDOCIN reduces basal plasma renin activity (PRA), as well as those elevations of PRA induced by furosemide
administration, or salt or volume depletion. These facts should be considered when evaluating plasma renin activity
in hypertensive patients.
It has been reported that the addition of triamterene to a maintenance schedule of INDOCIN resulted in reversible
acute renal failure in two of four healthy volunteers. INDOCIN and triamterene should not be administered
INDOCIN and potassium-sparing diuretics each may be associated with increased serum potassium levels. The
potential effects of INDOCIN and potassium-sparing diuretics on potassium kinetics and renal function should be
considered when these agents are administered concurrently.
Most of the above effects concerning diuretics have been attributed, at least in part, to mechanisms involving
inhibition of prostaglandin synthesis by INDOCIN.
Blunting of the antihypertensive effect of beta-adrenoceptor blocking agents by non-steroidal antiinflammatory
drugs including INDOCIN has been reported. Therefore, when using these blocking agents to treat hypertension,
patients should be observed carefully in order to confirm that the desired therapeutic effect has been obtained.
INDOCIN can reduce the antihypertensive effects of captopril and losartan.
False-negative results in the dexamethasone suppression test (DST) in patients being treated with INDOCIN have
been reported. Thus, results of the DST should be interpreted with caution in these patients.