Dosing & Uses
Dosage Forms & Strengths
tablet
- 150mg
- 200mg
Ankylosing Spondylitis, Osteoarthritis, Rheumatoid Arthritis
150-200 mg PO q12hr
No more than 400 mg
Use lowest effective dose for shortest possible duration
Shoulder Pain
200 mg PO q12hr for 7-14 days
Gout
200 mg PO q12hr for 7 days
Familial Adenomatous Polyposis (Off-label)
150-200 mg PO q12hr
Renal Impairment
Severe renal impairment: Not recommended; administer lower dose and monitor closely if administration necessary
Hepatic Impairment
Administer lower dose; discontinue if toxicity occurs
Administration
Take with food or 8-12 oz water to avoid GI effects
Other Indications & Uses
Bursitis/bursitis (shoulder), synovitis, tendonitis/tendonitis (shoulder), tenosynovitis
Safety & efficacy not established
Ankylosing spondylitis, osteoarthritis, rheumatoid arthritis
150-200 mg PO q12hr
No more than 400 mg
Use lowest effective dose for shortest possible duration
Shoulder Pain
200 mg PO q12hr for 7-14 days
Gout
200 mg PO q12hr for 7 days
Familial Adenomatous Polyposis (Off-label)
150-200 mg PO q12hr
Interactions
Interaction Checker
No Results
Contraindicated
Serious - Use Alternative
Significant - Monitor Closely
Minor
Contraindicated (0)
Serious - Use Alternative (21)
- aminolevulinic acid oral
aminolevulinic acid oral, sulindac. Either increases levels of the other by pharmacodynamic synergism. Avoid or Use Alternate Drug. Avoid administering other phototoxic drugs with aminolevulinic acid oral for 24 hr during perioperative period.
- aminolevulinic acid topical
sulindac, aminolevulinic acid topical. Either increases toxicity of the other by pharmacodynamic synergism. Avoid or Use Alternate Drug. Each drug may increase the photosensitizing effect of the other.
- apixaban
sulindac and apixaban both increase anticoagulation. Avoid or Use Alternate Drug.
- benazepril
sulindac, benazepril. pharmacodynamic antagonism. Avoid or Use Alternate Drug. Coadministration may result in a significant decrease in renal function. NSAIDs may diminish the antihypertensive effect of ACE inhibitors. The mechanism of these interactions is likely related to the ability of NSAIDs to reduce the synthesis of vasodilating renal prostaglandins.
- captopril
sulindac, captopril. pharmacodynamic antagonism. Avoid or Use Alternate Drug. Coadministration may result in a significant decrease in renal function. NSAIDs may diminish the antihypertensive effect of ACE inhibitors. The mechanism of these interactions is likely related to the ability of NSAIDs to reduce the synthesis of vasodilating renal prostaglandins.
- enalapril
sulindac, enalapril. pharmacodynamic antagonism. Avoid or Use Alternate Drug. Coadministration may result in a significant decrease in renal function. NSAIDs may diminish the antihypertensive effect of ACE inhibitors. The mechanism of these interactions is likely related to the ability of NSAIDs to reduce the synthesis of vasodilating renal prostaglandins.
- fosinopril
sulindac, fosinopril. pharmacodynamic antagonism. Avoid or Use Alternate Drug. Coadministration may result in a significant decrease in renal function. NSAIDs may diminish the antihypertensive effect of ACE inhibitors. The mechanism of these interactions is likely related to the ability of NSAIDs to reduce the synthesis of vasodilating renal prostaglandins.
- ketorolac
sulindac, ketorolac. Either increases toxicity of the other by pharmacodynamic synergism. Contraindicated.
- ketorolac intranasal
sulindac, ketorolac intranasal. Either increases toxicity of the other by pharmacodynamic synergism. Contraindicated.
- lisinopril
sulindac, lisinopril. pharmacodynamic antagonism. Avoid or Use Alternate Drug. Coadministration may result in a significant decrease in renal function. NSAIDs may diminish the antihypertensive effect of ACE inhibitors. The mechanism of these interactions is likely related to the ability of NSAIDs to reduce the synthesis of vasodilating renal prostaglandins.
- methotrexate
sulindac increases levels of methotrexate by decreasing renal clearance. Avoid or Use Alternate Drug. Concomitant administration of NSAIDs with high dose methotrexate has been reported to elevate and prolong serum methotrexate levels, resulting in deaths from severe hematologic and GI toxicity. NSAIDs may reduce tubular secretion of methotrexate and enhance toxicity. .
- methyl aminolevulinate
sulindac, methyl aminolevulinate. Either increases toxicity of the other by pharmacodynamic synergism. Avoid or Use Alternate Drug. Each drug may increase the photosensitizing effect of the other.
- moexipril
sulindac, moexipril. pharmacodynamic antagonism. Avoid or Use Alternate Drug. Coadministration may result in a significant decrease in renal function. NSAIDs may diminish the antihypertensive effect of ACE inhibitors. The mechanism of these interactions is likely related to the ability of NSAIDs to reduce the synthesis of vasodilating renal prostaglandins.
- pemetrexed
sulindac increases levels of pemetrexed by unspecified interaction mechanism. Avoid or Use Alternate Drug. Interrupt dosing in all patients taking NSAIDs with long elimination half-lives for at least 5d before, the day of, and 2d following pemetrexed administration. If coadministration of an NSAID is necessary, closely monitor patients for toxicity, especially myelosuppression, renal toxicity, and GI toxicity.
- perindopril
sulindac, perindopril. pharmacodynamic antagonism. Avoid or Use Alternate Drug. Coadministration may result in a significant decrease in renal function. NSAIDs may diminish the antihypertensive effect of ACE inhibitors. The mechanism of these interactions is likely related to the ability of NSAIDs to reduce the synthesis of vasodilating renal prostaglandins.
- pexidartinib
sulindac and pexidartinib both increase Other (see comment). Avoid or Use Alternate Drug. Pexidartinib can cause hepatotoxicity. Avoid coadministration of pexidartinib with other products know to cause hepatoxicity.
- pretomanid
sulindac, pretomanid. Either increases toxicity of the other by Other (see comment). Avoid or Use Alternate Drug. Comment: Pretomanid regimen associated with hepatotoxicity. Avoid alcohol and hepatotoxic agents, including herbal supplements and drugs other than bedaquiline and linezolid.
- quinapril
sulindac, quinapril. pharmacodynamic antagonism. Avoid or Use Alternate Drug. Coadministration may result in a significant decrease in renal function. NSAIDs may diminish the antihypertensive effect of ACE inhibitors. The mechanism of these interactions is likely related to the ability of NSAIDs to reduce the synthesis of vasodilating renal prostaglandins.
- ramipril
sulindac, ramipril. pharmacodynamic antagonism. Avoid or Use Alternate Drug. Coadministration may result in a significant decrease in renal function. NSAIDs may diminish the antihypertensive effect of ACE inhibitors. The mechanism of these interactions is likely related to the ability of NSAIDs to reduce the synthesis of vasodilating renal prostaglandins.
- tacrolimus
sulindac, tacrolimus. Either increases toxicity of the other by Other (see comment). Avoid or Use Alternate Drug. Comment: Concomitant administration increases risk of nephrotoxicity.
- trandolapril
sulindac, trandolapril. pharmacodynamic antagonism. Avoid or Use Alternate Drug. Coadministration may result in a significant decrease in renal function. NSAIDs may diminish the antihypertensive effect of ACE inhibitors. The mechanism of these interactions is likely related to the ability of NSAIDs to reduce the synthesis of vasodilating renal prostaglandins.
Monitor Closely (237)
- acebutolol
acebutolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of acebutolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - aceclofenac
aceclofenac and sulindac both increase anticoagulation. Use Caution/Monitor.
aceclofenac and sulindac both increase serum potassium. Use Caution/Monitor. - acemetacin
acemetacin and sulindac both increase anticoagulation. Use Caution/Monitor.
acemetacin and sulindac both increase serum potassium. Use Caution/Monitor. - agrimony
sulindac and agrimony both increase anticoagulation. Use Caution/Monitor.
- albuterol
sulindac increases and albuterol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- alfalfa
sulindac and alfalfa both increase anticoagulation. Use Caution/Monitor.
- alfuzosin
sulindac decreases effects of alfuzosin by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- aliskiren
sulindac will decrease the level or effect of aliskiren by Other (see comment). Use Caution/Monitor. In patients who are elderly, volume-depleted (including those on diuretic therapy), or with compromised renal function, coadministration of NSAIDs with drugs that affect RAAS may increase the risk of renal impairment (including acute renal failure) and cause loss of antihypertensive effect. Monitor renal function periodically.
- alteplase
sulindac and alteplase both increase anticoagulation. Use Caution/Monitor. Potential for increased risk of bleeding, caution is advised.
- American ginseng
sulindac and American ginseng both increase anticoagulation. Use Caution/Monitor.
- amiloride
amiloride and sulindac both increase serum potassium. Modify Therapy/Monitor Closely.
- antithrombin alfa
antithrombin alfa and sulindac both increase anticoagulation. Modify Therapy/Monitor Closely.
- antithrombin III
antithrombin III and sulindac both increase anticoagulation. Modify Therapy/Monitor Closely.
- arformoterol
sulindac increases and arformoterol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- argatroban
argatroban and sulindac both increase anticoagulation. Modify Therapy/Monitor Closely.
- asenapine
sulindac decreases effects of asenapine by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- aspirin
aspirin and sulindac both increase anticoagulation. Use Caution/Monitor.
aspirin and sulindac both increase serum potassium. Use Caution/Monitor. - aspirin rectal
aspirin rectal and sulindac both increase anticoagulation. Use Caution/Monitor.
aspirin rectal and sulindac both increase serum potassium. Use Caution/Monitor. - aspirin/citric acid/sodium bicarbonate
aspirin/citric acid/sodium bicarbonate and sulindac both increase anticoagulation. Use Caution/Monitor.
aspirin/citric acid/sodium bicarbonate and sulindac both increase serum potassium. Use Caution/Monitor. - atenolol
atenolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of atenolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - azficel-T
azficel-T, sulindac. Other (see comment). Use Caution/Monitor. Comment: Patients taking NSAIDS may experience increased bruising or bleeding at biopsy and/or injection sites. Concomitant use of NSAIDs is not recommended.
- azilsartan
sulindac, azilsartan. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals.
sulindac decreases effects of azilsartan by pharmacodynamic antagonism. Modify Therapy/Monitor Closely. NSAIDs decrease synthesis of vasodilating renal prostaglandins, and thus affect fluid homeostasis and may diminish antihypertensive effect. - bemiparin
bemiparin and sulindac both increase anticoagulation. Modify Therapy/Monitor Closely.
- benazepril
benazepril, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals.
- bendroflumethiazide
sulindac increases and bendroflumethiazide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- betaxolol
betaxolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of betaxolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - betrixaban
sulindac, betrixaban. Either increases levels of the other by anticoagulation. Use Caution/Monitor.
- bimatoprost
bimatoprost, sulindac. unspecified interaction mechanism. Use Caution/Monitor. There are conflicting reports from studies of either increased or decreased IOP when ophthalmic prostaglandins are coadministered with NSAIDs (either systemic or ophthalmic).
- bisoprolol
bisoprolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of bisoprolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - bivalirudin
bivalirudin and sulindac both increase anticoagulation. Modify Therapy/Monitor Closely.
- budesonide
sulindac, budesonide. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- bumetanide
sulindac increases and bumetanide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
sulindac decreases effects of bumetanide by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis. - candesartan
candesartan and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of candesartan by pharmacodynamic antagonism. Modify Therapy/Monitor Closely. NSAIDs decrease synthesis of vasodilating renal prostaglandins, and thus affect fluid homeostasis and may diminish antihypertensive effect.
candesartan, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals. - captopril
captopril, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals.
- carbenoxolone
sulindac increases and carbenoxolone decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- carvedilol
carvedilol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of carvedilol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - celecoxib
celecoxib and sulindac both increase anticoagulation. Use Caution/Monitor.
celecoxib and sulindac both increase serum potassium. Use Caution/Monitor. - celiprolol
celiprolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of celiprolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - chlorothiazide
sulindac increases and chlorothiazide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- chlorpropamide
sulindac increases effects of chlorpropamide by unknown mechanism. Use Caution/Monitor. Risk of hypoglycemia.
- chlorthalidone
sulindac increases and chlorthalidone decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- choline magnesium trisalicylate
choline magnesium trisalicylate and sulindac both increase anticoagulation. Use Caution/Monitor.
choline magnesium trisalicylate and sulindac both increase serum potassium. Use Caution/Monitor. - cinnamon
sulindac and cinnamon both increase anticoagulation. Use Caution/Monitor.
- ciprofloxacin
sulindac, ciprofloxacin. Other (see comment). Modify Therapy/Monitor Closely. Comment: Mechanism: unknown. Increased risk of CNS stimulation and seizures with high doses of fluoroquinolones.
- citalopram
citalopram, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. If possible, avoid concurrent use.
- clomipramine
clomipramine, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. Clomipramine inhib. serotonin uptake by platelets.
- clopidogrel
clopidogrel, sulindac. Either increases effects of the other by pharmacodynamic synergism. Modify Therapy/Monitor Closely. Clopidogrel and NSAIDs both inhibit platelet aggregation.
- cordyceps
sulindac and cordyceps both increase anticoagulation. Use Caution/Monitor.
- cortisone
sulindac, cortisone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- cyclopenthiazide
sulindac increases and cyclopenthiazide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- cyclosporine
sulindac, cyclosporine. Either increases toxicity of the other by nephrotoxicity and/or ototoxicity. Modify Therapy/Monitor Closely.
- dabigatran
dabigatran and sulindac both increase anticoagulation. Use Caution/Monitor. Caution is advised, both drugs have the potential to cause bleeding. Concomitant use may increase risk of bleeding.
- dalteparin
dalteparin and sulindac both increase anticoagulation. Modify Therapy/Monitor Closely.
- deferasirox
deferasirox, sulindac. Other (see comment). Use Caution/Monitor. Comment: Combination may increase GI bleeding, ulceration and irritation. Use with caution.
- defibrotide
defibrotide increases effects of sulindac by P-glycoprotein (MDR1) efflux transporter. Use Caution/Monitor. Defibrotide may enhance effects of platelet inhibitors.
- deflazacort
sulindac, deflazacort. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- dexamethasone
sulindac, dexamethasone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- diclofenac
diclofenac and sulindac both increase anticoagulation. Use Caution/Monitor.
diclofenac and sulindac both increase serum potassium. Use Caution/Monitor. - diflunisal
diflunisal and sulindac both increase anticoagulation. Use Caution/Monitor.
diflunisal and sulindac both increase serum potassium. Use Caution/Monitor. - digoxin
sulindac and digoxin both increase serum potassium. Use Caution/Monitor.
- dobutamine
sulindac increases and dobutamine decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- dong quai
sulindac and dong quai both increase anticoagulation. Use Caution/Monitor.
- dopexamine
sulindac increases and dopexamine decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- doxazosin
sulindac decreases effects of doxazosin by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- drospirenone
drospirenone and sulindac both increase serum potassium. Modify Therapy/Monitor Closely.
- duloxetine
duloxetine, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. SSRIs inhib. serotonin uptake by platelets.
- edoxaban
edoxaban, sulindac. Either increases toxicity of the other by anticoagulation. Modify Therapy/Monitor Closely. Both drugs have the potential to cause bleeding, monitor closely. Promptly evaluate any signs or symptoms of blood loss.
- eltrombopag
eltrombopag increases levels of sulindac by decreasing metabolism. Use Caution/Monitor. UGT inhibition; significance of interaction unclear.
- elvitegravir/cobicistat/emtricitabine/tenofovir DF
elvitegravir/cobicistat/emtricitabine/tenofovir DF, sulindac. Either increases toxicity of the other by decreasing renal clearance. Modify Therapy/Monitor Closely. Toxicity may result from coadministration of emtricitabine and tenofovir with other drugs that are also primarily excreted by glomerular filtration and/or active tubular secretion including high-dose or multiple-dose NSAIDs; alternatives to NSAIDs should be considered.
- emtricitabine
emtricitabine, sulindac. Either increases levels of the other by decreasing renal clearance. Modify Therapy/Monitor Closely. Toxicity may result from coadministration of emtricitabine with other drugs that are also primarily excreted by glomerular filtration and/or active tubular secretion including high-dose or multiple-dose NSAIDs; alternatives to NSAIDs should be considered.
- enalapril
enalapril, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals.
- enoxaparin
enoxaparin and sulindac both increase anticoagulation. Modify Therapy/Monitor Closely.
- ephedrine
sulindac increases and ephedrine decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- epinephrine
sulindac increases and epinephrine decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- epinephrine racemic
sulindac increases and epinephrine racemic decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- epoprostenol
sulindac and epoprostenol both increase anticoagulation. Use Caution/Monitor.
- eprosartan
eprosartan and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of eprosartan by pharmacodynamic antagonism. Modify Therapy/Monitor Closely. NSAIDs decrease synthesis of vasodilating renal prostaglandins, and thus affect fluid homeostasis and may diminish antihypertensive effect.
eprosartan, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals. - escitalopram
escitalopram, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. SSRIs inhib. serotonin uptake by platelets.
- esmolol
esmolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of esmolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - ethacrynic acid
sulindac increases and ethacrynic acid decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- etodolac
etodolac and sulindac both increase anticoagulation. Use Caution/Monitor.
etodolac and sulindac both increase serum potassium. Use Caution/Monitor. - fennel
sulindac and fennel both increase anticoagulation. Use Caution/Monitor.
- fenoprofen
fenoprofen and sulindac both increase anticoagulation. Use Caution/Monitor.
fenoprofen and sulindac both increase serum potassium. Use Caution/Monitor. - feverfew
sulindac and feverfew both increase anticoagulation. Use Caution/Monitor.
- fish oil triglycerides
fish oil triglycerides will increase the level or effect of sulindac by anticoagulation. Use Caution/Monitor. Prolonged bleeding reported in patients taking antiplatelet agents or anticoagulants and oral omega-3 fatty acids. Periodically monitor bleeding time in patients receiving fish oil triglycerides and concomitant antiplatelet agents or anticoagulants.
- fludrocortisone
sulindac, fludrocortisone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- fluoxetine
fluoxetine, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. SSRIs inhib. serotonin uptake by platelets.
- flurbiprofen
flurbiprofen and sulindac both increase anticoagulation. Use Caution/Monitor.
flurbiprofen and sulindac both increase serum potassium. Use Caution/Monitor. - fluvoxamine
fluvoxamine, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor.
- fondaparinux
fondaparinux and sulindac both increase anticoagulation. Modify Therapy/Monitor Closely.
- formoterol
sulindac increases and formoterol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- forskolin
sulindac and forskolin both increase anticoagulation. Use Caution/Monitor.
- fosinopril
fosinopril, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals.
- furosemide
sulindac increases and furosemide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- garlic
sulindac and garlic both increase anticoagulation. Use Caution/Monitor.
- gemifloxacin
gemifloxacin, sulindac. Other (see comment). Modify Therapy/Monitor Closely. Comment: Increased risk of CNS stimulation and seizures with high doses of fluoroquinolones.
- gentamicin
sulindac increases and gentamicin decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- ginger
sulindac and ginger both increase anticoagulation. Use Caution/Monitor.
- ginkgo biloba
sulindac and ginkgo biloba both increase anticoagulation. Use Caution/Monitor.
- glimepiride
sulindac increases effects of glimepiride by unknown mechanism. Use Caution/Monitor. Risk of hypoglycemia.
- glipizide
sulindac increases effects of glipizide by unknown mechanism. Use Caution/Monitor. Risk of hypoglycemia.
- glyburide
sulindac increases effects of glyburide by unknown mechanism. Use Caution/Monitor. Risk of hypoglycemia.
- green tea
green tea, sulindac. Other (see comment). Use Caution/Monitor. Comment: Combination may increase risk of bleeding.
- heparin
heparin and sulindac both increase anticoagulation. Modify Therapy/Monitor Closely.
- horse chestnut seed
sulindac and horse chestnut seed both increase anticoagulation. Use Caution/Monitor.
- hydralazine
sulindac decreases effects of hydralazine by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- hydrochlorothiazide
sulindac increases and hydrochlorothiazide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- hydrocortisone
sulindac, hydrocortisone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- ibrutinib
ibrutinib will increase the level or effect of sulindac by anticoagulation. Use Caution/Monitor. Ibrutinib may increase the risk of hemorrhage in patients receiving antiplatelet or anticoagulant therapies and monitor for signs of bleeding.
- ibuprofen
ibuprofen and sulindac both increase anticoagulation. Use Caution/Monitor.
ibuprofen and sulindac both increase serum potassium. Use Caution/Monitor. - ibuprofen IV
ibuprofen IV will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Use Caution/Monitor.
ibuprofen IV and sulindac both increase anticoagulation. Use Caution/Monitor.
ibuprofen IV and sulindac both increase serum potassium. Use Caution/Monitor. - imatinib
imatinib, sulindac. Either increases toxicity of the other by Other (see comment). Modify Therapy/Monitor Closely. Comment: Imatinib may cause thrombocytopenia; bleeding risk increased when imatinib is coadministered with anticoagulants, NSAIDs, platelet inhibitors, and thrombolytic agents.
- indapamide
sulindac increases and indapamide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- indomethacin
indomethacin and sulindac both increase anticoagulation. Use Caution/Monitor.
indomethacin and sulindac both increase serum potassium. Use Caution/Monitor. - irbesartan
irbesartan and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of irbesartan by pharmacodynamic antagonism. Modify Therapy/Monitor Closely. NSAIDs decrease synthesis of vasodilating renal prostaglandins, and thus affect fluid homeostasis and may diminish antihypertensive effect.
irbesartan, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals. - isoproterenol
sulindac increases and isoproterenol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- ketoprofen
ketoprofen and sulindac both increase anticoagulation. Use Caution/Monitor.
ketoprofen and sulindac both increase serum potassium. Use Caution/Monitor. - ketorolac
ketorolac and sulindac both increase anticoagulation. Use Caution/Monitor.
ketorolac and sulindac both increase serum potassium. Use Caution/Monitor. - ketorolac intranasal
ketorolac intranasal and sulindac both increase anticoagulation. Use Caution/Monitor.
ketorolac intranasal and sulindac both increase serum potassium. Use Caution/Monitor. - labetalol
labetalol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of labetalol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - latanoprost
latanoprost, sulindac. unspecified interaction mechanism. Use Caution/Monitor. There are conflicting reports from studies of either increased or decreased IOP when ophthalmic prostaglandins are coadministered with NSAIDs (either systemic or ophthalmic).
- latanoprostene bunod ophthalmic
latanoprostene bunod ophthalmic, sulindac. unspecified interaction mechanism. Use Caution/Monitor. There are conflicting reports from studies of either increased or decreased IOP when ophthalmic prostaglandins are coadministered with NSAIDs (either systemic or ophthalmic).
- levalbuterol
sulindac increases and levalbuterol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- levofloxacin
levofloxacin, sulindac. Other (see comment). Modify Therapy/Monitor Closely. Comment: Risk of CNS stimulation/seizure. Mechanism: Displacement of GABA from receptors in brain.
- levomilnacipran
levomilnacipran, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. SNRIs may further impair platelet activity in patients taking antiplatelet or anticoagulant drugs.
- lisinopril
lisinopril, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals.
- lithium
sulindac increases levels of lithium by decreasing renal clearance. Use Caution/Monitor.
- lornoxicam
lornoxicam and sulindac both increase anticoagulation. Use Caution/Monitor.
lornoxicam and sulindac both increase serum potassium. Use Caution/Monitor. - losartan
losartan and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of losartan by pharmacodynamic antagonism. Modify Therapy/Monitor Closely. NSAIDs decrease synthesis of vasodilating renal prostaglandins, and thus affect fluid homeostasis and may diminish antihypertensive effect.
losartan, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals. - meclofenamate
meclofenamate and sulindac both increase anticoagulation. Use Caution/Monitor.
meclofenamate and sulindac both increase serum potassium. Use Caution/Monitor. - mefenamic acid
mefenamic acid and sulindac both increase anticoagulation. Use Caution/Monitor.
mefenamic acid and sulindac both increase serum potassium. Use Caution/Monitor. - melatonin
melatonin increases effects of sulindac by anticoagulation. Use Caution/Monitor. Melatonin may decrease prothrombin time.
- meloxicam
meloxicam and sulindac both increase anticoagulation. Use Caution/Monitor.
meloxicam and sulindac both increase serum potassium. Use Caution/Monitor. - mesalamine
mesalamine, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Additive nephrotoxicity.
- metaproterenol
sulindac increases and metaproterenol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- methyclothiazide
sulindac increases and methyclothiazide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor. .
- methylprednisolone
sulindac, methylprednisolone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- metolazone
sulindac increases and metolazone decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- metoprolol
metoprolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of metoprolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - milnacipran
milnacipran, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. SSRIs inhib. serotonin uptake by platelets.
- mipomersen
mipomersen, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: Both drugs have potential to increase hepatic enzymes; monitor LFTs.
- mistletoe
sulindac increases and mistletoe decreases anticoagulation. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- moexipril
moexipril, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals.
- moxifloxacin
moxifloxacin, sulindac. Other (see comment). Modify Therapy/Monitor Closely. Comment: Increased risk of CNS stimulation and seizures with high doses of fluoroquinolones.
- moxisylyte
sulindac decreases effects of moxisylyte by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- mycophenolate
sulindac will increase the level or effect of mycophenolate by acidic (anionic) drug competition for renal tubular clearance. Use Caution/Monitor.
- nabumetone
nabumetone and sulindac both increase anticoagulation. Use Caution/Monitor.
nabumetone and sulindac both increase serum potassium. Use Caution/Monitor. - nadolol
nadolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of nadolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - naproxen
naproxen and sulindac both increase anticoagulation. Use Caution/Monitor.
naproxen and sulindac both increase serum potassium. Use Caution/Monitor. - nebivolol
nebivolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of nebivolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - nefazodone
nefazodone, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. SSRIs inhib. serotonin uptake by platelets.
- nettle
sulindac increases and nettle decreases anticoagulation. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- norepinephrine
sulindac increases and norepinephrine decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- olmesartan
olmesartan and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of olmesartan by pharmacodynamic antagonism. Modify Therapy/Monitor Closely. NSAIDs decrease synthesis of vasodilating renal prostaglandins, and thus affect fluid homeostasis and may diminish antihypertensive effect.
olmesartan, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals. - ospemifene
sulindac, ospemifene. Either increases levels of the other by plasma protein binding competition. Modify Therapy/Monitor Closely.
- oxaprozin
oxaprozin and sulindac both increase anticoagulation. Use Caution/Monitor.
oxaprozin and sulindac both increase serum potassium. Use Caution/Monitor. - panax ginseng
sulindac and panax ginseng both increase anticoagulation. Use Caution/Monitor.
- parecoxib
parecoxib and sulindac both increase anticoagulation. Use Caution/Monitor.
parecoxib and sulindac both increase serum potassium. Use Caution/Monitor. - paroxetine
paroxetine, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. SSRIs inhib. serotonin uptake by platelets.
- pau d'arco
sulindac and pau d'arco both increase anticoagulation. Use Caution/Monitor.
- pegaspargase
pegaspargase increases effects of sulindac by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of bleeding events.
- penbutolol
penbutolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of penbutolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - perindopril
perindopril, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals.
- phenindione
phenindione and sulindac both increase anticoagulation. Modify Therapy/Monitor Closely.
- phenoxybenzamine
sulindac decreases effects of phenoxybenzamine by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- phentolamine
sulindac decreases effects of phentolamine by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- phytoestrogens
sulindac and phytoestrogens both increase anticoagulation. Use Caution/Monitor.
- pindolol
pindolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of pindolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - pirbuterol
sulindac increases and pirbuterol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- piroxicam
piroxicam and sulindac both increase anticoagulation. Use Caution/Monitor.
piroxicam and sulindac both increase serum potassium. Use Caution/Monitor. - pivmecillinam
pivmecillinam, sulindac. Either increases levels of the other by plasma protein binding competition. Use Caution/Monitor.
pivmecillinam, sulindac. Either increases levels of the other by decreasing renal clearance. Use Caution/Monitor. - potassium acid phosphate
sulindac and potassium acid phosphate both increase serum potassium. Modify Therapy/Monitor Closely.
- potassium chloride
sulindac and potassium chloride both increase serum potassium. Modify Therapy/Monitor Closely.
- potassium citrate
sulindac and potassium citrate both increase serum potassium. Modify Therapy/Monitor Closely.
- potassium iodide
potassium iodide and sulindac both increase serum potassium. Use Caution/Monitor.
- pralatrexate
sulindac increases levels of pralatrexate by decreasing renal clearance. Use Caution/Monitor. NSAIDs may delay pralatrexate clearance, increasing drug exposure. Adjust the pralatrexate dose as needed.
- prasugrel
sulindac, prasugrel. Either increases effects of the other by anticoagulation. Use Caution/Monitor. Chronic use of NSAIDs with prasugrel may increase bleeding risk.
- prazosin
sulindac decreases effects of prazosin by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- prednisolone
sulindac, prednisolone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- prednisone
sulindac, prednisone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- probenecid
sulindac will increase the level or effect of probenecid by acidic (anionic) drug competition for renal tubular clearance. Use Caution/Monitor.
- propranolol
propranolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of propranolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - protamine
protamine and sulindac both increase anticoagulation. Modify Therapy/Monitor Closely.
- quinapril
quinapril, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals.
- ramipril
ramipril, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals.
- reishi
sulindac and reishi both increase anticoagulation. Use Caution/Monitor.
- reteplase
sulindac and reteplase both increase anticoagulation. Use Caution/Monitor. Potential for increased risk of bleeding, caution is advised.
- rivaroxaban
rivaroxaban, sulindac. Other (see comment). Use Caution/Monitor. Comment: NSAIDs are known to increase bleeding. Bleeding risk may be increased when NSAIDs are used concomitantly with rivaroxaban. Monitor for signs/symptoms of blood loss.
- rivastigmine
rivastigmine increases toxicity of sulindac by pharmacodynamic synergism. Use Caution/Monitor. Monitor patients for symptoms of active or occult gastrointestinal bleeding.
- sacubitril/valsartan
sacubitril/valsartan and sulindac both increase serum potassium. Use Caution/Monitor.
sacubitril/valsartan, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals.
sulindac decreases effects of sacubitril/valsartan by pharmacodynamic antagonism. Modify Therapy/Monitor Closely. NSAIDs decrease synthesis of vasodilating renal prostaglandins, and thus affect fluid homeostasis and may diminish antihypertensive effect. - salicylates (non-asa)
salicylates (non-asa) and sulindac both increase anticoagulation. Use Caution/Monitor.
salicylates (non-asa) and sulindac both increase serum potassium. Use Caution/Monitor. - salmeterol
sulindac increases and salmeterol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- salsalate
salsalate and sulindac both increase anticoagulation. Use Caution/Monitor.
salsalate and sulindac both increase serum potassium. Use Caution/Monitor. - saw palmetto
saw palmetto increases toxicity of sulindac by unspecified interaction mechanism. Use Caution/Monitor. May increase risk of bleeding.
- sertraline
sertraline, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. SSRIs inhib. serotonin uptake by platelets.
- Siberian ginseng
sulindac and Siberian ginseng both increase anticoagulation. Use Caution/Monitor.
- silodosin
sulindac decreases effects of silodosin by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- sodium picosulfate/magnesium oxide/anhydrous citric acid
sulindac, sodium picosulfate/magnesium oxide/anhydrous citric acid. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May be associated with fluid and electrolyte imbalances.
- sodium sulfate/?magnesium sulfate/potassium chloride
sodium sulfate/?magnesium sulfate/potassium chloride increases toxicity of sulindac by Other (see comment). Use Caution/Monitor. Comment: Coadministration with medications that cause fluid and electrolyte abnormalities may increase the risk of adverse events of seizure, arrhythmias, and renal impairment.
- sodium sulfate/potassium sulfate/magnesium sulfate
sodium sulfate/potassium sulfate/magnesium sulfate increases toxicity of sulindac by Other (see comment). Use Caution/Monitor. Comment: Coadministration with medications that cause fluid and electrolyte abnormalities may increase the risk of adverse events of seizure, arrhythmias, and renal impairment.
- sodium sulfate/potassium sulfate/magnesium sulfate/polyethylene glycol
sulindac, sodium sulfate/potassium sulfate/magnesium sulfate/polyethylene glycol. Other (see comment). Use Caution/Monitor. Comment: Caution when bowel preps are used with drugs that cause SIADH or NSAIDs; increased risk for water retention or electrolyte imbalance.
- sotalol
sotalol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of sotalol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - sparsentan
sulindac and sparsentan both increase nephrotoxicity and/or ototoxicity. Use Caution/Monitor. Coadministration of NSAIDS, including selective COX-2 inhibitors, may result in deterioration of kidney function (eg, possible kidney failure). Monitor for signs of worsening renal function with concomitant use with NSAIDs.
- spironolactone
spironolactone and sulindac both increase serum potassium. Modify Therapy/Monitor Closely.
- succinylcholine
sulindac and succinylcholine both increase serum potassium. Use Caution/Monitor.
- sulfasalazine
sulfasalazine and sulindac both increase anticoagulation. Use Caution/Monitor.
sulfasalazine and sulindac both increase serum potassium. Use Caution/Monitor. - tafluprost
tafluprost, sulindac. unspecified interaction mechanism. Use Caution/Monitor. There are conflicting reports from studies of either increased or decreased IOP when ophthalmic prostaglandins are coadministered with NSAIDs (either systemic or ophthalmic).
- telmisartan
telmisartan and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of telmisartan by pharmacodynamic antagonism. Modify Therapy/Monitor Closely. NSAIDs decrease synthesis of vasodilating renal prostaglandins, and thus affect fluid homeostasis and may diminish antihypertensive effect.
telmisartan, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals. - temocillin
temocillin, sulindac. Either increases levels of the other by plasma protein binding competition. Use Caution/Monitor.
temocillin, sulindac. Either increases levels of the other by decreasing renal clearance. Use Caution/Monitor. - tenecteplase
sulindac and tenecteplase both increase anticoagulation. Use Caution/Monitor. Potential for increased risk of bleeding, caution is advised.
- tenofovir DF
tenofovir DF, sulindac. Either increases levels of the other by decreasing renal clearance. Modify Therapy/Monitor Closely. Toxicity may result from coadministration of tenofovir DF with other drugs that are also primarily excreted by glomerular filtration and/or active tubular secretion including high-dose or multiple-dose NSAIDs; alternatives to NSAIDs should be considered.
- terazosin
sulindac decreases effects of terazosin by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- terbutaline
sulindac increases and terbutaline decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- ticagrelor
ticagrelor, sulindac. Either increases effects of the other by anticoagulation. Use Caution/Monitor. Increased risk of bleeding with use of ticagrelor and chronic NSAID use. .
- ticarcillin
ticarcillin, sulindac. Either increases levels of the other by plasma protein binding competition. Use Caution/Monitor.
ticarcillin, sulindac. Either increases levels of the other by decreasing renal clearance. Use Caution/Monitor. - timolol
timolol and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of timolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - tobramycin inhaled
tobramycin inhaled and sulindac both increase nephrotoxicity and/or ototoxicity. Modify Therapy/Monitor Closely. Avoid concurrent or sequential use to decrease risk for ototoxicity
- tolazamide
sulindac increases effects of tolazamide by unknown mechanism. Use Caution/Monitor. Risk of hypoglycemia.
- tolbutamide
sulindac increases effects of tolbutamide by unknown mechanism. Use Caution/Monitor. Risk of hypoglycemia.
- tolfenamic acid
sulindac and tolfenamic acid both increase anticoagulation. Use Caution/Monitor.
sulindac and tolfenamic acid both increase serum potassium. Use Caution/Monitor. - tolmetin
sulindac and tolmetin both increase anticoagulation. Use Caution/Monitor.
sulindac and tolmetin both increase serum potassium. Use Caution/Monitor. - tolvaptan
sulindac and tolvaptan both increase serum potassium. Use Caution/Monitor.
- torsemide
sulindac increases and torsemide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- trandolapril
trandolapril, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals.
- travoprost ophthalmic
travoprost ophthalmic, sulindac. unspecified interaction mechanism. Use Caution/Monitor. There are conflicting reports from studies of either increased or decreased IOP when ophthalmic prostaglandins are coadministered with NSAIDs (either systemic or ophthalmic).
- trazodone
trazodone, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. SSRIs inhib. serotonin uptake by platelets.
- triamcinolone acetonide injectable suspension
sulindac, triamcinolone acetonide injectable suspension. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Concomitant use of NSAIDS and corticosteroids increases the risk of gastrointestinal side effects. .
- triamterene
triamterene and sulindac both increase serum potassium. Modify Therapy/Monitor Closely.
- valsartan
valsartan and sulindac both increase serum potassium. Use Caution/Monitor.
sulindac decreases effects of valsartan by pharmacodynamic antagonism. Modify Therapy/Monitor Closely. NSAIDs decrease synthesis of vasodilating renal prostaglandins, and thus affect fluid homeostasis and may diminish antihypertensive effect.
valsartan, sulindac. Either increases toxicity of the other by Other (see comment). Use Caution/Monitor. Comment: May result in renal function deterioration, particularly in elderly or volume depleted individuals. - venlafaxine
venlafaxine, sulindac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. SSRIs inhib. serotonin uptake by platelets.
- vitamin K1 (phytonadione)
sulindac increases and vitamin K1 (phytonadione) decreases anticoagulation. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- voclosporin
voclosporin, sulindac. Either increases toxicity of the other by nephrotoxicity and/or ototoxicity. Modify Therapy/Monitor Closely. Coadministration with drugs associated with nephrotoxicity may increase the risk for acute and/or chronic nephrotoxicity.
- vorapaxar
sulindac, vorapaxar. Either increases effects of the other by pharmacodynamic synergism. Use Caution/Monitor. Additive antiplatelet effect may occur.
- vortioxetine
sulindac, vortioxetine. Either increases effects of the other by anticoagulation. Use Caution/Monitor.
- warfarin
sulindac, warfarin. Either increases effects of the other by pharmacodynamic synergism. Modify Therapy/Monitor Closely. Drugs with antiplatelet properties may increase anticoagulation effect of warfarin.
- zanubrutinib
sulindac, zanubrutinib. Either increases effects of the other by anticoagulation. Modify Therapy/Monitor Closely. Zanubrutinib-induced cytopenias increases risk of hemorrhage. Coadministration of zanubritinib with antiplatelets or anticoagulants may further increase this risk.
- zotepine
sulindac decreases effects of zotepine by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
Minor (75)
- aceclofenac
aceclofenac will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- acemetacin
acemetacin will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- acyclovir
sulindac will increase the level or effect of acyclovir by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- alendronate
sulindac, alendronate. Either increases toxicity of the other by pharmacodynamic synergism. Minor/Significance Unknown. Increased risk of GI ulceration.
- amikacin
sulindac increases levels of amikacin by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in preterm infants.
- aminohippurate sodium
sulindac will increase the level or effect of aminohippurate sodium by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- anamu
sulindac and anamu both increase anticoagulation. Minor/Significance Unknown.
- aspirin
aspirin will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- aspirin rectal
aspirin rectal will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- aspirin/citric acid/sodium bicarbonate
aspirin/citric acid/sodium bicarbonate will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- balsalazide
sulindac will increase the level or effect of balsalazide by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- bendroflumethiazide
bendroflumethiazide will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- cefadroxil
cefadroxil will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- cefamandole
cefamandole will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- cefpirome
cefpirome will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- ceftibuten
ceftibuten will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- celecoxib
celecoxib will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- cephalexin
cephalexin will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- chlorothiazide
chlorothiazide will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- chlorpropamide
sulindac will increase the level or effect of chlorpropamide by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- chlorthalidone
chlorthalidone will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- choline magnesium trisalicylate
choline magnesium trisalicylate will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- creatine
creatine, sulindac. Mechanism: pharmacodynamic synergism. Minor/Significance Unknown. (Theoretical interaction) Combination may have additive nephrotoxic effects.
- cyclopenthiazide
cyclopenthiazide will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- danshen
sulindac and danshen both increase anticoagulation. Minor/Significance Unknown.
- devil's claw
sulindac and devil's claw both increase anticoagulation. Minor/Significance Unknown.
- diclofenac
diclofenac will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- diclofenac topical
diclofenac topical, sulindac. Either increases effects of the other by pharmacodynamic synergism. Minor/Significance Unknown. Although low, there is systemic exposure to diclofenac topical; theoretically, concomitant administration with systemic NSAIDS or aspirin may result in increased NSAID adverse effects.
- diflunisal
diflunisal will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- entecavir
sulindac, entecavir. Either increases effects of the other by decreasing renal clearance. Minor/Significance Unknown. Coadministration with drugs that reduce renal function or compete for active tubular secretion may increase serum concentrations of either entecavir or the coadministered drug.
- eplerenone
sulindac decreases effects of eplerenone by pharmacodynamic antagonism. Minor/Significance Unknown. NSAIDs decrease prostaglandin synthesis.
- etodolac
etodolac will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- fenoprofen
fenoprofen will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- feverfew
sulindac decreases effects of feverfew by pharmacodynamic antagonism. Minor/Significance Unknown.
- flurbiprofen
flurbiprofen will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- furosemide
sulindac decreases effects of furosemide by pharmacodynamic antagonism. Minor/Significance Unknown. NSAIDs decrease prostaglandin synthesis.
- ganciclovir
sulindac will increase the level or effect of ganciclovir by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- gentamicin
sulindac increases levels of gentamicin by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in preterm infants.
- hydrochlorothiazide
hydrochlorothiazide will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- ibuprofen
ibuprofen will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- imidapril
sulindac decreases effects of imidapril by pharmacodynamic antagonism. Minor/Significance Unknown. NSAIDs decrease prostaglandin synthesis.
- indapamide
indapamide will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- indomethacin
indomethacin will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- ketoprofen
ketoprofen will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- ketorolac
ketorolac will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- ketorolac intranasal
ketorolac intranasal will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- lornoxicam
lornoxicam will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- meclofenamate
meclofenamate will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- mefenamic acid
mefenamic acid will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- meloxicam
meloxicam will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- mesalamine
sulindac will increase the level or effect of mesalamine by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- methyclothiazide
methyclothiazide will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- metolazone
metolazone will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- nabumetone
nabumetone will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- naproxen
naproxen will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- neomycin PO
sulindac increases levels of neomycin PO by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in preterm infants.
- nitazoxanide
nitazoxanide, sulindac. Either increases levels of the other by Mechanism: plasma protein binding competition. Minor/Significance Unknown.
- noni juice
sulindac and noni juice both increase serum potassium. Minor/Significance Unknown.
- ofloxacin
ofloxacin, sulindac. Other (see comment). Minor/Significance Unknown. Comment: Risk of CNS stimulation/seizure. Mechanism: Displacement of GABA from receptors in brain.
- oxaprozin
oxaprozin will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- parecoxib
parecoxib will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- paromomycin
sulindac increases levels of paromomycin by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in preterm infants.
- piroxicam
piroxicam will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- rose hips
rose hips will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- salicylates (non-asa)
salicylates (non-asa) will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- salsalate
salsalate will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- streptomycin
sulindac increases levels of streptomycin by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in preterm infants.
- sulfasalazine
sulfasalazine will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- tobramycin
sulindac increases levels of tobramycin by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in preterm infants.
- tolfenamic acid
sulindac will increase the level or effect of tolfenamic acid by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- tolmetin
sulindac will increase the level or effect of tolmetin by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- triamterene
triamterene, sulindac. Other (see comment). Minor/Significance Unknown. Comment: Risk of acute renal failure. Mechanism: NSAIDs decrease prostaglandin synthesis, which normally protect against nephrotoxicity.
sulindac increases toxicity of triamterene by pharmacodynamic antagonism. Minor/Significance Unknown. NSAIDs decrease prostaglandin synthesis, increasing the risk of nephrotoxicity. - valganciclovir
sulindac will increase the level or effect of valganciclovir by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- vancomycin
sulindac increases levels of vancomycin by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in neonates.
- willow bark
sulindac will increase the level or effect of willow bark by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
Adverse Effects
1-10%
GI pain (10%)
Constipation (3-9%)
Diarrhea (3-9%)
Dizziness (3-9%)
Dyspepsia (3-9%)
Headache (3-9%)
Nausea (3-9%)
Rash (3-9%)
Abdominal cramps (1-3%)
Anorexia (1-3%)
Edema (1-3%)
Nervousness (1-3%)
Pruritus (1-3%)
Tinnitus (1-3%)
Vomiting (1-3%)
<1%
Hypersensitivity reactions (including anaphylaxis, angioedema, bronchospasm, dyspnea) Sulindac therapy should be discontinued & not reinstituted if unexplained fever or other evidence of hypersensitivity occurs
Thrombocytopenia
Ecchymosis
Purpura
Leukopenia
Agranulocytosis
Neutropenia
Bone marrow depression
CHF (<1%)
Hematuria (<1%)
Renal impairment (including renal failure)
Interstitial nephritis
Nephrotic syndrome
Warnings
Black Box Warnings
Cardiovascular Risk
- NSAIDs may increase risk of serious cardiovascular thrombotic events, myocardial infarction (MI), & stroke, which can be fatal
- Risk may increase with duration of use
- Patients with risk factors for or existing cardiovascular disease may be at greater risk
- NSAIDs are contraindicated for perioperative pain in the setting of coronary artery bypass graft (CABG) surgery (increased risk of MI & stroke)
Gastrointestinal Risk
- NSAIDs increase risk of serious GI adverse events including bleeding, ulceration, & perforation of the stomach or intestines, which can be fatal
- GI adverse events may occur at any time during use & without warning symptoms
- Elderly patients are at greater risk for serious GI events
Contraindications
Hypersensitivity to drug or excipients
In the setting of CABG surgery
History of asthma, urticaria, or any other type of reaction after taking aspirin or other NSAIDs
Cautions
Sulindac metabolites have been reported rarely as the major or a minor component in renal stones in association with other calculus components; the drug should be used with caution in patients with a history of renal lithiasis, and they should be kept well hydrated while receiving therapy
Pancreatitis has been reported in patients receiving therapy; should pancreatitis be suspected, the drug should be discontinued and not restarted, supportive medical therapy instituted, and patient monitored closely with appropriate laboratory studies (eg, serum and urine amylase, amylase/creatinine clearance ratio, electrolytes, serum calcium, glucose, lipase, etc.); a search for other causes of pancreatitis as well as those conditions which mimic pancreatitis should be conducted
Because of reports of adverse eye findings with non-steroidal anti-inflammatory agents, it is recommended that patients who develop eye complaints during treatment have ophthalmologic studies
In patients with poor liver function, delayed, elevated and prolonged circulating levels of the sulfide and sulfone metabolites may occur; such patients should be monitored closely; a reduction of daily dosage may be required
In patients with systemic lupus erythematosus (SLE) and mixed connective tissue disease, there may be an increased risk of aseptic meningitis
Patients receiving corticosteroids
- Sulindac cannot be expected to substitute for corticosteroids or to treat corticosteroid insufficiency; abrupt discontinuation of corticosteroids may lead to disease exacerbation
- Patients on prolonged corticosteroid therapy should have their therapy tapered slowly if a decision is made to discontinue corticosteroids
- The pharmacological activity of sulindac in reducing fever and inflammation may diminish the utility of these diagnostic signs in detecting complications of presumed noninfectious, painful conditions
Cardiovascular effects
- May increase risk of serious cardiovascular (CV) thrombotic events, myocardial infarction, and stroke, which can be fatal
- Patients with known CV disease or risk factors for CV disease may be at greater risk; to minimize potential risk for an adverse CV event in patients treated with an NSAID, the lowest effective dose should be used for the shortest duration possible; physicians and patients should remain alert for the development of such events, even in absence of previous CV symptoms
- Patients should be informed about signs and/or symptoms of serious CV events and 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; the concurrent use of aspirin and an NSAID does increase risk of serious GI events
Hypertension
- NSAIDs can lead to new onset of hypertension or worsening of pre-existing hypertension, either of which may contribute to the increased incidence of CV events.
- Use with caution in patients with hypertension
- Closely monitor blood pressure during initiation and during therapy
- Patients taking angiotensin converting enzyme (ACE) inhibitors, thiazides, or loop diuretics may have impaired response to these therapies when taking NSAIDs
Gastrointestinal effects
- Therapy can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the stomach, small intestine, or large intestine, which can be fatal
- These serious adverse events can occur at any time, with or without warning symptoms; these trends continue with longer duration of use, increasing the likelihood of developing a serious GI event at some time during the course of therapy; however, even short-term therapy is not without risk
- NSAIDs should be prescribed with extreme caution in those with prior history of ulcer disease or gastrointestinal bleeding; patients with a prior history of peptic ulcer disease and/or gastrointestinal bleeding 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 NSAIDs include concomitant use of oral corticosteroids or anticoagulants, longer duration of NSAID therapy, smoking, use of alcohol, older age, and poor general health status
- Most spontaneous reports of fatal GI events are in elderly or debilitated patients and therefore, 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 possible 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
Hepatic effects
- In addition to hypersensitivity reactions involving liver, in some patients the findings are consistent with those of cholestatic hepatitis
- As with other non-steroidal anti-inflammatory drugs, borderline elevation of one or more liver tests without any other signs and symptoms may occur in patients taking NSAIDs; these laboratory abnormalities may progress, may remain essentially unchanged, or may be transient with continued therapy
- The SGPT (ALT) test is probably the most sensitive indicator of liver dysfunction; meaningful (3 times the upper limit of normal) elevations of SGPT or SGOT (AST) reported in clinical trials
- Notable elevations of ALT or AST (approximately three or more times the upper limit of normal) reported; in addition, rare cases of severe hepatic reactions, including jaundice and fatal fulminant hepatitis, liver necrosis and hepatic failure, some of them with fatal outcomes reported
- A patient with symptoms and/or signs suggesting liver dysfunction, or in whom an abnormal liver test has occurred, should be evaluated for evidence of development of a more severe hepatic reaction while on therapy
- Although such reactions as described above are rare, if abnormal liver tests persist or worsen, if clinical signs and symptoms consistent with liver disease develop, or if systemic manifestations occur (eg, eosinophilia, rash, etc.), therapy should be discontinued
- In clinical trials the use of doses of 600 mg/day has been associated with an increased incidence of mild liver test abnormalities
Renal effects
- Long-term administration of NSAIDs has resulted in renal papillary necrosis and other renal injury; renal toxicity has also been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion; in these patients, administration of a non-steroidal anti-inflammatory drug may cause a dose-dependent reduction in prostaglandin formation and, secondarily, in renal blood flow, which may precipitate overt renal decompensation
- Patients at greatest risk of this reaction are those with impaired renal function, heart failure, liver dysfunction, those taking diuretics and ACE inhibitors, patients who are volume-depleted, and the elderly; discontinuation of NSAID therapy is usually followed by recovery to the pretreatment state
- No information is available from controlled clinical studies regarding use in patients with advanced renal disease; therefore, treatment with sulindac is not recommended in these patients with advanced renal disease; If therapy must be initiated, close monitoring of the patient’s renal function advisable
Anaphylactic reactions
- As with other NSAIDs, anaphylactic/anaphylactoid reactions may occur in patients without known prior exposure to sulindac; therapy should not be given to patients with the aspirin triad; this symptom complex 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 NSAIDs
- Emergency help should be sought in cases where an anaphylactic/anaphylactoid reaction occurs
Heart failure risk
- NSAIDS have the potential to trigger HF by prostaglandin inhibition that leads to sodium and water retention, increased systemic vascular resistance, and blunted response to diuretics
- NSAIDS should be avoided or withdrawn whenever possible
- Heart failure: risk is higher if you administer more than directed or for longer than directed
- AHA/ACC Heart Failure Guidelines; Circulation. 2016; 134
Skin and drug reactions with eosinophilia and systemic symptoms
- NSAIDS 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 first appearance of skin rash or any other sign of hypersensitivity
- Drug reaction with eosinophilia and systemic symptoms (DRESS) reported; some of these events have been fatal or life-threatening; DRESS typically, although not exclusively, presents with fever, rash, lymphadenopathy, and/or facial swelling
- Other clinical manifestations may include hepatitis, nephritis, hematological abnormalities, myocarditis, or myositis; sometimes symptoms of DRESS may resemble an acute viral infection
- Eosinophilia is often present; because this disorder is variable in its presentation, other organ systems not noted here may be involved
- Early manifestations of hypersensitivity, such as fever or lymphadenopathy, may be present even though rash is not evident; if such signs or symptoms are present, discontinue therapy and evaluate the patient immediately
Hematologic effects
- Anemia is sometimes seen in patients receiving NSAIDs; this may be due to fluid retention, occult or gross GI blood loss, or an incompletely described effect upon erythropoiesis
- Patients on long-term treatment with NSAIDs, should have their hemoglobin or hematocrit checked if they exhibit any signs or symptoms of anemia; NSAIDs inhibit platelet aggregation 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 who may be adversely affected by alterations in platelet function, such as those with coagulation disorders or patients receiving anticoagulants, should be carefully monitored
Preexisting asthma
- 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 non-steroidal anti-inflammatory drugs has been reported in such aspirin-sensitive patients, sulindac should not be administered to patients with this form of aspirin sensitivity and should be used with caution in patients with preexisting asthma
Drug interaction overview
·Drugs that interfere with hemostasis
- Monitor for bleeding
- Diclofenac and anticoagulants such as warfarin have a synergistic effect on bleeding. Use with anticoagulants have an increased risk of serious bleeding
- Serotonin release by platelets plays an important role in hemostasis
- Monitor for signs of bleeding in patients concomitantly using anticoagulants (eg, warfarin), antiplatelet agents (eg, aspirin), selective serotonin reuptake inhibitors, and serotonin norepinephrine reuptake inhibitors
·Salicylates
- Not generally recommended
- Diclofenac with other NSAIDs or salicylates (eg, diflunisal, salsalate) increases the risk of GI toxicity, with little or no increase in efficacy
- ACE inhibitors, angiotensin receptor blockers (ARBs), beta-blockers H5
- Monitor for signs of worsening renal function in high-risk patients (eg, elderly patients, volume depleted, renal impaired patients)
- NSAIDs may diminish the antihypertensive effect of ACE inhibitors, ARBs, or beta-blockers
·Diuretics
- Monitor patients to assure diuretic efficacy including antihypertensive effects
- NSAIDs can reduce natriuretic effect of loop and thiazide diuretics
·Digoxin
- Monitor serum digoxin level
- Diclofenac can increase serum concentration and prolong half-life of digoxin
·Pemetrexed
- Monitor for myelosuppression, renal, and GI toxicity during coadministration of NSAIDS with pemetrexed in renally impaired patients (CrCl 45-79 mL/min)
- Avoid NSAIDs with short elimination half-lives (eg, diclofenac, indomethacin) for a period of 2 days before, the day of, and 2 days following administration of pemetrexed
- Interrupt dosing of NSAIDs with longer half-lives (eg, meloxicam, nabumetone) for at least 5 days before, during, and 2 days following pemetrexed administration
- Diclofenac may increase the risk of pemetrexed-associated myelosuppression, renal, and GI toxicity
Pregnancy & Lactation
Pregnancy Category: B; D if used for prolonged periods, or near term (may cause premature closure of ductus arteriosus)
The Quebec Pregnancy Registry identified 4705 women who had spontaneous abortions by 20 weeks' gestation; each case was matched to 10 control subjects (n=47,050) who had not had spontaneous abortions; exposure to nonaspirin NSAIDs during pregnancy was documented in approximately 7.5% of cases of spontaneous abortions and in approximately 2.6% of controls. (CMAJ, September 6, 2011; DOI:10.1503/cmaj.110454)
Lactation: not known if distributed in milk
Pregnancy Categories
A: Generally acceptable. Controlled studies in pregnant women show no evidence of fetal risk.
B: May be acceptable. Either animal studies show no risk but human studies not available or animal studies showed minor risks and human studies done and showed no risk. C: Use with caution if benefits outweigh risks. Animal studies show risk and human studies not available or neither animal nor human studies done. D: Use in LIFE-THREATENING emergencies when no safer drug available. Positive evidence of human fetal risk. X: Do not use in pregnancy. Risks involved outweigh potential benefits. Safer alternatives exist. NA: Information not available.Pharmacology
Mechanism of Action
Inhibits synthesis of prostaglandins in body tissues by inhibiting at least 2 cyclooxygenase isoenzymes, cyclooxygenase-1 (COX-1) and -2 (COX-2)
May inhibit chemotaxis, may alter lymphocyte activity, decrease proinflammatory cytokine activity, and may inhibit neutrophil aggregation. These effects may contribute to its anti-inflammatory activity
Pharmacokinetics
Half-life: Sulindac (8 hr); sulfide metabolite (16.4 hr)
Peak Plasma Time: 2 hr (sulindac); 5-6 hr (sulfide metabolites)
Concentration: 3-6 mcg/mL
Excretion: Urine (50%); feces (25%)
Bioavailability: 90%
Protein Bound: Approx 93% (sulindac); approx 98% (sulfide metabolite)
Metabolism: Hepatic reduction; significant enterohepatic circulation
Metabolites: Sulfide and sulfone metabolites
Dialyzable: Unknown
Enzymes inhibited: Cyclooxygenase
Images
| BRAND | FORM. | UNIT PRICE | PILL IMAGE |
|---|---|---|---|
| sulindac oral - | 200 mg tablet |  | |
| sulindac oral - | 200 mg tablet |  | |
| sulindac oral - | 200 mg tablet |  | |
| sulindac oral - | 150 mg tablet |  | |
| sulindac oral - | 200 mg tablet |  | |
| sulindac oral - | 150 mg tablet |  | |
| sulindac oral - | 150 mg tablet |  | |
| sulindac oral - | 150 mg tablet |  |
Copyright © 2010 First DataBank, Inc.
Patient Handout
sulindac oral
SULINDAC - ORAL
(SUL-in-dak)
COMMON BRAND NAME(S): Clinoril
WARNING: Nonsteroidal anti-inflammatory drugs (including sulindac) may rarely increase the risk of a heart attack or stroke. This effect can happen at any time while taking this drug but is more likely if you take it for a long time. The risk may be greater in older adults or if you have heart disease or increased risk for heart disease (for example, due to smoking, family history of heart disease, or conditions such as high blood pressure or diabetes). Do not take this drug right before or after heart bypass surgery (CABG).Also, this drug may rarely cause serious (rarely fatal) bleeding from the stomach or intestines. This effect can occur without warning symptoms at any time while taking this drug. Older adults may be at higher risk for this effect.Stop taking sulindac and get medical help right away if you notice any of these rare but serious side effects: stomach/abdominal pain that doesn't go away, black/tarry stools, vomit that looks like coffee grounds, chest/jaw/left arm pain, shortness of breath, unusual sweating, confusion, weakness on one side of the body, trouble speaking, sudden vision changes.Talk to your doctor or pharmacist about the benefits and risks of taking this drug.
USES: See also Warning section.Sulindac is used to reduce pain, swelling, and joint stiffness from arthritis. It is also used to treat arthritis of the spine, gouty arthritis, and shoulder bursitis/tendonitis.Sulindac is known as a nonsteroidal anti-inflammatory drug (NSAID). It works by blocking your body's production of certain natural substances that cause inflammation. This effect helps to decrease swelling, pain, or fever.If you are treating a chronic condition such as arthritis, ask your doctor about non-drug treatments and/or using other medications to treat your pain.
HOW TO USE: Read the Medication Guide provided by your pharmacist before you start taking sulindac and each time you get a refill. If you have any questions, ask your doctor or pharmacist.Take this medication by mouth as directed by your doctor, usually twice daily. Take this medication with a full glass of water (8 ounces/240 milliliters), unless your doctor directs you otherwise. Do not lie down for at least 10 minutes after taking this medication. If stomach upset occurs while taking this medication, take it with food, milk, or an antacid.The dosage is based on your medical condition and response to treatment. To reduce your risk of stomach bleeding and other side effects, take this medication at the lowest effective dose for the shortest possible time. Do not increase your dose or take this drug more often or for longer than prescribed. Discuss the risks and benefits with your doctor or pharmacist.For certain conditions (such as arthritis), it may take 1-2 weeks of taking this drug regularly until you get the full benefit.If you are taking this drug "as needed" (not on a regular schedule), remember that pain medications work best if they are used as the first signs of pain occur. If you wait until the pain has worsened, the medicine may not work as well.Tell your doctor if your condition gets worse.
SIDE EFFECTS: See also Warning section.Upset stomach, nausea, vomiting, gas, diarrhea, constipation, dizziness, or headache may occur. If any of these effects last or get worse, tell your doctor or pharmacist promptly.Remember that this medication has been prescribed because your doctor has judged that the benefit to you is greater than the risk of side effects. Many people using this medication do not have serious side effects.This medication may raise your blood pressure. Check your blood pressure regularly and tell your doctor if the results are high.Tell your doctor right away if you have any serious side effects, including: hearing changes (such as ringing in the ears), mental/mood changes, easy bleeding/bruising, difficult/painful swallowing, symptoms of heart failure (such as swelling ankles/feet, unusual tiredness, unusual/sudden weight gain).Get medical help right away if you have any very serious side effects, including: signs of kidney problems (such as change in the amount of urine, pink/bloody urine), unexplained stiff neck.Sulindac may rarely cause serious (possibly fatal) liver disease. Get medical help right away if you have any symptoms of liver damage, such as: nausea/vomiting that doesn't stop, loss of appetite, stomach/abdominal pain, yellowing eyes/skin, dark urine.A very serious allergic reaction to this drug is rare. However, get medical help right away if you notice any symptoms of a serious allergic reaction, including: fever, swollen lymph nodes, rash, itching/swelling (especially of the face/tongue/throat), severe dizziness, trouble breathing.This is not a complete list of possible side effects. If you notice other effects not listed above, contact your doctor or pharmacist.In the US -Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088 or at www.fda.gov/medwatch.In Canada - Call your doctor for medical advice about side effects. You may report side effects to Health Canada at 1-866-234-2345.
PRECAUTIONS: See also Warning section.Before taking sulindac, tell your doctor or pharmacist if you are allergic to it; or to aspirin or other NSAIDs (such as ibuprofen, naproxen, celecoxib); or if you have any other allergies. This product may contain inactive ingredients, which can cause allergic reactions or other problems. Talk to your pharmacist for more details.Before using this medication, tell your doctor or pharmacist your medical history, especially of: asthma (including a history of worsening breathing after taking aspirin or other NSAIDs), blood disorders (such as anemia, bleeding/clotting problems), growths in the nose (nasal polyps), heart disease (such as previous heart attack), high blood pressure, kidney stones, liver disease, stroke, swelling (edema, fluid retention), stomach/intestinal/esophagus problems (such as bleeding, heartburn, ulcers).Kidney problems can sometimes occur with the use of NSAID medications, including sulindac. Problems are more likely to occur if you are dehydrated, have heart failure or kidney disease, are an older adult, or if you take certain medications (see also Drug Interactions section). Drink plenty of fluids as directed by your doctor to prevent dehydration and tell your doctor right away if you have pink/bloody urine or any unusual change in the amount of urine.This drug may make you dizzy. Alcohol or marijuana (cannabis) can make you more dizzy. Do not drive, use machinery, or do anything that needs alertness until you can do it safely. Limit alcoholic beverages. Talk to your doctor if you are using marijuana (cannabis).This medicine may cause stomach bleeding. Daily use of alcohol and tobacco, especially when combined with this medicine, may increase your risk for stomach bleeding. Limit alcohol and stop smoking.This medication may make you more sensitive to the sun. Limit your time in the sun. Avoid tanning booths and sunlamps. Use sunscreen and wear protective clothing when outdoors. Tell your doctor right away if you get sunburned or have skin blisters/redness.Before having surgery, tell your doctor or dentist about all the products you use (including prescription drugs, nonprescription drugs, and herbal products).Older adults may be at greater risk for stomach/intestinal bleeding, kidney problems, heart attack, and stroke while using this drug.Before using this medication, women of childbearing age should talk with their doctor(s) about the benefits and risks. Tell your doctor if you are pregnant or if you plan to become pregnant. This medication may harm an unborn baby and cause problems with normal labor/delivery. It is not recommended for use in pregnancy from 20 weeks until delivery. If your doctor decides that you need to use this medication between 20 and 30 weeks of pregnancy, you should use the lowest effective dose for the shortest possible time. You should not use this medication after 30 weeks of pregnancy.It is unknown if this medication passes into breast milk. Breast-feeding while using this drug is not recommended. Consult your doctor before breast-feeding.
DRUG INTERACTIONS: Drug interactions may change how your medications work or increase your risk for serious side effects. This document does not contain all possible drug interactions. Keep a list of all the products you use (including prescription/nonprescription drugs and herbal products) and share it with your doctor and pharmacist. Do not start, stop, or change the dosage of any medicines without your doctor's approval.Some products that may interact with this drug are: aliskiren, ACE inhibitors (such as benazepril, lisinopril), angiotensin II receptor blockers (such as losartan, valsartan), cidofovir, corticosteroids (such as dexamethasone, prednisone), dimethyl sulfoxide (DMSO), lithium, methotrexate, "water pills" (diuretics such as furosemide).This medication may increase the risk of bleeding when taken with other drugs that also may cause bleeding. Examples include anti-platelet drugs such as clopidogrel, "blood thinners" such as dabigatran/enoxaparin/warfarin, among others.Check all prescription and nonprescription medicine labels carefully since many medications contain pain relievers/fever reducers (aspirin, NSAIDs such as ibuprofen, ketorolac, naproxen). These drugs are similar to sulindac and may increase your risk of side effects if taken together. However, if your doctor has directed you to take low-dose aspirin to prevent heart attack or stroke (usually 81-162 milligrams a day), you should keep taking the aspirin unless your doctor instructs you otherwise. Ask your doctor or pharmacist for more details.
OVERDOSE: If someone has overdosed and has serious symptoms such as passing out or trouble breathing, call 911. Otherwise, call a poison control center right away. US residents can call their local poison control center at 1-800-222-1222. Canada residents can call a provincial poison control center. Symptoms of overdose may include: severe stomach pain, slow/shallow breathing, extreme drowsiness, loss of consciousness.
NOTES: Do not share this medication with others.Lab and/or medical tests (such as complete blood count, liver/kidney function, blood pressure) may be done while you are using this medication. Keep all medical and lab appointments. Consult your doctor for more details.Lifestyle changes (such as weight loss if needed, strengthening/conditioning exercises) may help improve your flexibility and joint function. Consult your doctor for specific instructions.
MISSED DOSE: If you are prescribed this drug on a regular schedule (not just "as needed") and you miss a dose, take it as soon as you remember. If it is near the time of the next dose, skip the missed dose. Take your next dose at the regular time. Do not double the dose to catch up.
STORAGE: Store at room temperature away from light and moisture. Do not store in the bathroom. Keep all medications away from children and pets.Do not flush medications down the toilet or pour them into a drain unless instructed to do so. Properly discard this product when it is expired or no longer needed. Consult your pharmacist or local waste disposal company.
Information last revised August 2022. Copyright(c) 2023 First Databank, Inc.
IMPORTANT: HOW TO USE THIS INFORMATION: This is a summary and does NOT have all possible information about this product. This information does not assure that this product is safe, effective, or appropriate for you. This information is not individual medical advice and does not substitute for the advice of your health care professional. Always ask your health care professional for complete information about this product and your specific health needs.
Formulary
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