Dosing & Uses
Dosage Forms & Strengths
diclofenac/misoprostol
tablet
- 50mg/200mcg
- 75mg/200mcg
Osteoarthritis
50 mg/200 mcg: 1 tab PO three times daily; not to exceed 200 mcg misoprostol/dose or 800 mcg/day
75mg/200mcg: 1 tab PO three times daily; not to exceed 200 mcg misoprostol/dose or 800 mcg/day
If not tolerated, may reduce frequency to twice daily
Three times daily dose of misoprostol is more protective than when given twice daily
Rheumatoid Arthritis
50 mg/200 mcg: 1 tab PO three or four times daily; not to exceed 200 mcg misoprostol/dose or 800 mcg/day
75mg/200mcg: 1 tab PO three or four times daily; not to exceed 200 mcg misoprostol/dose or 800 mcg/day
If not tolerated may reduce frequency to twice daily
Three times daily dose of misoprostol is more protective than when given twice daily
Administration
Swallow tablet whole, do not chew or crush
Do not take with antacids
Safety & efficacy not established
Interactions
Interaction Checker
No Results

Contraindicated
Serious - Use Alternative
Significant - Monitor Closely
Minor

Contraindicated (1)
- fezolinetant
diclofenac will increase the level or effect of fezolinetant by affecting hepatic enzyme CYP1A2 metabolism. Contraindicated. Fezolinetant AUC and peak plasma concentration are increased if coadministered with drugs that are weak, moderate, or strong CYP1A2 inhibitors
Serious - Use Alternative (21)
- aluminum hydroxide/magnesium carbonate
aluminum hydroxide/magnesium carbonate, misoprostol. unknown mechanism. Avoid or Use Alternate Drug. Antacids reduce the bioavailability of misoprostol acid. Magnesium-containing antacids may potentiate misoprostol-induced diarrhea. If an antacid is needs, use an aluminum- or calcium- containing antacids.
- aluminum hydroxide/magnesium trisilicate
aluminum hydroxide/magnesium trisilicate, misoprostol. unknown mechanism. Avoid or Use Alternate Drug. Antacids reduce the bioavailability of misoprostol acid. Magnesium-containing antacids may potentiate misoprostol-induced diarrhea. If an antacid is needs, use an aluminum- or calcium- containing antacids.
- aminolevulinic acid oral
aminolevulinic acid oral, diclofenac. Either increases toxicity 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
diclofenac, 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
diclofenac and apixaban both increase anticoagulation. Avoid or Use Alternate Drug.
- benazepril
diclofenac, 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
diclofenac, 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.
- citric acid/glucono-delta-lactone/magnesium carbonate
citric acid/glucono-delta-lactone/magnesium carbonate, misoprostol. unknown mechanism. Avoid or Use Alternate Drug. Antacids reduce the bioavailability of misoprostol acid. Magnesium-containing antacids may potentiate misoprostol-induced diarrhea. If an antacid is needs, use an aluminum- or calcium- containing antacids.
- enalapril
diclofenac, 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
diclofenac, 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.
- ivosidenib
ivosidenib will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Avoid or Use Alternate Drug. Avoid coadministration of sensitive CYP2C9 substrates with ivosidenib or replace with alternate therapies. If coadministration is unavoidable, monitor patients for loss of therapeutic effect of these drugs.
- ketorolac
diclofenac, ketorolac. Either increases toxicity of the other by pharmacodynamic synergism. Contraindicated.
- ketorolac intranasal
diclofenac, ketorolac intranasal. Either increases toxicity of the other by pharmacodynamic synergism. Contraindicated.
- lisinopril
diclofenac, 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.
- lonafarnib
diclofenac will increase the level or effect of lonafarnib by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Avoid or Use Alternate Drug. If coadministration of lonafarnib (a sensitive CYP3A substrate) with weak CYP3A inhibitors is unavoidable, reduce to, or continue lonafarnib at starting dose. Closely monitor for arrhythmias and events (eg, syncope, heart palpitations) since lonafarnib effect on QT interval is unknown.
- magnesium gluconate
magnesium gluconate, misoprostol. unknown mechanism. Avoid or Use Alternate Drug. Antacids reduce the bioavailability of misoprostol acid. Magnesium-containing antacids may potentiate misoprostol-induced diarrhea. If an antacid is needs, use an aluminum- or calcium- containing antacids.
- methotrexate
diclofenac 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
diclofenac, 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
diclofenac, 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.
- oxytocin
misoprostol increases effects of oxytocin by pharmacodynamic synergism. Avoid or Use Alternate Drug. Misoprostol may augment the effects oxytocic agents, especially when given less than 4 hours before initiating oxytocin. .
- pemetrexed
diclofenac 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.
Monitor Closely (269)
- acebutolol
acebutolol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of acebutolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - aceclofenac
aceclofenac and diclofenac both increase anticoagulation. Use Caution/Monitor.
aceclofenac and diclofenac both increase serum potassium. Use Caution/Monitor. - acemetacin
acemetacin and diclofenac both increase anticoagulation. Use Caution/Monitor.
acemetacin and diclofenac both increase serum potassium. Use Caution/Monitor. - agrimony
diclofenac and agrimony both increase anticoagulation. Use Caution/Monitor.
- albuterol
diclofenac increases and albuterol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- alfalfa
diclofenac and alfalfa both increase anticoagulation. Use Caution/Monitor.
- alfuzosin
diclofenac decreases effects of alfuzosin by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- aliskiren
diclofenac 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.
- alpelisib
alpelisib will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Modify Therapy/Monitor Closely.
- alteplase
diclofenac and alteplase both increase anticoagulation. Use Caution/Monitor. Potential for increased risk of bleeding, caution is advised.
- American ginseng
diclofenac and American ginseng both increase anticoagulation. Use Caution/Monitor.
- amiloride
amiloride and diclofenac both increase serum potassium. Modify Therapy/Monitor Closely.
- antithrombin alfa
antithrombin alfa and diclofenac both increase anticoagulation. Modify Therapy/Monitor Closely.
- antithrombin III
antithrombin III and diclofenac both increase anticoagulation. Modify Therapy/Monitor Closely.
- apalutamide
apalutamide will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Coadministration of apalutamide, a weak CYP2C9 inducer, with drugs that are CYP2C9 substrates can result in lower exposure to these medications. Evaluate for loss of therapeutic effect if medication must be coadministered.
- arformoterol
diclofenac increases and arformoterol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- argatroban
argatroban and diclofenac both increase anticoagulation. Modify Therapy/Monitor Closely.
- artesunate
diclofenac will increase the level or effect of artesunate by decreasing metabolism. Use Caution/Monitor. Coadministration may increase active artesunate metabolite (DHA) by inhibiting UGT. Monitor for increased adverse effects.
- asenapine
diclofenac decreases effects of asenapine by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- aspirin
aspirin and diclofenac both increase anticoagulation. Use Caution/Monitor.
aspirin and diclofenac both increase serum potassium. Use Caution/Monitor. - aspirin rectal
aspirin rectal and diclofenac both increase anticoagulation. Use Caution/Monitor.
aspirin rectal and diclofenac both increase serum potassium. Use Caution/Monitor. - aspirin/citric acid/sodium bicarbonate
aspirin/citric acid/sodium bicarbonate and diclofenac both increase anticoagulation. Use Caution/Monitor.
aspirin/citric acid/sodium bicarbonate and diclofenac both increase serum potassium. Use Caution/Monitor. - atazanavir
atazanavir increases levels of diclofenac by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Use Caution/Monitor. Potential for increased toxicity. .
- atenolol
atenolol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of atenolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - atogepant
diclofenac will increase the level or effect of atogepant by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Use Caution/Monitor.
- avapritinib
diclofenac will increase the level or effect of avapritinib by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Use Caution/Monitor.
- axitinib
diclofenac increases levels of axitinib by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Use Caution/Monitor.
- azficel-T
azficel-T, diclofenac. 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
diclofenac, 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.
diclofenac 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.
azilsartan decreases effects of diclofenac 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 diclofenac both increase anticoagulation. Modify Therapy/Monitor Closely.
- benazepril
benazepril, diclofenac. 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
diclofenac increases and bendroflumethiazide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- betaxolol
betaxolol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of betaxolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - betrixaban
diclofenac, betrixaban. Either increases levels of the other by anticoagulation. Use Caution/Monitor.
- bimatoprost
bimatoprost, diclofenac. 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 diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of bisoprolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - bivalirudin
bivalirudin and diclofenac both increase anticoagulation. Modify Therapy/Monitor Closely.
- budesonide
diclofenac, budesonide. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- bumetanide
diclofenac increases and bumetanide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
diclofenac decreases effects of bumetanide by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis. - candesartan
candesartan and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac 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, diclofenac. 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. - cannabidiol
cannabidiol will increase the level or effect of diclofenac by decreasing metabolism. Modify Therapy/Monitor Closely. Cannabidiol may potentially inhibit CYP2C9 activity. Consider reducing the dose when concomitantly using CYP2C9 substrates.
- capecitabine
capecitabine will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Do not exceed diclofenac dose of 50 mg BID
- captopril
captopril, diclofenac. 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
diclofenac increases and carbenoxolone decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- carvedilol
carvedilol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of carvedilol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - celecoxib
celecoxib and diclofenac both increase anticoagulation. Use Caution/Monitor.
celecoxib and diclofenac both increase serum potassium. Use Caution/Monitor. - celiprolol
celiprolol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of celiprolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - chlorothiazide
diclofenac increases and chlorothiazide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- chlorpropamide
diclofenac increases effects of chlorpropamide by unknown mechanism. Use Caution/Monitor. Risk of hypoglycemia.
- chlorthalidone
diclofenac increases and chlorthalidone decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- cholestyramine
cholestyramine decreases levels of diclofenac by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor.
- choline magnesium trisalicylate
diclofenac and choline magnesium trisalicylate both increase anticoagulation. Use Caution/Monitor.
diclofenac and choline magnesium trisalicylate both increase serum potassium. Use Caution/Monitor. - cinnamon
diclofenac and cinnamon both increase anticoagulation. Use Caution/Monitor.
- ciprofloxacin
diclofenac, 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, diclofenac. 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, diclofenac. 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, diclofenac. Either increases effects of the other by pharmacodynamic synergism. Modify Therapy/Monitor Closely. Clopidogrel and NSAIDs both inhibit platelet aggregation.
- cordyceps
diclofenac and cordyceps both increase anticoagulation. Use Caution/Monitor.
- cortisone
diclofenac, cortisone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- cyclopenthiazide
diclofenac increases and cyclopenthiazide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- cyclosporine
diclofenac, cyclosporine. Either increases toxicity of the other by nephrotoxicity and/or ototoxicity. Modify Therapy/Monitor Closely. Potential for dangerous interaction. Use with caution and monitor closely.
- dabigatran
dabigatran and diclofenac 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 diclofenac both increase anticoagulation. Modify Therapy/Monitor Closely.
- deferasirox
deferasirox, diclofenac. Other (see comment). Use Caution/Monitor. Comment: Combination may increase GI bleeding, ulceration and irritation. Use with caution.
- deferiprone
diclofenac will increase the level or effect of deferiprone by decreasing metabolism. Use Caution/Monitor. Coadministration with UGT1A6 inhibitors may increase serum concentration of deferiprone.
- defibrotide
defibrotide increases effects of diclofenac by P-glycoprotein (MDR1) efflux transporter. Use Caution/Monitor. Defibrotide may enhance effects of platelet inhibitors.
- deflazacort
diclofenac, deflazacort. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- dexamethasone
diclofenac, dexamethasone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- diflunisal
diclofenac and diflunisal both increase anticoagulation. Use Caution/Monitor.
diclofenac and diflunisal both increase serum potassium. Use Caution/Monitor. - digoxin
diclofenac and digoxin both increase serum potassium. Use Caution/Monitor.
- dobutamine
diclofenac increases and dobutamine decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- dong quai
diclofenac and dong quai both increase anticoagulation. Use Caution/Monitor.
- dopexamine
diclofenac increases and dopexamine decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- doxazosin
diclofenac decreases effects of doxazosin by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- drospirenone
drospirenone and diclofenac both increase serum potassium. Modify Therapy/Monitor Closely.
- duloxetine
duloxetine, diclofenac. 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, diclofenac. 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.
- efavirenz
efavirenz will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor.
- eltrombopag
eltrombopag increases levels of diclofenac by decreasing metabolism. Use Caution/Monitor. UGT inhibition; significance of interaction unclear.
- elvitegravir/cobicistat/emtricitabine/tenofovir DF
elvitegravir/cobicistat/emtricitabine/tenofovir DF decreases levels of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Elvitegravir is a moderate CYP2C9 inducer.
elvitegravir/cobicistat/emtricitabine/tenofovir DF, diclofenac. 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, diclofenac. 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, diclofenac. 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 diclofenac both increase anticoagulation. Modify Therapy/Monitor Closely.
- ephedrine
diclofenac increases and ephedrine decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- epinephrine
diclofenac increases and epinephrine decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- epinephrine racemic
diclofenac increases and epinephrine racemic decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- epoprostenol
diclofenac and epoprostenol both increase anticoagulation. Use Caution/Monitor.
- eprosartan
eprosartan and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac 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, diclofenac. 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, diclofenac. 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 diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of esmolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - ethacrynic acid
diclofenac increases and ethacrynic acid decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- etodolac
diclofenac and etodolac both increase anticoagulation. Use Caution/Monitor.
diclofenac and etodolac both increase serum potassium. Use Caution/Monitor. - fenbufen
diclofenac and fenbufen both increase anticoagulation. Use Caution/Monitor.
diclofenac and fenbufen both increase serum potassium. Use Caution/Monitor. - fennel
diclofenac and fennel both increase anticoagulation. Use Caution/Monitor.
- fenoprofen
diclofenac and fenoprofen both increase anticoagulation. Use Caution/Monitor.
diclofenac and fenoprofen both increase serum potassium. Use Caution/Monitor. - feverfew
diclofenac and feverfew both increase anticoagulation. Use Caution/Monitor.
- finerenone
diclofenac will increase the level or effect of finerenone by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Modify Therapy/Monitor Closely. Monitor serum potassium during initiation and dosage adjustment of either finererone or weak CYP3A4 inhibitors. Adjust finererone dosage as needed.
- fish oil triglycerides
fish oil triglycerides will increase the level or effect of diclofenac 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.
- flibanserin
diclofenac will increase the level or effect of flibanserin by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Use Caution/Monitor. Increased flibanserin adverse effects may occur if coadministered with multiple weak CYP3A4 inhibitors.
- fluconazole
fluconazole will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Do not exceed diclofenac dose of 50 mg BID
- fludrocortisone
diclofenac, fludrocortisone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- fluorouracil
fluorouracil will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Do not exceed diclofenac dose of 50 mg BID
- fluoxetine
fluoxetine will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor.
fluoxetine, diclofenac. 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
diclofenac and flurbiprofen both increase anticoagulation. Use Caution/Monitor.
diclofenac and flurbiprofen both increase serum potassium. Use Caution/Monitor. - fluvoxamine
fluvoxamine, diclofenac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. SSRIs inhib. serotonin uptake by platelets.
- fondaparinux
fondaparinux and diclofenac both increase anticoagulation. Modify Therapy/Monitor Closely.
- formoterol
diclofenac increases and formoterol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- forskolin
diclofenac and forskolin both increase anticoagulation. Use Caution/Monitor.
- fosinopril
fosinopril, diclofenac. 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
diclofenac increases and furosemide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- garlic
diclofenac and garlic both increase anticoagulation. Use Caution/Monitor.
- gemfibrozil
gemfibrozil will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Do not exceed diclofenac dose of 50 mg BID
- gemifloxacin
gemifloxacin, diclofenac. Other (see comment). Modify Therapy/Monitor Closely. Comment: Increased risk of CNS stimulation and seizures with high doses of fluoroquinolones.
- gentamicin
diclofenac increases and gentamicin decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- ginger
diclofenac and ginger both increase anticoagulation. Use Caution/Monitor.
- ginkgo biloba
diclofenac and ginkgo biloba both increase anticoagulation. Use Caution/Monitor.
- glimepiride
diclofenac increases effects of glimepiride by unknown mechanism. Use Caution/Monitor. Risk of hypoglycemia.
- glipizide
diclofenac increases effects of glipizide by unknown mechanism. Use Caution/Monitor. Risk of hypoglycemia.
- glyburide
diclofenac increases effects of glyburide by unknown mechanism. Use Caution/Monitor. Risk of hypoglycemia.
- green tea
green tea, diclofenac. Other (see comment). Use Caution/Monitor. Comment: Combination may increase risk of bleeding.
- heparin
heparin and diclofenac both increase anticoagulation. Modify Therapy/Monitor Closely.
- horse chestnut seed
diclofenac and horse chestnut seed both increase anticoagulation. Use Caution/Monitor.
- hydralazine
diclofenac decreases effects of hydralazine by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- hydrochlorothiazide
diclofenac increases and hydrochlorothiazide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- hydrocortisone
diclofenac, 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 diclofenac 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
diclofenac and ibuprofen both increase anticoagulation. Use Caution/Monitor.
diclofenac and ibuprofen both increase serum potassium. Use Caution/Monitor. - ibuprofen IV
diclofenac will increase the level or effect of ibuprofen IV by acidic (anionic) drug competition for renal tubular clearance. Use Caution/Monitor.
diclofenac and ibuprofen IV both increase anticoagulation. Use Caution/Monitor.
diclofenac and ibuprofen IV both increase serum potassium. Use Caution/Monitor. - imatinib
imatinib will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor.
imatinib, diclofenac. 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
diclofenac increases and indapamide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- indomethacin
diclofenac and indomethacin both increase anticoagulation. Use Caution/Monitor.
diclofenac and indomethacin both increase serum potassium. Use Caution/Monitor. - irbesartan
irbesartan and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac 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, diclofenac. 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. - isavuconazonium sulfate
diclofenac will increase the level or effect of isavuconazonium sulfate by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Use Caution/Monitor.
- isoproterenol
diclofenac increases and isoproterenol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- ivacaftor
diclofenac increases levels of ivacaftor by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Use Caution/Monitor. Monitor when coadministered with weak CYP3A4 inhibitors .
- ketoconazole
ketoconazole will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Do not exceed diclofenac dose of 50 mg BID
- ketoprofen
diclofenac and ketoprofen both increase anticoagulation. Use Caution/Monitor.
diclofenac and ketoprofen both increase serum potassium. Use Caution/Monitor. - ketorolac
diclofenac and ketorolac both increase anticoagulation. Use Caution/Monitor.
diclofenac and ketorolac both increase serum potassium. Use Caution/Monitor. - ketorolac intranasal
diclofenac and ketorolac intranasal both increase anticoagulation. Use Caution/Monitor.
diclofenac and ketorolac intranasal both increase serum potassium. Use Caution/Monitor. - labetalol
labetalol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of labetalol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - latanoprost
latanoprost, diclofenac. 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, diclofenac. 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).
- lemborexant
diclofenac will increase the level or effect of lemborexant by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Modify Therapy/Monitor Closely. Lower nightly dose of lemborexant recommended if coadministered with weak CYP3A4 inhibitors. See drug monograph for specific dosage modification.
- levalbuterol
diclofenac increases and levalbuterol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- levofloxacin
levofloxacin, diclofenac. Other (see comment). Modify Therapy/Monitor Closely. Comment: Risk of CNS stimulation/seizure. Mechanism: Displacement of GABA from receptors in brain.
- levoketoconazole
levoketoconazole will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Do not exceed diclofenac dose of 50 mg BID
- levomilnacipran
levomilnacipran, diclofenac. 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, diclofenac. 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
diclofenac increases levels of lithium by decreasing renal clearance. Use Caution/Monitor.
- lomitapide
diclofenac increases levels of lomitapide by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Use Caution/Monitor. Lomitapide dose should not exceed 30 mg/day.
- lornoxicam
diclofenac and lornoxicam both increase anticoagulation. Use Caution/Monitor.
diclofenac and lornoxicam both increase serum potassium. Use Caution/Monitor. - losartan
losartan and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac 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, diclofenac. 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. - lumacaftor/ivacaftor
lumacaftor/ivacaftor, diclofenac. affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. In vitro studies suggest that lumacaftor may induce and ivacaftor may inhibit CYP2C9 substrates. .
- meclofenamate
diclofenac and meclofenamate both increase anticoagulation. Use Caution/Monitor.
diclofenac and meclofenamate both increase serum potassium. Use Caution/Monitor. - mefenamic acid
diclofenac and mefenamic acid both increase anticoagulation. Use Caution/Monitor.
diclofenac and mefenamic acid both increase serum potassium. Use Caution/Monitor. - melatonin
melatonin increases effects of diclofenac by anticoagulation. Use Caution/Monitor. Melatonin may decrease prothrombin time.
- meloxicam
diclofenac and meloxicam both increase anticoagulation. Use Caution/Monitor.
diclofenac and meloxicam both increase serum potassium. Use Caution/Monitor. - mesalamine
mesalamine, diclofenac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Additive nephrotoxicity.
- metaproterenol
diclofenac increases and metaproterenol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- methyclothiazide
diclofenac increases and methyclothiazide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor. .
- methylprednisolone
diclofenac, methylprednisolone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- metolazone
diclofenac increases and metolazone decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- metoprolol
metoprolol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of metoprolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - midazolam intranasal
diclofenac will increase the level or effect of midazolam intranasal by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Use Caution/Monitor. Coadministration of mild CYP3A4 inhibitors with midazolam intranasal may cause higher midazolam systemic exposure, which may prolong sedation.
- milnacipran
milnacipran, diclofenac. 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, diclofenac. 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
diclofenac increases and mistletoe decreases anticoagulation. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- moexipril
moexipril, diclofenac. 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, diclofenac. Other (see comment). Modify Therapy/Monitor Closely. Comment: Increased risk of CNS stimulation and seizures with high doses of fluoroquinolones.
- moxisylyte
diclofenac decreases effects of moxisylyte by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- mycophenolate
diclofenac will increase the level or effect of mycophenolate by acidic (anionic) drug competition for renal tubular clearance. Use Caution/Monitor.
- nabumetone
diclofenac and nabumetone both increase anticoagulation. Use Caution/Monitor.
diclofenac and nabumetone both increase serum potassium. Use Caution/Monitor. - nadolol
nadolol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of nadolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - naproxen
diclofenac and naproxen both increase anticoagulation. Use Caution/Monitor.
diclofenac and naproxen both increase serum potassium. Use Caution/Monitor. - nebivolol
nebivolol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of nebivolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - nefazodone
nefazodone, diclofenac. 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
diclofenac increases and nettle decreases anticoagulation. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- nicardipine
nicardipine will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Do not exceed diclofenac dose of 50 mg BID
- nitisinone
nitisinone will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Nitisinone inhibits CYP2C9. Caution if CYP2C9 substrate coadministered, particularly those with a narrow therapeutic index.
- norepinephrine
diclofenac increases and norepinephrine decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- olmesartan
olmesartan and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac 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, diclofenac. 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. - oxaprozin
diclofenac and oxaprozin both increase anticoagulation. Use Caution/Monitor.
diclofenac and oxaprozin both increase serum potassium. Use Caution/Monitor. - panax ginseng
diclofenac and panax ginseng both increase anticoagulation. Use Caution/Monitor.
- parecoxib
diclofenac and parecoxib both increase anticoagulation. Use Caution/Monitor.
diclofenac and parecoxib both increase serum potassium. Use Caution/Monitor. - paroxetine
paroxetine, diclofenac. 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
diclofenac and pau d'arco both increase anticoagulation. Use Caution/Monitor.
- pegaspargase
pegaspargase increases effects of diclofenac by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of bleeding events.
- peginterferon alfa 2b
peginterferon alfa 2b decreases levels of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. When patients are administered peginterferon alpha-2b with CYP2C9 substrates, the therapeutic effect of these drugs may be altered. .
- penbutolol
penbutolol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of penbutolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - perindopril
perindopril, diclofenac. 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 diclofenac both increase anticoagulation. Modify Therapy/Monitor Closely.
- phenoxybenzamine
diclofenac decreases effects of phenoxybenzamine by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- phentolamine
diclofenac decreases effects of phentolamine by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- phytoestrogens
diclofenac and phytoestrogens both increase anticoagulation. Use Caution/Monitor.
- pindolol
pindolol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of pindolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - pirbuterol
diclofenac increases and pirbuterol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- piroxicam
diclofenac and piroxicam both increase anticoagulation. Use Caution/Monitor.
diclofenac and piroxicam both increase serum potassium. Use Caution/Monitor. - pivmecillinam
pivmecillinam, diclofenac. Either increases levels of the other by plasma protein binding competition. Use Caution/Monitor.
pivmecillinam, diclofenac. Either increases levels of the other by decreasing renal clearance. Use Caution/Monitor. - potassium acid phosphate
diclofenac and potassium acid phosphate both increase serum potassium. Modify Therapy/Monitor Closely.
- potassium chloride
diclofenac and potassium chloride both increase serum potassium. Modify Therapy/Monitor Closely.
- potassium citrate
diclofenac and potassium citrate both increase serum potassium. Modify Therapy/Monitor Closely.
- potassium iodide
potassium iodide and diclofenac both increase serum potassium. Use Caution/Monitor.
- pralatrexate
diclofenac 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
diclofenac, prasugrel. Either increases effects of the other by anticoagulation. Use Caution/Monitor. Chronic use of NSAIDs with prasugrel may increase bleeding risk.
- prazosin
diclofenac decreases effects of prazosin by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- prednisolone
diclofenac, prednisolone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- prednisone
diclofenac, prednisone. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of GI ulceration.
- probenecid
diclofenac will increase the level or effect of probenecid by acidic (anionic) drug competition for renal tubular clearance. Use Caution/Monitor.
- propranolol
propranolol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of propranolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - protamine
protamine and diclofenac both increase anticoagulation. Modify Therapy/Monitor Closely.
- quinapril
quinapril, diclofenac. 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, diclofenac. 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
diclofenac and reishi both increase anticoagulation. Use Caution/Monitor.
- reteplase
diclofenac and reteplase both increase anticoagulation. Use Caution/Monitor. Potential for increased risk of bleeding, caution is advised.
- rivaroxaban
rivaroxaban, diclofenac. 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 diclofenac by pharmacodynamic synergism. Use Caution/Monitor. Monitor patients for symptoms of active or occult gastrointestinal bleeding.
- rucaparib
rucaparib will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Modify Therapy/Monitor Closely. Adjust dosage of CYP2C9 substrates, if clinically indicated.
- sacubitril/valsartan
sacubitril/valsartan and diclofenac both increase serum potassium. Use Caution/Monitor.
sacubitril/valsartan, diclofenac. 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.
diclofenac 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)
diclofenac and salicylates (non-asa) both increase anticoagulation. Use Caution/Monitor.
diclofenac and salicylates (non-asa) both increase serum potassium. Use Caution/Monitor. - salmeterol
diclofenac increases and salmeterol decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- salsalate
diclofenac and salsalate both increase anticoagulation. Use Caution/Monitor.
diclofenac and salsalate both increase serum potassium. Use Caution/Monitor. - saw palmetto
saw palmetto increases toxicity of diclofenac by unspecified interaction mechanism. Use Caution/Monitor. May increase risk of bleeding.
- sertraline
sertraline, diclofenac. 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
diclofenac and Siberian ginseng both increase anticoagulation. Use Caution/Monitor.
- silodosin
diclofenac decreases effects of silodosin by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- sodium picosulfate/magnesium oxide/anhydrous citric acid
diclofenac, 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 diclofenac 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 diclofenac 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
diclofenac, 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 diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of sotalol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - sparsentan
diclofenac 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.
sparsentan will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Sparsentan (a CYP2C9 inducer) decreases exposure of CYP2C9 substrates and reduces efficacy related to these substrates. - spironolactone
spironolactone and diclofenac both increase serum potassium. Modify Therapy/Monitor Closely.
- succinylcholine
diclofenac and succinylcholine both increase serum potassium. Use Caution/Monitor.
- sulfadiazine
sulfadiazine will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Do not exceed diclofenac dose of 50 mg BID
- sulfasalazine
diclofenac and sulfasalazine both increase anticoagulation. Use Caution/Monitor.
diclofenac and sulfasalazine both increase serum potassium. Use Caution/Monitor. - sulindac
diclofenac and sulindac both increase anticoagulation. Use Caution/Monitor.
diclofenac and sulindac both increase serum potassium. Use Caution/Monitor. - tafluprost
tafluprost, diclofenac. 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).
- tazemetostat
diclofenac will increase the level or effect of tazemetostat by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Use Caution/Monitor.
- telmisartan
telmisartan and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac 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, diclofenac. 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, diclofenac. Either increases levels of the other by plasma protein binding competition. Use Caution/Monitor.
temocillin, diclofenac. Either increases levels of the other by decreasing renal clearance. Use Caution/Monitor. - tenecteplase
diclofenac and tenecteplase both increase anticoagulation. Use Caution/Monitor. Potential for increased risk of bleeding, caution is advised.
- tenofovir DF
tenofovir DF, diclofenac. 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
diclofenac decreases effects of terazosin by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
- terbutaline
diclofenac increases and terbutaline decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- teriflunomide
teriflunomide increases levels of diclofenac by Other (see comment). Use Caution/Monitor. Comment: Teriflunomide inhibits CYP2C8; caution when coadministered with CYP2C8 substrates.
- ticagrelor
ticagrelor, diclofenac. 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, diclofenac. Either increases levels of the other by plasma protein binding competition. Use Caution/Monitor.
ticarcillin, diclofenac. Either increases levels of the other by decreasing renal clearance. Use Caution/Monitor. - timolol
timolol and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac decreases effects of timolol by pharmacodynamic antagonism. Use Caution/Monitor. Long term (>1 wk) NSAID use. NSAIDs decrease prostaglandin synthesis. - tinidazole
diclofenac will increase the level or effect of tinidazole by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Use Caution/Monitor.
- tolazamide
diclofenac increases effects of tolazamide by unknown mechanism. Use Caution/Monitor. Risk of hypoglycemia.
- tolbutamide
diclofenac increases effects of tolbutamide by unknown mechanism. Use Caution/Monitor. Risk of hypoglycemia.
tolbutamide will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Do not exceed diclofenac dose of 50 mg BID - tolfenamic acid
diclofenac and tolfenamic acid both increase anticoagulation. Use Caution/Monitor.
diclofenac and tolfenamic acid both increase serum potassium. Use Caution/Monitor. - tolmetin
diclofenac and tolmetin both increase anticoagulation. Use Caution/Monitor.
diclofenac and tolmetin both increase serum potassium. Use Caution/Monitor. - tolvaptan
diclofenac and tolvaptan both increase serum potassium. Use Caution/Monitor.
- torsemide
diclofenac increases and torsemide decreases serum potassium. Effect of interaction is not clear, use caution. Use Caution/Monitor.
- trandolapril
trandolapril, diclofenac. 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, diclofenac. 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, diclofenac. 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
diclofenac, 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 diclofenac both increase serum potassium. Modify Therapy/Monitor Closely.
- valsartan
valsartan and diclofenac both increase serum potassium. Use Caution/Monitor.
diclofenac 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, diclofenac. 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, diclofenac. Either increases toxicity of the other by pharmacodynamic synergism. Use Caution/Monitor. Increased risk of upper GI bleeding. SSRIs inhib. serotonin uptake by platelets.
- voclosporin
voclosporin, diclofenac. 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
diclofenac, vorapaxar. Either increases effects of the other by pharmacodynamic synergism. Use Caution/Monitor. Additive antiplatelet effect may occur.
- voriconazole
voriconazole will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Use Caution/Monitor. Do not exceed diclofenac dose of 50 mg BID
- vortioxetine
diclofenac, vortioxetine. Either increases effects of the other by anticoagulation. Use Caution/Monitor.
- warfarin
diclofenac, 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
diclofenac, 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
diclofenac decreases effects of zotepine by pharmacodynamic antagonism. Use Caution/Monitor. NSAIDs decrease prostaglandin synthesis.
Minor (101)
- aceclofenac
aceclofenac will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- acemetacin
acemetacin will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- acyclovir
diclofenac will increase the level or effect of acyclovir by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- alendronate
diclofenac, alendronate. Either increases toxicity of the other by pharmacodynamic synergism. Minor/Significance Unknown. Increased risk of GI ulceration.
- amikacin
diclofenac increases levels of amikacin by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in preterm infants.
- aminohippurate sodium
diclofenac will increase the level or effect of aminohippurate sodium by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- amiodarone
amiodarone will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- amobarbital
amobarbital will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- anamu
diclofenac and anamu both increase anticoagulation. Minor/Significance Unknown.
- aspirin
aspirin will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- aspirin rectal
aspirin rectal will increase the level or effect of diclofenac 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 diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- balsalazide
diclofenac 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 diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- bosentan
bosentan will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- butabarbital
butabarbital will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- butalbital
butalbital will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- carbamazepine
carbamazepine will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- cefadroxil
cefadroxil will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- cefamandole
cefamandole will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- cefpirome
cefpirome will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- celecoxib
celecoxib will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- cephalexin
cephalexin will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- chlorothiazide
chlorothiazide will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- chlorpropamide
diclofenac 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 diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- choline magnesium trisalicylate
diclofenac will increase the level or effect of choline magnesium trisalicylate by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- cimetidine
cimetidine will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- colestipol
colestipol decreases levels of diclofenac by inhibition of GI absorption. Applies only to oral form of both agents. Minor/Significance Unknown.
- creatine
creatine, diclofenac. Mechanism: pharmacodynamic synergism. Minor/Significance Unknown. (Theoretical interaction) Combination may have additive nephrotoxic effects.
- cyclopenthiazide
cyclopenthiazide will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- danshen
diclofenac and danshen both increase anticoagulation. Minor/Significance Unknown.
- devil's claw
diclofenac and devil's claw both increase anticoagulation. Minor/Significance Unknown.
- diclofenac topical
diclofenac topical, diclofenac. 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
diclofenac will increase the level or effect of diflunisal by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- disulfiram
disulfiram will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- eplerenone
diclofenac decreases effects of eplerenone by pharmacodynamic antagonism. Minor/Significance Unknown. NSAIDs decrease prostaglandin synthesis.
- etodolac
diclofenac will increase the level or effect of etodolac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- etravirine
etravirine will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- felbamate
felbamate will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- fenbufen
diclofenac will increase the level or effect of fenbufen by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- fenoprofen
diclofenac will increase the level or effect of fenoprofen by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- feverfew
diclofenac decreases effects of feverfew by pharmacodynamic antagonism. Minor/Significance Unknown.
- flurbiprofen
diclofenac will increase the level or effect of flurbiprofen by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- furosemide
diclofenac decreases effects of furosemide by pharmacodynamic antagonism. Minor/Significance Unknown. NSAIDs decrease prostaglandin synthesis.
- ganciclovir
diclofenac will increase the level or effect of ganciclovir by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- gentamicin
diclofenac 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 diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- ibuprofen
diclofenac will increase the level or effect of ibuprofen by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- imidapril
diclofenac decreases effects of imidapril by pharmacodynamic antagonism. Minor/Significance Unknown. NSAIDs decrease prostaglandin synthesis.
- indapamide
indapamide will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- indomethacin
diclofenac will increase the level or effect of indomethacin by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- ketoprofen
diclofenac will increase the level or effect of ketoprofen by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- ketorolac
diclofenac will increase the level or effect of ketorolac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- ketorolac intranasal
diclofenac will increase the level or effect of ketorolac intranasal by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- leflunomide
leflunomide will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- lornoxicam
diclofenac will increase the level or effect of lornoxicam by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- meclofenamate
diclofenac will increase the level or effect of meclofenamate by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- mefenamic acid
diclofenac will increase the level or effect of mefenamic acid by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- meloxicam
diclofenac will increase the level or effect of meloxicam by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- mesalamine
diclofenac 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 diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- metolazone
metolazone will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- metronidazole
metronidazole will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- miconazole vaginal
miconazole vaginal will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- nabumetone
diclofenac will increase the level or effect of nabumetone by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- naproxen
diclofenac will increase the level or effect of naproxen by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- nateglinide
nateglinide will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- neomycin PO
diclofenac increases levels of neomycin PO by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in preterm infants.
- nilotinib
nilotinib will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- noni juice
diclofenac and noni juice both increase serum potassium. Minor/Significance Unknown.
- ofloxacin
ofloxacin, diclofenac. Other (see comment). Minor/Significance Unknown. Comment: Risk of CNS stimulation/seizure. Mechanism: Displacement of GABA from receptors in brain.
- oxaprozin
diclofenac will increase the level or effect of oxaprozin by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- parecoxib
diclofenac will increase the level or effect of parecoxib by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- paromomycin
diclofenac increases levels of paromomycin by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in preterm infants.
- pentobarbital
pentobarbital will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- phenobarbital
phenobarbital will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- piroxicam
diclofenac will increase the level or effect of piroxicam by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- primidone
primidone will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- rifampin
rifampin will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- rifapentine
rifapentine will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- rose hips
rose hips will increase the level or effect of diclofenac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- ruxolitinib
diclofenac will increase the level or effect of ruxolitinib by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Minor/Significance Unknown.
- ruxolitinib topical
diclofenac will increase the level or effect of ruxolitinib topical by affecting hepatic/intestinal enzyme CYP3A4 metabolism. Minor/Significance Unknown.
- salicylates (non-asa)
diclofenac will increase the level or effect of salicylates (non-asa) by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- salsalate
diclofenac will increase the level or effect of salsalate by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- secobarbital
secobarbital will decrease the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- streptomycin
diclofenac increases levels of streptomycin by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in preterm infants.
- sulfamethoxazole
sulfamethoxazole will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- sulfasalazine
diclofenac will increase the level or effect of sulfasalazine by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- sulindac
diclofenac will increase the level or effect of sulindac by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- ticlopidine
ticlopidine will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- tobramycin
diclofenac increases levels of tobramycin by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in preterm infants.
- tolfenamic acid
diclofenac will increase the level or effect of tolfenamic acid by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- tolmetin
diclofenac will increase the level or effect of tolmetin by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- triamterene
triamterene, diclofenac. Other (see comment). Minor/Significance Unknown. Comment: Risk of acute renal failure. Mechanism: NSAIDs decrease prostaglandin synthesis, which normally protect against nephrotoxicity.
diclofenac increases toxicity of triamterene by pharmacodynamic antagonism. Minor/Significance Unknown. NSAIDs decrease prostaglandin synthesis, increasing the risk of nephrotoxicity. - valganciclovir
diclofenac will increase the level or effect of valganciclovir by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- valproic acid
valproic acid will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
- vancomycin
diclofenac increases levels of vancomycin by decreasing renal clearance. Minor/Significance Unknown. Interaction mainly occurs in neonates.
- willow bark
diclofenac will increase the level or effect of willow bark by acidic (anionic) drug competition for renal tubular clearance. Minor/Significance Unknown.
- zafirlukast
zafirlukast will increase the level or effect of diclofenac by affecting hepatic enzyme CYP2C9/10 metabolism. Minor/Significance Unknown.
Adverse Effects
>10%
Rash including erythematous, rash macular and maculo-papular (18%)
Pyrexia (15%)
Urticaria (13%)
Flushing (13%)
1-10%
Hypertension (10%)
Hyperhydrosis (8%)
Decreased oxygen saturation (8%)
Cough (8%)
Tachypnea (8%)
Tachycardia (8%)
Urticaria (8%)
Anaphylaxis (7%
Chest discomfort (7%)
Muscle twitching (7%)
Erythema (5%)
Vomiting (5%)
Rigors (5%)
Pallor (5%)
Cyanosis (5%)
Agitation (5%)
Tremor (5%)
Myalgia (5%)
Flushing (5%)
Peripheral edema (3%)
Pruritus (3%)
Rash, papular (3%)
Throat tightness (3%)
<1%
Fatigue
Malaise
Chills
Edema
Atrial fibrillation
Congestive heart failure
Myocardial infarction
Phlebitis
Vasculitis
Syncope
Dysphagia
Enteritis
Peptic ulcer
Vaginitis
Breast pain
Dysmenorrhea
Uterine cramping
Ulcerative stomatitis
Impotence
Perineal pain
Glycosuria
Alopecia
Postmarketing reports
Increased alanine aminotransferase
Increased alkaline phosphatase
Increased aspartate aminotransferase
Increased BUN
Dehydration
Glycosuria
Gout
Hypercholesterolemia
Hyperglycemia
Hyperuricemia
Hypoglycemia
Hyponatremia
Periorbital edema porphyria
Weight changes
Fluid retention
Body as a whole: Death, fever, infection, sepsis
Cardiovascular system: Arrhythmia, hypotension, increased creatinine phosphokinase, increased lactate dehydrogenase, palpitations, premature ventricular contractions, syncope
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 and patients with a prior history of peptic ulcer disease and/or GI bleeding are at greater risk for serious GI events
Women with childbearing potential
- Patient should be advised to use effective contraception during treatment
- Advise patient or abortificient property and warn not to give to others; not for women of childbearing potential unless patient requires nonsteroidal anti-inflammatory drug (NSAID) therapy and is at high risk of developing gastric or duodenal ulceration or complications from gastric or duodenal ulcers associated with NSAID use
- Administration to women who are pregnant can cause abortion, premature birth, birth defects, or uttering rupture
- Uterine rupture reported when misoprostol was administered in pregnant women to induce labor or abortion
- Risk of uterine rupture increases with advancing gestational ages and with prior uttering surgery, including cesarean delivery; drug should not be administered to women who are pregnant
- Prescribe to patients of childbearing potential only if the following conditions are met:
- Has had a negative serum pregnancy test within 2 wk prior to beginning therapy
- Is capable of complying with effective contraceptive measures
- Has received both oral and written warnings of hazards of misoprostol, the risk of possible contraception failure, and danger to other women of childbearing potential should the drug be taken by mistake
- Will begin diclofenac only on second or third day of the next normal menstrual period
Contraindications
Hypersensitivity drugs or related products
Perioperative pain in the setting of coronary artery bypass graft (CABG) surgery; active gastrointestinal bleeding
Patients who have experienced asthma, urticaria, or other allergic-type reactions after taking aspirin or other NSAIDs
Pregnancy
Cautions
Caution in women of childbearing potential (see mfr's package insert for restrictions)
NSAIDs increase risk of premature closure of the fetal ductus arteriosus at about 30 weeks of gestation and later
Avoid pregnancy during & for at least 1 month after treatment
Avoid use of this drug in patients with a recent MI unless benefits are expected to outweigh risk of recurrent CV thrombotic events; if this drug is used in patients with recent MI, monitor patients for signs of cardiac ischemia
May cause blurred vision, drowsiness, dizziness
May increase risk of aseptic meningitis especially in patients with mixed connective tissue disorders and systemic lupus erythematous
Severe bronchospasm may occur in patients with asthma
Use caution in hepatic impairment, porphyria (avoid if possible), or hypertension
Avoid use of diclofenac/misoprostol with concomitant NSAIDs including COX inhibitors
Use lowest effective dose in patients with known cardiovascular (CV) disease or risk factors for CV
Concurrent use of aspirin with NSAIDs in mitigating CV thrombotic events not shown conclusively; increased risk of serious GI adverse reactions likely
Serious gastrointestinal adverse events including inflammation, bleeding, ulceration, and perforation of stomach, small intestine, or large intestine, which can be fatal may occur
Toxic epidermal necrolysis, reported with NSAID use, especially within first month of therapy; discontinue use at first appearance of skin rash
Use of NSAIDs may diminish ability to diagnose conditions associated with pain or inflammation
Use caution in patients with coagulation disorders or receiving anticoagulants; NSAIDs inhibit platelet aggregation
Therapy has been associated with anaphylactic reactions in patients with and without known hypersensitivity to the individual components of diclofenac sodium and misoprostol and in patients with aspirin-sensitive asthma
NSAIDs can cause serious skin adverse reactions such as exfoliative dermatitis, Stevens-Johnson Syndrome (SJS), and toxic epidermal necrolysis (TEN), which can be fatal; these serious events may occur without warning; inform patients about the signs and symptoms of serious skin reactions, and to discontinue the use of this drug at the first appearance of skin rash or any other sign of hypersensitivity; this medication is contraindicated in patients with previous serious skin reactions to NSAIDs
Because serious GI bleeding, hepatotoxicity and renal injury can occur without warning symptoms or signs, consider monitoring patients on long-term NSAID treatment with a complete blood count (CBC) and a chemistry profile periodically
Heart failure
- Fluid retention and edema may occur with therapy; use with caution in patients with heart failure
- In patients with heart failure, NSAID use have increased risk of MI, hospitalization for heart failure, and death; treat these medical conditions (eg, diuretics, ACE inhibitors, or angiotensin receptor blockers [ARBs])
- Avoid use in patients with severe heart failure unless the benefits are expected to outweigh risk of worsening heart failure; if this drug is used in patients with severe heart failure, monitor patients for signs of worsening heart failure
Hypertension
- Use caution in patients with hypertension
- NSAIDs, can lead to new onset of hypertension or worsening of pre-existing hypertension, either of which may contribute to increased incidence of CV events
- Patients taking angiotensin-converting enzyme (ACE) inhibitors, thiazide diuretics, or loop diuretics may have impaired response to these therapies when taking NSAIDs
- Monitor blood pressure (BP) during initiation of NSAID treatment and throughout course of therapy
Cardiovascular thrombotic events
- Patients with known CV disease or risk factors may have higher absolute incidence of excess serious CV thrombotic events, due to their increased baseline rate; some observational studies have found that the increased risk of serious CV thrombotic events may begin as early as first weeks of treatment; increase in CV thrombotic risk has been observed most consistently at higher doses
- To minimize potential risk for adverse CV event in NSAID-treated patients, use lowest effective dose for shortest duration possible; physicians and patients should remain alert for development of such events, throughout entire treatment course, even in absence of previous CV symptoms; patients should be informed about symptoms of serious CV events and the steps to take if they occur
Exacerbation of asthma-related aspirin sensitivity
- A subpopulation of patients with asthma may have aspirin-sensitive asthma which may include chronic rhinosinusitis complicated by nasal polyps; severe, potentially fatal bronchospasm; and/or intolerance to aspirin and other NSAIDs
- Because cross-reactivity between aspirin and other NSAIDs has been reported in such aspirin-sensitive patients, this therapy is contraindicated in patients with this form of aspirin sensitivity
- When this medication is used in patients with preexisting asthma (without known aspirin sensitivity), monitor patients for changes in the signs and symptoms of asthma
Hematologic toxicity
- Anemia has occurred in NSAID-treated patients; this may be due to occult or gross bloodloss, fluid retention, or an incompletely described effect on erythropoiesis; if a patient treated with this drug has any signs or symptoms of anemia, monitor hemoglobin or hematocrit
- NSAIDs may increase the risk of bleeding events; co-morbid conditions such as coagulation disorders or concomitant use of warfarin and other anticoagulants, antiplatelet drugs (eg, aspirin), and SSRIs and serotonin-norepinephrine reuptake inhibitors (SNRIs) may increase this risk; monitor these patients for signs of bleeding
Geriatric use
- Geriatric patients (those 65 years of age and older), compared to younger adult patients, are at greater risk for NSAID-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions; the risk of diclofenac-associated adverse reactions may be greater in geriatric patients with renal impairment or those taking concomitant ACE inhibitors or ARBs
- Avoid use in geriatric patients with cardiovascular and/or renal risk factors; if use cannot be avoided, use lowest recommended dosage for shortest duration and monitor for cardiac and renal adverse reactions
- Monitor renal function in geriatric patients during treatment, especially in patients with concomitant use of ACE inhibitors or ARBs
- No clinically meaningful differences in the pharmacokinetics of diclofenac and misoprostol were observed in geriatric patients compared to younger adult patients
Renal toxicity and hyperkalemia
- 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 an NSAID 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, dehydration, hypovolemia, heart failure, liver dysfunction, those taking diuretics and ACE inhibitors or ARBs, and the elderly; discontinuation of NSAID therapy is usually followed by recovery to pretreatment state
- No information available from controlled clinical studies regarding use of this drug in patients with advanced renal disease; the renal effects of this medication may hasten the progression of renal dysfunction in patients with pre-existing renal disease
- Correct volume status in dehydrated or hypovolemic patients prior to initiating therapy; monitor renal function in patients with renal or hepatic impairment, heart failure, dehydration, or hypovolemia during use of this drug
- Avoid use in patients with advanced renal disease unless benefits are expected to outweigh risk of worsening renal function; if this drug is used in patients with advanced renal disease, monitor patients for signs of worsening renal function
- Increases in serum potassium concentration, including hyperkalemia, reported, with use of NSAIDs, even in some patients without renal impairment; in patients with normal renal function, these effects have been attributed to a hyporeninemic-hypoaldosteronism state
- Avoid use of this medication in patients with advanced renal disease; if use cannot be avoided in patients with advanced renal disease, use lowest dosage for shortest duration, monitor patient’s renal function, and monitor for clinical signs of worsening renal function
Oligohydramnios/neonatal renal impairment
- Use of NSAIDs, including diclofenac, at about 20 weeks gestation or later in pregnancy may cause fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment; these adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after NSAID initiation
- Oligohydramnios is often, but not always, reversible with treatment discontinuation; complications of prolonged oligohydramnios may, for example, include limb contractures and delayed lung maturation; in some postmarketing cases of impaired neonatal renal function, invasive procedures such as exchange transfusion or dialysis were required
GI bleeding
- Serious gastrointestinal adverse events including inflammation, bleeding, ulceration, and perforation of stomach, small intestine, or large intestine, which can be fatal may occur
- Patients with a prior history of peptic ulcer disease and/or GI bleeding who used NSAIDs had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors
- Other factors that increase risk of GI bleeding in patients treated with NSAIDs include longer duration of NSAID therapy; concomitant use of oral corticosteroids, antiplatelet drugs (such as aspirin), anticoagulants, or selective serotonin reuptake inhibitors (SSRIs); smoking; use of alcohol; older age; and poor general health status; most postmarketing reports of fatal GI events occurred in elderly or debilitated patients; additionally, patients with advanced liver disease and/or coagulopathy are at increased risk for GI bleeding
- Upper GI ulcers, gross bleeding, or perforation caused by NSAIDs may occur in 1% patients treated for 3-6 months, and in about 2-4% of patients treated for one year; however, even short-term NSAID therapy is not without risk
-
Strategies to minimize GI risks in NSAID-treated patients
- Use lowest effective dosage for shortest possible duration
- Avoid administration of more than one NSAID at a time
- Remain alert for signs and symptoms of GI ulceration and bleeding during NSAID therapy
- If a serious GI adverse event is suspected, promptly initiate evaluation and treatment, and discontinue therapy until a serious GI adverse event is ruled out
- In the setting of concomitant use of low-dose aspirin for cardiac prophylaxis, monitor patients more closely for evidence of GI bleeding
Hepatotoxicity
- Meaningful elevations (ie, more than 3 times the ULN) of alanine aminotransferase (ALT) (serum glutamic pyruvic transaminase [SGPT], aspartate aminotransferase (AST) (serum glutamic-oxaloacetic transaminase [SGOT]) reported; these increases were generally transient, and enzyme levels returned to within the normal range upon discontinuation of therapy misoprostol component does not appear to exacerbate hepatic effects caused by diclofenac sodium component
- Elevations of ALT or AST reported in patients receiving diclofenac when compared to other NSAIDs; elevations in transaminases were seen more frequently in patients with osteoarthritis than in those with rheumatoid arthritis
- Almost all meaningful elevations in transaminases have been detected before patients became symptomatic; in postmarketing reports, cases of drug-induced hepatotoxicity have been reported in first month, and in some cases, first 2 months of therapy, but can occur at any time during treatment with diclofenac
- Postmarketing surveillance has reported cases of severe hepatic reactions, including liver necrosis, jaundice, fulminant hepatitis with and without jaundice, and liver failure; some of these reported cases resulted in fatalities or liver transplantation
- Physicians should measure transaminases at baseline and periodically in patients receiving long-term therapy with diclofenac, because severe hepatotoxicity may develop without a prodrome of distinguishing symptoms
- Optimum times for making first and subsequent transaminase measurements are not known; based on clinical trial data and postmarketing experiences, transaminases should be monitored within 4-8 weeks after initiating treatment with diclofenac; however, severe hepatic reactions can occur at any time during treatment with diclofenac
- If abnormal liver tests persist or worsen, if clinical signs and/or symptoms consistent with liver disease develop, or if systemic manifestations occur (eg, eosinophilia, rash, abdominal pain, diarrhea, dark urine, etc), therapy should be discontinued immediately
- To minimize potential risk for adverse liver related event in patients treated with this drug, the lowest effective dose should be used for shortest duration possible
- Exercise caution when prescribing this drug with concomitant drugs that are known to be potentially hepatotoxic (eg, antibiotics, anti-epileptics)
Drug reaction with eosinophilia and systemic symptoms (DRESS)
- Drug Reaction reported in patients taking NSAIDs; 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
Pregnancy & Lactation
Pregnancy
Not recommended in women of childbearing potential; if prescribed, patient must be advised of abortifacient property and warned not to give drug to others; advise females to inform their healthcare provider of a known or suspected pregnancy
Drug combination is contraindicated in pregnant women; there are no adequate and well-controlled studies in pregnant women; however, there is information available about the active drug components diclofenac sodium and misoprostol
Administration of misoprostol to pregnant women can cause abortion, premature birth, birth defects or uterine rupture; congenital anomalies sometimes associated with fetal death have been reported subsequent to unsuccessful use of misoprostol as an abortifacient, but the drug’s teratogenic mechanism has not been demonstrated
Use of NSAIDS, including diclofenac can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment
There are clinical considerations when misoprostol and diclofenac are used in pregnant women In reproduction studies with pregnant rabbits, there were no skeletal or visceral malformations when the combination of diclofenac sodium and misoprostol was administered during organogenesis at doses less than the maximum recommended human doses (MRHD); however, embryotoxicity was observed at this exposure
Based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization
In animal studies, administration of prostaglandin synthesis inhibitors such as diclofenac, resulted in increased pre-and post-implantation loss; if a woman becomes pregnant while taking drug combination, discontinue drug and advise the woman of the potential risks to her and to a fetus
Maternal adverse reactions
- Misoprostol may produce uterine contractions, uterine bleeding, and expulsion of the products of conception; misoprostol has been used to ripen the cervix, to induce labor, and to treat postpartum hemorrhage, outside of its approved indication
- A major adverse effect of these uses is hyperstimulation of the uterus; uterine rupture, amniotic fluid embolism, severe bleeding, shock, and maternal death have been reported when misoprostol was administered to pregnant women to induce labor to induce abortion beyond the eighth weeks of pregnancy
- Higher doses of misoprostol, including the 100 mcg tablet, may increase the risk of complications from uterine hyperstimulation; the drug combination, which contains 200 mcg of misoprostol, is likely to have a greater risk of uterine hyperstimulation than the 100 mcg tablet of misoprostol
- Abortions caused by misoprostol may be incomplete; cases of amniotic fluid embolism, which resulted in maternal and fetal death, have been reported with use of misoprostol during pregnancy
- Severe vaginal bleeding, retained placenta, shock, and pelvic pain have also been reported; these women were administered misoprostol vaginally and/or orally over a range of doses; if a woman is or becomes pregnant while taking this drug, the drug should be discontinued and the patient apprised of the potential hazard to the fetus
- Drug combination is contraindicated in pregnant women
Fetal toxicity
- Misoprostol may endanger pregnancy (may cause abortion) and thereby cause harm to the fetus when administered to a pregnant woman; use of misoprostol for the induction of labor in the third trimester was associated with uterine hyperstimulation with resulting changes in the fetal heart rate (fetal bradycardia) and fetal death (misoprostol is not approved for this use)
- NSAIDs can cause premature closure of the fetal ductus arteriosus at about 30 weeks gestation and later in pregnancy and at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment
- If an NSAID is necessary at about 20 weeks gestation or later in pregnancy, limit the use to the lowest effective dose and shortest duration possible. If treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. If oligohydramnios occurs, discontinue treatment and follow up according to clinical practice
Labor or delivery
- There are no studies on the effects of drug combination or diclofenac during labor or delivery; in animal studies, NSAIDS, including diclofenac, are known to inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth;
- In humans, some case reports and studies have associated misoprostol with risk of stillbirth, uterine hyperstimulation, perineal tear, amniotic fluid embolism, severe bleeding, shock, uterine rupture and death
- The risk of uterine rupture associated with misoprostol use in pregnancy may occur at any gestational age, and increases with advancing gestational ages and with prior uterine surgery, including cesarean delivery; grand multiparity also appears to be a risk factor for uterine rupture
Infertility
- Based on mechanism of action, NSAIDs, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women
- Animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin-mediated follicular rupture required for ovulation; small studies in women have also shown a reversible delay in ovulation in women treated with NSAIDs; consider withdrawal of NSAIDs, in women who have difficulties conceiving or who are undergoing investigation of infertility
Animal data
- In reproduction studies with pregnant rabbits, there were no skeletal or visceral malformations when drug combination was administered during organogenesis at doses less than maximum recommended human doses (MRHD); however, embryotoxicity was observed at this exposure
- Based on animal data, prostaglandins have been shown to have important role in endometrial vascular permeability, blastocyst implantation, and decidualization; in animal studies, administration of prostaglandin synthesis inhibitors such as diclofenac, resulted in increased pre-and post-implantation loss; if a woman becomes pregnant while receiving therapy, discontinue drug and advise woman of potential risks to her and to a fetus
- In animal studies, NSAIDs are known to inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth
Lactation
No lactation studies conducted; however, limited published literature reports that diclofenac and active metabolite of misoprostol are present in breast milk; developmental and health benefits of breastfeeding should be considered along with mother’s clinical need for therapy and any potential adverse effects on breastfed infant from therapy or from underlying maternal condition
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
Diclofenac: Inhibits cyclooxygenase-1 (COX-1) & -2 (COX-2), thereby inhibiting prostaglandin synthesis; has anti-inflammatory, antipyresis, and analgesic properties
Misoprostol: Replaces protective prostaglandins consumed by prostaglandin-inhibiting therapies (NSAID-induced ulcers)
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