Skip to main content

Piroxicam (Monograph)

Brand name: Feldene
Drug class: Other Nonsteroidal Anti-inflammatory Agents
VA class: MS120
Chemical name: 4-Hydroxy-2-methyl-N2-pyridinyl-2H-1,2-benzothiazine-3-carboxamide 1,1-dioxide
Molecular formula: C15H13N3O4S
CAS number: 36322-90-4

Medically reviewed by on Nov 29, 2021. Written by ASHP.


    Cardiovascular Risk
  • Increased risk of serious (sometimes fatal) cardiovascular thrombotic events (e.g., MI, stroke). Risk may occur early in treatment and may increase with duration of use. (See Cardiovascular Thrombotic Effects under Cautions.)

  • Contraindicated in the setting of CABG surgery.

    GI Risk
  • Increased risk of serious (sometimes fatal) GI events (e.g., bleeding, ulceration, perforation of the stomach or intestine). Serious GI events can occur at any time and may not be preceded by warning signs and symptoms. Geriatric individuals are at greater risk for serious GI events. (See GI Effects under Cautions.)


Prototypical NSAIA; an oxicam derivative.

Uses for Piroxicam

Consider potential benefits and risks of piroxicam therapy as well as alternative therapies before initiating therapy with the drug. Use lowest possible effective dosage and shortest duration of therapy consistent with patient's treatment goals.

Inflammatory Diseases

Symptomatic treatment of rheumatoid arthritis and osteoarthritis.

Has been used for the symptomatic relief of acute gouty arthritis [off-label] and ankylosing spondylitis [off-label]; has also been used for symptomatic treatment of acute musculoskeletal disorders [off-label].


Has been used for symptomatic relief of postoperative [off-label] or postpartum pain [off-label].


Has been used for the management of dysmenorrhea.

Piroxicam Dosage and Administration


  • Consider potential benefits and risks of piroxicam therapy as well as alternative therapies before initiating therapy with the drug.


Oral Administration

Administered orally, usually as a single daily dose. May be administered in divided doses daily.


To minimize the potential risk of adverse cardiovascular and/or GI events, use lowest effective dosage and shortest duration of therapy consistent with patient's treatment goals. Adjust dosage based on individual requirements and response; attempt to titrate to lowest effective dosage.


Inflammatory Diseases
Osteoarthritis or Rheumatoid Arthritis

Initially, 20 mg daily. Adjust dosage based on response and tolerance; 30 or 40 mg daily may be required for maintenance therapy, although 20 mg daily is usually adequate.

Prescribing Limits


Inflammatory Diseases

Dosages >20 mg daily associated with increased frequency of adverse GI effects.

Special Populations

Hepatic Impairment

Inflammatory Diseases

Dosage reduction may be required.

CYP2C9 Poor or Intermediate Metabolizers

Manufacturer states to consider dosage reduction in known or suspected CYP2C9 poor metabolizers.

Clinical Pharmacogenetics Implementation Consortium (CPIC) guidelines recommend avoiding piroxicam use in CYP2C9 poor metabolizers and in intermediate metabolizers with a diplotype functional activity score (AS) of 1. Select an alternative agent that is not metabolized by CYP2C9 or is not substantially affected by CYP2C9 genetic variants in vivo; alternatively, consider an NSAIA that is metabolized by CYP2C9 but has a shorter half-life. (See Pharmacogenomic Precautions under Cautions.)

Intermediate metabolizers with an AS of 1.5 may receive dosages recommended for normal metabolizers.

Cautions for Piroxicam


  • Known hypersensitivity to piroxicam or any ingredient in the formulation.

  • History of asthma, urticaria, or other sensitivity reaction precipitated by aspirin or other NSAIAs.

  • In the setting of CABG surgery.



Cardiovascular Thrombotic Effects

NSAIAs (selective COX-2 inhibitors, prototypical NSAIAs) increase the risk of serious adverse cardiovascular thrombotic events (e.g., MI, stroke) in patients with or without cardiovascular disease or risk factors for cardiovascular disease.

Findings of FDA review of observational studies, meta-analysis of randomized controlled trials, and other published information indicate that NSAIAs may increase the risk of such events by 10–50% or more, depending on the drugs and dosages studied.

Relative increase in risk appears to be similar in patients with or without known underlying cardiovascular disease or risk factors for cardiovascular disease, but the absolute incidence of serious NSAIA-associated cardiovascular thrombotic events is higher in those with cardiovascular disease or risk factors for cardiovascular disease because of their elevated baseline risk.

Increased risk may occur early (within the first weeks) following initiation of therapy and may increase with higher dosages and longer durations of use.

In controlled studies, increased risk of MI and stroke observed in patients receiving a selective COX-2 inhibitor for analgesia in first 10–14 days following CABG surgery.

In patients receiving NSAIAs following MI, increased risk of reinfarction and death observed beginning in the first week of treatment.

Increased 1-year mortality rate observed in patients receiving NSAIAs following MI; absolute mortality rate declined somewhat after the first post-MI year, but the increased relative risk of death persisted over at least the next 4 years.

Some systematic reviews of controlled observational studies and meta-analyses of randomized studies suggest naproxen may be associated with lower risk of cardiovascular thrombotic events compared with other NSAIAs. FDA states that limitations of these studies and indirect comparisons preclude definitive conclusions regarding relative risks of NSAIAs.

Use NSAIAs with caution and careful monitoring (e.g., monitor for development of cardiovascular events throughout therapy, even in those without prior cardiovascular symptoms) and at the lowest effective dose for the shortest duration necessary.

Some clinicians suggest that it may be prudent to avoid NSAIA use, whenever possible, in patients with cardiovascular disease. Avoid use in patients with recent MI unless benefits of therapy are expected to outweigh risk of recurrent cardiovascular thrombotic events; if used, monitor for cardiac ischemia. Contraindicated in the setting of CABG surgery.

No consistent evidence that concomitant use of low-dose aspirin mitigates the increased risk of serious adverse cardiovascular events associated with NSAIAs. (See Specific Drugs under Interactions.)

GI Effects

Serious GI toxicity (e.g., bleeding, ulceration, perforation) can occur with or without warning symptoms; increased risk in those with a history of GI bleeding or ulceration, geriatric patients, smokers, those with alcohol dependence, and those in poor general health.

For patients at high risk for complications from NSAIA-induced GI ulceration (e.g., bleeding, perforation), consider concomitant use of misoprostol; alternatively, consider concomitant use of a proton-pump inhibitor (e.g., omeprazole) or use of an NSAIA that is a selective inhibitor of COX-2 (e.g., celecoxib).


Hypertension and worsening of preexisting hypertension reported; either event may contribute to the increased incidence of cardiovascular events. Use with caution in patients with hypertension; monitor BP.

Impaired response to ACE inhibitors, angiotensin II receptor antagonists, β-blockers, and certain diuretics may occur. (See Specific Drugs under Interactions.)

Heart Failure and Edema

Fluid retention and edema reported.

NSAIAs (selective COX-2 inhibitors, prototypical NSAIAs) may increase morbidity and mortality in patients with heart failure.

NSAIAs may diminish cardiovascular effects of diuretics, ACE inhibitors, or angiotensin II receptor antagonists used to treat heart failure or edema. (See Specific Drugs under Interactions.)

Manufacturer recommends avoiding use in patients with severe heart failure unless benefits of therapy are expected to outweigh risk of worsening heart failure; if used, monitor for worsening heart failure.

Some experts recommend avoiding use, whenever possible, in patients with reduced left ventricular ejection fraction and current or prior symptoms of heart failure.

Renal Effects

Direct renal injury, including renal papillary necrosis, reported in patients receiving long-term NSAIA therapy.

Potential for overt renal decompensation. Increased risk of renal toxicity in patients with renal or hepatic impairment or heart failure, in geriatric patients, in patients with volume depletion, and in those receiving a diuretic, ACE inhibitor, or angiotensin II receptor antagonist. (See Renal Impairment under Cautions.)

Sensitivity Reactions

Hypersensitivity Reactions

Anaphylactoid reactions reported. Immediate medical intervention and discontinuance for anaphylaxis.

Avoid in patients with aspirin triad (aspirin sensitivity, asthma, nasal polyps); caution in patients with asthma.

Potentially fatal or life-threatening syndrome of multi-organ hypersensitivity (i.e., drug reaction with eosinophilia and systemic symptoms [DRESS]) reported in patients receiving NSAIAs. Clinical presentation is variable, but typically includes eosinophilia, fever, rash, lymphadenopathy, and/or facial swelling, possibly associated with other organ system involvement (e.g., hepatitis, nephritis, hematologic abnormalities, myocarditis, myositis). Symptoms may resemble those of acute viral infection. Early manifestations of hypersensitivity (e.g., fever, lymphadenopathy) may be present in the absence of rash. If signs or symptoms of DRESS develop, discontinue the NSAIA and immediately evaluate the patient.

Dermatologic Reactions

Serious skin reactions (e.g., exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis) reported; can occur without warning. Discontinue at first appearance of rash or any other sign of hypersensitivity (e.g., blisters, fever, pruritus).

General Precautions

Hepatic Effects

Severe reactions including jaundice, fatal fulminant hepatitis, liver necrosis, and hepatic failure (sometimes fatal) reported rarely with NSAIAs.

Elevations of serum ALT or AST reported.

Monitor for symptoms and/or signs suggesting liver dysfunction; monitor abnormal liver function test results. Discontinue if signs or symptoms of liver disease or systemic manifestations (e.g., eosinophilia, rash) occur or if liver function test abnormalities persist or worsen.

Hematologic Effects

Anemia reported rarely. Determine hemoglobin concentration or hematocrit in patients receiving long-term therapy if signs or symptoms of anemia occur.

May inhibit platelet aggregation and prolong bleeding time.

Pharmacogenomic Precautions

CYP2C9 poor metabolizers: Piroxicam metabolism may be decreased substantially, half-life may be prolonged, and higher plasma concentrations of the drug may increase likelihood and/or severity of adverse effects. (See Special Populations under Pharmacokinetics.)

CYP2C9 intermediate metabolizers: Piroxicam metabolism may be moderately or mildly reduced in those with an AS of 1 or 1.5, respectively. Higher plasma piroxicam concentrations in intermediate metabolizers with an AS of 1 may increase likelihood of adverse effects. Presence of other factors affecting piroxicam clearance (e.g., hepatic impairment, advanced age) also may increase risk of adverse effects in intermediate metabolizers.

Piroxicam's long half-life enhances the risks in patients with reduced CYP2C9 metabolism.

Avoidance of piroxicam may be recommended depending on CYP2C9 phenotype. (See CYP2C9 Poor or Intermediate Metabolizers under Dosage and Administration.)

Consult Clinical Pharmacogenetics Implementation Consortium Guideline (CPIC) for CYP2C9 and Nonsteroidal Anti-Inflammatory Drugs for additional information on interpretation of CYP2C9 genotype testing.

Ocular Effects

Visual disturbances reported; ophthalmic evaluation recommended if visual changes occur.

Other Precautions

Not a substitute for corticosteroid therapy; not effective in the management of adrenal insufficiency.

May mask certain signs of infection.

Obtain CBC and chemistry profile periodically during long-term use.

Specific Populations


No adequate and well-controlled studies of piroxicam in pregnant women.

Use of NSAIAs during pregnancy at about ≥30 weeks’ gestation can cause premature closure of the fetal ductus arteriosus; use at about ≥20 weeks’ gestation associated with fetal renal dysfunction resulting in oligohydramnios and, in some cases, neonatal renal impairment.

Effects of NSAIAs on the human fetus during third trimester of pregnancy include prenatal constriction of the ductus arteriosus, tricuspid incompetence, and pulmonary hypertension; nonclosure of the ductus arteriosus during the postnatal period (which may be resistant to medical management); and myocardial degenerative changes, platelet dysfunction with resultant bleeding, intracranial bleeding, renal dysfunction or renal failure, renal injury or dysgenesis potentially resulting in prolonged or permanent renal failure, oligohydramnios, GI bleeding or perforation, and increased risk of necrotizing enterocolitis.

Avoid use of NSAIAs in pregnant women at about ≥30 weeks’ gestation; if use required between about 20 and 30 weeks’ gestation, use lowest effective dosage and shortest possible duration of treatment, and consider monitoring amniotic fluid volume via ultrasound examination if treatment duration >48 hours; if oligohydramnios occurs, discontinue drug and follow up according to clinical practice. (See Advice to Patients.)

Fetal renal dysfunction resulting in oligohydramnios and, in some cases, neonatal renal impairment observed, on average, following days to weeks of maternal NSAIA use; infrequently, oligohydramnios observed as early as 48 hours after initiation of NSAIAs. Oligohydramnios is often, but not always, reversible (generally within 3–6 days) following NSAIA discontinuance. Complications of prolonged oligohydramnios may include limb contracture and delayed lung maturation. In limited number of cases, neonatal renal dysfunction (sometimes irreversible) occurred without oligohydramnios. Some neonates have required invasive procedures (e.g., exchange transfusion, dialysis). Deaths associated with neonatal renal failure also reported. Limitations of available data (lack of control group; limited information regarding dosage, duration, and timing of drug exposure; concomitant use of other drugs) preclude a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal NSAIA use. Available data on neonatal outcomes generally involved preterm infants; extent to which risks can be generalized to full-term infants is uncertain.

Animal data indicate important roles for prostaglandins in kidney development and endometrial vascular permeability, blastocyst implantation, and decidualization. In animal studies, inhibitors of prostaglandin synthesis increased pre- and post-implantation losses; also impaired kidney development at clinically relevant doses.

No evidence of teratogenicity in animal studies of piroxicam; postimplantation loss, delayed parturition, and increased incidence of stillbirth observed.

Effects of piroxicam on labor or delivery not known.


Distributed into milk at approximately 1–3% of maternal concentration. No accumulation in milk relative to maternal plasma.

Consider developmental and health benefits of breast-feeding along with the mother's clinical need for piroxicam and any potential adverse effects on the breast-fed infant from the drug or underlying maternal condition.


NSAIAs may be associated with reversible infertility in some women. Reversible delays in ovulation observed in limited studies in women receiving NSAIAs; animal studies indicate that inhibitors of prostaglandin synthesis can disrupt prostaglandin-mediated follicular rupture required for ovulation.

Consider withdrawal of NSAIAs in women experiencing difficulty conceiving or undergoing evaluation of infertility.

Pediatric Use

Safety and efficacy not established.

Geriatric Use

Caution advised. Geriatric adults appear to tolerate NSAIA-induced adverse effects less well than younger individuals. Fatal adverse GI effects reported more frequently in geriatric patients than younger adults.

Consider lowest effective dosage for the shortest possible duration.

Hepatic Impairment

Monitor closely. (See Hepatic Impairment under Dosage and Administration.)

Renal Impairment

Use not recommended in patients with advanced renal disease; close monitoring of renal function advised if used.

Common Adverse Effects

Dyspepsia, nausea, diarrhea, constipation, rash, dizziness, headache, edema, tinnitus.

Interactions for Piroxicam

Protein-bound Drugs

Pharmacokinetic interaction possible with other highly protein-bound drugs; monitor patient; dosage adjustment may be needed.

Specific Drugs




ACE inhibitors

Reduced BP response to ACE inhibitor

Monitor BP

Angiotensin II receptor antagonists

Reduced BP response to angiotensin II receptor antagonist

Monitor BP

Antacids (magnesium- or aluminum-containing)

Pharmacokinetic interaction unlikely

Anticoagulants (warfarin)

Possible bleeding complications

Increased risk of major bleeding or supratherapeutic INRs in patients with reduced CYP2C9 function receiving concomitant warfarin (CYP2C9 substrate) and NSAIAs

Use with caution; monitor PT; adjust anticoagulant dosage as needed

Some experts recommend avoiding concomitant use of warfarin and NSAIAs in CYP2C9 intermediate or poor metabolizers

Diuretics (furosemide, thiazides)

Reduced natriuretic effects

Monitor for diuretic efficacy and renal failure


Increased plasma lithium concentrations

Monitor plasma lithium concentrations when initiating or discontinuing piroxicam; monitor for lithium toxicity


Increased plasma methotrexate concentrations, particularly with high methotrexate dosage

Use with caution


NSAIAs including aspirin: Increased risk of GI ulceration and other complications

Aspirin: No consistent evidence that use of low-dose aspirin mitigates the increased risk of serious cardiovascular events associated with NSAIAs

Decreased plasma piroxicam concentrations with concomitant use of 20 mg piroxicam and 3.9 g aspirin daily

Concomitant use not recommended


Possible increased risk of pemetrexed-associated myelosuppression, renal toxicity, and GI toxicity

Short half-life NSAIAs (e. g., diclofenac, indomethacin): Avoid administration beginning 2 days before and continuing through 2 days after pemetrexed administration

Longer half-life NSAIAs (e.g., meloxicam, nabumetone): In the absence of data, avoid administration beginning at least 5 days before and continuing through 2 days after pemetrexed administration

Patients with Clcr 45–79 mL/minute: Monitor for myelosuppression, renal toxicity, and GI toxicity

Thrombolytic agents (streptokinase)

Possible bleeding complications

Use with caution

Piroxicam Pharmacokinetics



Well absorbed following oral administration; peak plasma concentrations usually attained within 3 to 5 hours.


Decreases rate but not extent of absorption.



Distributed into synovial fluid.

Distributed into human milk.

May accumulate slowly in cartilage.

Plasma Protein Binding




Extensively metabolized, principally by CYP2C9-mediated hydroxylation and glucuronide conjugation of the hydroxy metabolite.

Elimination Route

Excreted principally in urine and feces, with urinary excretion approximately twice the fecal excretion. Excreted principally as metabolites; <5% excreted unchanged.


50 hours (range: 14–158 hours).

Special Populations

CYP2C9 *1/*2 or *1/*3 diplotype: Piroxicam concentrations following a single oral dose increased 1.7-fold compared with normal metabolizers; elimination half-life in those with the *1/*3 diplotype also increased 1.7-fold.

CYP2C9 *3/*3 diplotype: Piroxicam concentrations increased 5.3-fold following a single oral dose and elimination half-life increased 8.8-fold compared with normal metabolizers.





Tight, light-resistant containers at <30°C.


  • Inhibits cyclooxygenase-1 (COX-1) and COX-2.

  • Pharmacologic actions similar to those of other prototypical NSAIAs; exhibits anti-inflammatory, analgesic, and antipyretic activity.

Advice to Patients

  • Importance of reading the medication guide for NSAIAs that is provided to the patient each time the drug is dispensed.

  • Risk of serious cardiovascular events (e.g., MI, stroke).

  • Risk of GI bleeding and ulceration.

  • Risk of serious skin reactions, DRESS, and anaphylactoid and other sensitivity reactions.

  • Risk of hepatotoxicity.

  • Importance of seeking immediate medical attention if signs and symptoms of a cardiovascular event (chest pain, dyspnea, weakness, slurred speech) occur.

  • Importance of notifying clinician if signs and symptoms of GI ulceration or bleeding, unexplained weight gain, or edema develops.

  • Advise patients to stop taking the drug immediately if they develop any type of rash or fever and to promptly contact their clinician. Importance of seeking immediate medical attention if an anaphylactic reaction occurs.

  • Importance of discontinuing therapy and contacting clinician immediately if signs and symptoms of hepatotoxicity (nausea, fatigue, lethargy, pruritus, jaundice, upper right quadrant tenderness, flu-like symptoms) occur.

  • Risk of heart failure or edema; importance of reporting dyspnea, unexplained weight gain, or edema.

  • Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.

  • Importance of avoiding NSAIA use beginning at 20 weeks’ gestation unless otherwise advised by a clinician; importance of avoiding NSAIAs beginning at 30 weeks’ gestation because of risk of premature closure of the fetal ductus arteriosus; monitoring for oligohydramnios may be necessary if NSAIA therapy required for >48 hours’ duration between about 20 and 30 weeks’ gestation.

  • Advise women who are trying to conceive that NSAIAs may be associated with a reversible delay in ovulation.

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant diseases.

  • Importance of informing patients of other important precautionary information. (See Cautions.)


Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name



Dosage Forms


Brand Names




10 mg*



20 mg*



AHFS DI Essentials™. © Copyright 2023, Selected Revisions November 29, 2021. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

† Off-label: Use is not currently included in the labeling approved by the US Food and Drug Administration.

Reload page with references included