Version May 2024
Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction (MI) and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use.
Meloxicam is contraindicated in the setting of coronary artery bypass graft (CABG) surgery.
NSAIDs cause an increased risk of serious GI adverse events, including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal. These events can occur at any time during use and 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.
Dosage guidance:
Safety: Avoid or use with caution in patients at risk for or with existing cardiovascular disease, GI disease, kidney impairment, chronic liver disease, or a bleeding diathesis due to greater risk for adverse events. Consider proton pump inhibitor coadministration in patients at risk for GI bleeding (eg, taking dual antiplatelet therapy or an anticoagulant, ≥60 years of age, high meloxicam doses) (Ref).
Dosing: Use the lowest effective dose for the shortest duration of time. Lower doses (eg, ≤7.5 mg/day) may be relatively COX-2 selective, but this relative selectivity is lost at higher doses (eg, 15 mg/day) (Ref).
Dosage form information: Capsules, orally disintegrating tablets, oral suspension, and tablets do not have equivalent systemic exposure and are not interchangeable, even if the total milligram strength is the same.
Acute pain:
Note: Due to slow onset, other oral nonsteroidal anti-inflammatory drugs (NSAIDs) are generally preferred; however, some experts use for postoperative pain management (Ref).
IV: 30 mg once daily.
Capsule: Oral (off-label route): 5 mg to 10 mg once daily; maximum dose: 10 mg/day (Ref).
Orally disintegrating tablet (Omiiz ODT): Oral (off-label route): 7.5 mg to 15 mg once daily; maximum dose: 15 mg/day (Ref). Note: Qmiiz ODT has been discontinued in the United States for >1 year.
Suspension: Oral (off-label route): 7.5 mg to 15 mg once daily; maximum dose: 15 mg/day (Ref).
Tablet: Oral (off-label route): 7.5 mg to 15 mg once daily; maximum dose: 15 mg/day (Ref).
Gout, treatment, acute flares (off-label use):
Tablet: Oral: 15 mg once daily (Ref); initiate within 24 to 48 hours of flare onset; reduce dose as symptoms improve. Discontinue a few days after resolution of clinical signs (usual total duration: 5 to 7 days); longer duration may be required if therapy is delayed (Ref).
Osteoarthritis:
Capsule: Oral: Initial: 5 mg once daily; may increase to a maximum of 10 mg once daily.
Orally disintegrating tablet: Oral: Initial: 7.5 mg once daily; may increase to a maximum of 15 mg once daily. Note: Qmiiz ODT has been discontinued in the United States for >1 year.
Suspension: Oral: Initial: 7.5 mg once daily; may increase to a maximum of 15 mg once daily.
Tablet: Oral: Initial: 7.5 mg once daily; may increase to a maximum of 15 mg once daily.
Rheumatoid arthritis:
Orally disintegrating tablet: Oral: Initial: 7.5 mg once daily; may increase to a maximum of 15 mg once daily. Note: Qmiiz ODT has been discontinued in the United States for >1 year.
Suspension: Oral: Initial: 7.5 mg once daily; may increase to a maximum of 15 mg once daily.
Tablet: Oral: Initial: 7.5 mg once daily; may increase to a maximum of 15 mg once daily.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
IV:
eGFR ≥60 mL/minute/1.73 m2: No dosage adjustment necessary.
eGFR <60 mL/minute/1.73 m2: Use is not recommended; contraindicated in patients who are at risk for renal failure due to volume depletion.
Oral:
Altered kidney function:
CrCl ≥60 mL/minute: No dosage adjustment necessary (Ref).
CrCl >30 to <60 mL/minute: No dosage adjustment necessary (Ref). Use of analgesics other than nonsteroidal anti-inflammatory drugs may be preferred. If necessary, use the lowest effective dose for the shortest duration possible; avoid in patients at high risk for acute kidney injury (ie, volume depleted, hypotensive, elderly, or taking concurrent nephrotoxic medications) (Ref).
CrCl ≤30 mL/minute: Avoid use due to increased risk of acute kidney injury (Ref).
Hemodialysis, intermittent (thrice weekly): Not significantly dialyzable (Ref): Avoid use, as patients with end-stage kidney disease may be at increased risk for bleeding (eg, GI), cardiovascular adverse effects, and loss of residual kidney function (Ref).
Peritoneal dialysis: Avoid use, as patients with end-stage kidney disease may be at increased risk for bleeding (eg, GI), cardiovascular adverse effects, and loss of residual kidney function (Ref).
CRRT: Avoid use (Ref).
PIRRT (eg, sustained, low-efficiency diafiltration): Avoid use (Ref).
IV: Mild to severe impairment: There are no dosage adjustments provided in the manufacturer's labeling (has not been studied); use with caution to avoid adverse effects and discontinue if hepatic function worsens.
Oral:
Mild to moderate impairment (Child-Pugh class A or B): No dosage adjustment necessary.
Severe impairment (Child-Pugh class C): There are no dosage adjustments provided in the manufacturer's labeling (has not been studied); use with caution to avoid adverse effects and discontinue if hepatic function worsens.
Note: Unless alternative agents are ineffective and a gastroprotective agent can be administered, avoid short-term scheduled use in combination with corticosteroids, anticoagulants, or antiplatelet agents or chronic use with or without medications that increase risk for bleeding (Ref).
Refer to adult dosing; initiate oral dose at lower end of the dosing range.
(For additional information see "Meloxicam: Pediatric drug information")
Dosage guidance:
Dose form information: Orally disintegrating tablets, capsules, tablets, and oral suspension do not have equivalent systemic exposure and are not interchangeable, even if the total milligram strength is the same; do not substitute similar dose strengths of other meloxicam products.
Juvenile idiopathic arthritis (JIA): Note: To reduce the risk of adverse cardiovascular and GI effects, use the lowest effective dose for the shortest period of time; adjust dose to patient's clinical needs; higher doses have not demonstrated additional benefit in clinical trials.
Oral suspension:
Children ≥2 years and Adolescents: Oral: 0.125 mg/kg once daily; maximum dose: 7.5 mg/dose.
Orally disintegrating tablets (Qmiiz ODT): Note: Qmiiz ODT has been discontinued in the United States for >1 year.
Children and Adolescents weighing ≥60 kg: Oral: 7.5 mg once daily.
Tablets:
Children and Adolescents weighing ≥60 kg: Oral: 7.5 mg once daily.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Children ≥2 years and Adolescents: Oral:
Mild to moderate impairment: No dosage adjustment necessary.
Severe renal impairment: Use is not recommended (has not been studied).
Hemodialysis: Not dialyzable; additional doses are not required after hemodialysis; maximum dose: 7.5 mg/dose.
KDIGO guidelines provide the following recommendations for NSAIDs (Ref):
eGFR 30 to <60 mL/minute/1.73 m2: Temporarily discontinue in patients with intercurrent disease that increases risk of acute kidney injury.
eGFR <30 mL/minute/1.73 m2: Avoid use.
Children ≥2 years and Adolescents: Oral:
Mild to moderate impairment: No dosage adjustments are recommended.
Severe impairment: There are no dosage adjustments provided in the manufacturer's labeling (has not been studied); use with caution; meloxicam is significantly metabolized in the liver.
Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with an increased risk of serious adverse cardiovascular (CV) events, including acute myocardial infarction (MI), cerebrovascular accident, and CV death. New-onset hypertension or exacerbation of hypertension may occur with NSAID use which may also contribute to an increased risk of CV events (Ref). New-onset or exacerbation of heart failure may also occur with nonselective NSAIDs (eg, naproxen), cyclooxygenase (COX)-2 selective NSAIDs (ie, coxibs), and relatively selective COX-2 inhibitors (eg, meloxicam), resulting in an increased risk of hospitalizations for heart failure and death in patients with heart failure (Ref).
Data collected by the Coxib and traditional NSAID Trialists’ (CNT) Collaborative has shown that use of COX-2 selective NSAIDs, including celecoxib, may increase the risk of major vascular events as compared to nonselective NSAIDs (Ref); however, data from the PRECISION trial showed no difference with regards to risk between celecoxib, naproxen, or ibuprofen after a treatment duration of therapy of ~3 years (Ref). A nested matched case-control trial found that use of meloxicam resulted in a 38% increase in the risk of MI (Ref). Additional trial and registry data are also conflicted with regards to the comparative risk of CV events among the COX-2 selective and nonselective NSAIDs (Ref). However, data in those with established heart disease consistently reveals an increased risk of harm with NSAID use (Ref). The FDA states that there is insufficient data to determine if risk of MI or stroke is definitely higher or lower for any particular NSAID as compared to another (Ref).
Mechanism: Dose- and time-related; inhibition of COX-2 by NSAIDs results in a reduction in the production of prostaglandin I2 (prostacyclin) in the vascular endothelium (Ref); animal studies have shown that reduced prostacyclin activity may result in a predisposition to vascular injury (Ref). In addition, prostaglandins inhibit sodium resorption in the thick ascending loop of Henle and collecting tubule; therefore, a reduction in prostaglandin synthesis by NSAIDs may cause sodium and fluid retention and result in hypertension and decreased efficacy of diuretics (Ref).
Onset: Varied; increased risk may be apparent within the first weeks following initiation of treatment (Ref); longer duration of therapy may further increase risk (Ref).
Risk factors:
• ≥65 years of age
• Higher doses (especially with regards to CV thrombotic risk) (Ref)
• Longer duration of use and frequent use (eg, ≥22 days per month) (Ref)
• Preexisting cardiovascular disease (CVD) or presence of risk factors for CVD, including use following coronary artery bypass graft surgery (Ref)
- Note: Relative risk appears to be similar in those with and without known CVD or risk factors for CVD; however, absolute incidence of serious CV thrombotic events appears to be higher in patients with known CVD or risk factors for CVD due to an increased baseline risk (Ref)
Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with an increased risk of serious gastrointestinal (GI) adverse events, including GI inflammation, gastrointestinal hemorrhage, gastrointestinal ulcer, and gastrointestinal perforation; severity may range from asymptomatic to fatal (Ref). Selective cyclooxygenase (COX)-2 NSAIDs, including relatively selective COX-2 inhibitors (eg, meloxicam), appear to be associated with a lower risk of significant GI adverse events as compared to nonselective NSAIDs; the concomitant use of low-dose aspirin therapy may diminish the safety advantage of COX-2 selective NSAIDs over nonselective NSAIDs (Ref).
Mechanism: Dose- and time-related; inhibition of COX-1 by NSAIDs results in a reduction in the production of mucosal-protective prostaglandin E2. COX-2 selective NSAIDs may block COX-1 in the GI tract, albeit to a lesser degree as compared to nonselective NSAIDs, and therefore have the ability to cause damage (Ref).
Onset: Varied; GI events can occur at any time during use and without warning symptoms.
Risk factors:
• ≥65 years of age (Ref)
• Longer duration of use
• Higher doses (eg, meloxicam 15 mg daily (Ref))
• Prior history of peptic ulcer disease and/or GI bleeding
• Concomitant use of agents known to increase the risk of GI bleeding (eg, aspirin (Ref); anticoagulants, corticosteroids (Ref); selective serotonin reuptake inhibitors (Ref))
• Comorbid Helicobacter pylori infection (Ref)
• Advanced liver disease/cirrhosis
• Coagulopathy
• Smoking
• Consumption of alcohol
• People with poor general health status
• Small intestine damage: Small intestine bacterial overgrowth (SIBO), including SIBO induced by proton pump inhibitor therapy, may be associated with an increased risk of small intestine damage (Ref)
Use of nonsteroidal anti-inflammatory drugs (NSAIDs) may result in anemia; drug-induced hemolytic anemia has been reported with use of other NSAIDs, including both non-selective and cyclooxygenase (COX)-2 selective agents (Ref). Use of meloxicam may result in a prolonged bleeding time and an increased risk for hemorrhage (Ref); however, nonselective NSAIDs (eg, ibuprofen) may be more likely to impact platelet function and cause prolonged bleeding time compared to selective and relatively selective COX-2 inhibitors (coxibs and meloxicam respectively) (Ref). Rarely, NSAID use, including meloxicam, has been associated with potentially severe blood dyscrasias (eg, agranulocytosis, thrombocytopenia (Ref), aplastic anemia).
Mechanism:
Anemia: Not clearly established; anemia may be due to occult or gross blood loss, fluid retention, or an incompletely described effect on erythropoiesis.
Prolonged bleeding time: Inhibition of COX-1 causes a decrease in the production of prostaglandins, prostacyclins, and thromboxanes, including thromboxane A2 (TxA2) (Ref). Therefore, patients exposed to NSAIDs, especially nonselective NSAIDs (eg, naproxen), may exhibit a decrease in platelet adhesion and aggregation and subsequent prolonged bleeding time (Ref).
Onset: Prolonged bleeding time: Rapid; suppression of platelet COX-1 activity occurs within hours of administration (Ref). In patients receiving antithrombotic therapy after myocardial infarction, the use of NSAIDs, including COX-2 selective NSAIDs, has been associated with an increased risk of bleeding and excess thrombotic events even after short-term treatment (eg, <3 days) (Ref).
Risk factors:
• Bleeding events:
- Preexisting coagulation disorders
- Concomitant use of agents known to increase the risk of bleeding (eg, anticoagulants, antithrombotics (Ref); antiplatelet agents [eg, aspirin], selective serotonin reuptake inhibitors (Ref); or serotonin norepinephrine reuptake inhibitors).
Nonsteroidal anti-inflammatory drugs (NSAIDs) may cause mild transaminase elevations (Ref); meloxicam has been associated with both cholestatic and hepatocellular patterns of transaminase elevations (Ref). The incidence of hepatic adverse events appears similar between cyclooxygenase (COX)-2 selective NSAIDs (ie, coxibs) and nonselective NSAIDs (eg, naproxen, ibuprofen) (Ref); diclofenac exhibits a higher rate of hepatotoxic events compared to other NSAIDs (Ref). Rarely, serious liver injury may occur, such as fulminant hepatitis, hepatic necrosis, and/or hepatic failure; meloxicam-induced autoimmune hepatitis, cholestatic hepatitis, hepatotoxicity, and jaundice have been reported (Ref).
Mechanism: Not clearly established; possible mechanisms include a toxic metabolite or a hypersensitivity reaction (Ref).
Onset: Varied; onset of NSAID-induced hepatotoxicity is generally classified as moderate (30 to 90 days) to long (>90 days) (Ref). For meloxicam, onset was <1 month in a few cases (Ref).
Risk factors:
• Prior “oxicam” NSAID (eg, piroxicam)-related liver injury (theoretical risk factor) (Ref)
Hypersensitivity reactions to meloxicam may involve the skin (eg, angioedema, urticaria), airways (eg, dyspnea, rhinorrhea), and/or other organs (Ref). Clinical phenotypes of nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity reactions include NSAID-exacerbated respiratory disease (NERD), NSAID-induced urticaria/angioedema (NIUA), NSAID-exacerbated cutaneous disease (NECD), and single NSAID-induced urticaria/angioedema or anaphylaxis (Ref). Delayed hypersensitivity reactions ranging from mild reactions such as fixed drug eruption (Ref) to more serious reactions including Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) (Ref) have been reported with meloxicam.
Mechanism:
Immediate hypersensitivity reactions: Non–dose-related; most reactions (ie, NERD, NECD, NIUA) are non-immunologic related to inhibition of cyclooxygenase (COX)-1 with subsequent activation of mast cells and eosinophils causing release of inflammatory mediators including cysteinyl-leukotrienes (cysLTs) (Ref). Meloxicam preferentially inhibits COX-2 at lower doses, but at higher doses also inhibits the COX-1 enzyme (Ref).
Delayed hypersensitivity reactions: T-cell-mediated (Ref).
Onset:
Immediate hypersensitivity reactions: Rapid; occur within 1 hour of administration but may occur several hours after exposure (Ref).
Delayed hypersensitivity reactions (including SJS/TEN): Varied, generally occurs after 1 to 8 weeks after initiation (Ref), although time to onset with meloxicam may be 2 to 3 days (Ref).
Risk factors:
• Preferential COX-2 inhibitors (eg, meloxicam) are generally tolerated (especially in low to therapeutic doses) in patients with NERD (Ref) and in many patients with cutaneous reactions to NSAIDs (Ref); ~4% to 9% of NECD, NERD, and NIUA patients may develop reactions with meloxicam (Ref)
• Cross-reactions with meloxicam and other enolic acid derivatives (“oxicams”) NSAIDs (eg, piroxicam, tenoxicam) may occur (Ref)
Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with an increased risk of several kidney-specific effects: hemodynamically-mediated acute kidney injury (AKI), interstitial nephritis (with or without nephrotic syndrome), and renal papillary necrosis.
Hemodynamically-mediated AK): Hemodynamically-mediated AKI may occur following use of either cyclooxygenase (COX)-2 selective NSAIDs (ie, coxibs) or nonselective NSAIDs (Ref); the risk may be greater with nonselective NSAIDs, especially indomethacin (Ref). The risk of developing AKI is decreased upon discontinuation (Ref). In patients who develop AKI, kidney function is likely to return to baseline following prompt discontinuation of the offending NSAID and supportive care (Ref); however, the mechanism of the damage and other concurrent factors can contribute to irreversibility.
Acute interstitial nephritis (AIN) with or without nephrotic syndrome: Patients may develop NSAID-associated proteinuria combined with interstitial nephritis and varying degrees of kidney impairment; the “classic triad” of fever, rash, and eosinophilia is less commonly observed in NSAID-associated AIN than with antibiotic-induced AIN (Ref). In patients with concurrent nephrotic syndrome, kidney histology may reveal minimal change glomerulonephritis or membranous nephropathy (Ref). While use of meloxicam has been associated with this clinical picture (Ref); the risk may be greatest with fenoprofen as compared to other NSAIDS (Ref). Proteinuria generally improves within weeks following discontinuation; full recovery may require treatment and take up to a year (Ref).
Papillary necrosis: Chronic use of NSAIDs has resulted in the development of papillary necrosis which may occur in conjunction with chronic interstitial nephritis and progressive decline in glomerular filtration rate as a clinical syndrome known as analgesic nephropathy (Ref). However, controversy exists on the degree to which NSAID use increases the risk for chronic kidney disease and analgesic nephropathy (Ref). Acute papillary necrosis may occur following NSAID overdose, especially in a setting of severe dehydration or intravascular volume depletion (Ref).
Mechanism:
Hemodynamically-mediated AKI: Dose- and time-related; inhibition of COX-1 and COX-2 by NSAIDs results in a reduced production of nephroprotective prostaglandins and subsequent attenuation of renal vasodilation (Ref). In addition, an increase in vasoconstriction of the afferent arteriole and impaired renal blood flow causes a reduction in the glomerular capillary pressure and filtration (Ref).
AIN with or without nephrotic syndrome: Not clearly established. Following inhibition of COX-1 and COX-2 by NSAIDs, arachidonic acid is formed which may be further metabolized to leukotrienes via the lipoxygenase pathway; leukotrienes may increase vascular permeability within glomerular capillaries and peritubular capillaries and increase lymphocyte recruitment and activation (Ref).
Papillary necrosis: Time-related; exact mechanism is not clearly established; may be due to direct toxicity and/or inhibition of prostaglandin-mediated vasodilation resulting in ischemic necrosis (Ref).
Onset:
AKI: Rapid; may occur within days of treatment initiation (Ref).
AIN with or without nephrotic syndrome: Varied; mean time of onset of ~5 months (range: 2 weeks to 18 months) has been described following use of nonselective NSAIDs (Ref).
Risk factors:
• AKI:
- Preexisting kidney impairment
- Chronic kidney disease; Note: Higher cumulative doses may increase the risk for progression of chronic kidney disease (Ref)
- ≥65 years of age(Ref); Note: NSAID-associated AKI may also occur in pediatric patients, even at therapeutic doses (Ref)
• Hemodynamically-mediated AKI:
- Preexisting conditions which result in decreased effective arterial circulation (ie, conditions where renal blood flow/renal perfusion may be dependent on prostaglandin-mediated vasodilation) (Ref)
Volume depletion (eg, due to concomitant diuretic use, nausea, or vomiting)
Heart failure (Ref)
Cirrhosis and ascites (Ref)
Nephrotic syndrome
- Concomitant use of diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, or calcineurin inhibitors (Ref)
• AIN with or without nephrotic syndrome: Prior history of NSAID-induced nephrotic syndrome; recurrence has been described with a nonselective NSAID (Ref)
• Papillary necrosis (acute):
- Massive NSAID ingestion (Ref)
- Dehydration (Ref)
- Intravascular volume depletion (Ref)
• Papillary necrosis (chronic)/analgesic nephropathy: Chronic concomitant use of other analgesics (eg, aspirin, acetaminophen) (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
1% to 10%:
Cardiovascular: Acute myocardial infarction (<2%), angina pectoris (<2%), cardiac arrhythmia (<2%), edema (≤5%), heart failure (<2%), hypertension (<2%), hypotension (<2%), palpitations (<2%), presyncope (<2%), syncope (<2%), tachycardia (<2%), vasculitis (<2%)
Dermatologic: Alopecia (<2%), bullous rash (<2%), diaphoresis (<2%), ecchymoses (<2%), pruritus (<2%), skin photosensitivity (<2%), skin rash (<2%), urticaria (<2%)
Endocrine & metabolic: Albuminuria (<2%), dehydration (<2%), hot flash (<2%), hypokalemia (<2%), hypomagnesemia (<2%), weight gain (<2%), weight loss (<2%)
Gastrointestinal: Abdominal distention (<2%), abdominal distress (<2%), abdominal pain (≤3%; more common in pediatric patients), aphthous stomatitis (<2%), colitis (<2%), constipation (8%), diarrhea (≤8%; more common in pediatric patients), duodenal ulcer (<2%; duodenal ulcer with hemorrhage: <2%), dysgeusia (<2%), dyspepsia (6%), epigastric discomfort (<2%), eructation (<2%), esophagitis (<2%), flatulence (<2%), gastric ulcer (<2%; gastric ulcer with hemorrhage: <2%), gastritis (<2%), gastroenteritis (<2%), gastroesophageal reflux disease (<2%), gastrointestinal hemorrhage (<2%), gastrointestinal pain (<2%), gastrointestinal perforation (<2%; including duodenal, gastric), hematemesis (<2%), increased appetite (<2%), intestinal perforation (<2%), melena (<2%), nausea (2% to 4%), pancreatitis (<2%), rectal hemorrhage (<2%), xerostomia (<2%)
Genitourinary: Hematuria (<2%), pollakiuria (<2%), urinary retention (<2%)
Hematologic & oncologic: Anemia (2%) (table 1), leukopenia (<2%), neutropenia (<2%), prolonged bleeding time (<2%), purpuric disease (<2%), thrombocytopenia (<2%), thrombocytosis (<2%), wound hematoma (IV only: <2%)
|
Drug (Meloxicam) |
Placebo |
Dosage Form |
Number of Patients (Meloxicam) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
2% |
1% |
IV injection |
748 |
393 |
Hepatic: Abnormal hepatic function tests (<2%), hepatitis (<2%), hyperbilirubinemia (<2%), increased gamma-glutamyl transferase (≤3%), increased serum alanine aminotransferase (<2%), increased serum aspartate aminotransferase (<2%)
Hypersensitivity: Angioedema (<2%), facial edema (<2%), hypersensitivity reaction (<2%)
Local: Incision-site hemorrhage (IV only: <2%), infusion-site reaction (IV only: <2%), localized rash (IV only, infusion site: <2%)
Nervous system: Abnormal dreams (<2%), anxiety (<2%), asthenia (<2%), confusion (<2%), depression (<2%), disturbance in attention (<2%), dizziness (4%), drowsiness (<2%), falling (3%), fatigue (<2%), headache (2%; more common in pediatric patients), insomnia (<2%), malaise (<2%), migraine (<2%), nervousness (<2%), noncardiac chest pain (<2%), paresthesia (<2%), seizure (<2%), tremor (<2%), vertigo (<2%)
Neuromuscular & skeletal: Back pain (<2%), muscle spasm (<2%)
Ophthalmic: Visual disturbance (<2%)
Otic: Tinnitus (<2%)
Renal: Increased blood urea nitrogen (<2%), increased serum creatinine (<2%), renal failure syndrome (<2%)
Respiratory: Asthma (<2%), bronchospasm (<2%), dyspnea (<2%), epistaxis (<2%), flu-like symptoms (3% to 6%), pharyngitis (3%), upper respiratory tract infection (3% to 7%)
Miscellaneous: Accidental injury (3% to 5%), fever (<2%; more common in pediatric patients), wound dehiscence (<2%)
Frequency not defined:
Cardiovascular: Thrombosis
Gastrointestinal: Vomiting (more common in pediatric patients)
Nervous system: Cerebrovascular accident
Postmarketing:
Dermatologic: Erythema multiforme (Nikas 1999), exfoliative dermatitis, fixed drug eruption (Ozdemir 2011), Stevens-Johnson syndrome (Ishiguro 2020), toxic epidermal necrolysis (Nguyen 2019; Papay 2012)
Hematologic & oncologic: Agranulocytosis, hemorrhage (Kurien 2005)
Hepatic: Autoimmune hepatitis (Martínez-Odriozola 2010), cholestatic hepatitis (Schmeltzer 2016), hepatic failure, hepatotoxicity (idiosyncratic) (Chalasani 2021), jaundice (Staerkel 1999)
Hypersensitivity: Anaphylactic shock, anaphylaxis (Bavbek 2006), drug reaction with eosinophilia and systemic symptoms (Helmandollar 2018), nonimmune anaphylaxis
Nervous system: Mood changes
Renal: Interstitial nephritis, nephrotic syndrome (Vega 2012), renal papillary necrosis, renal tubular necrosis (Vega 2012)
Hypersensitivity to meloxicam or any component of the formulation; history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nonsteroidal anti-inflammatory drugs; use in the setting of coronary artery bypass graft surgery; phenylketonuria (orally disintegrating tablet only); moderate to severe renal insufficiency patients who are at risk for renal failure due to volume depletion (injection only).
Canadian labeling: Additional contraindications (not in US labeling): Pregnancy (third trimester); breastfeeding; severe uncontrolled heart failure; active or recent GI/gastric/duodenal/peptic ulceration/perforation; active GI bleeding; cerebrovascular bleeding or other bleeding disorders; inflammatory bowel disease (Crohn disease or ulcerative colitis); severe liver impairment or active liver disease; severe renal impairment (creatinine clearance [CrCl] <30 mL/minute or 0.5 mL/second) or deteriorating renal disease; known hyperkalemia; pediatric patients <18 years; rare hereditary conditions that may be incompatible with an excipient of the product.
Concerns related to adverse effects:
• CNS effects: May cause drowsiness, dizziness, blurred vision, and other neurologic effects that may impair physical or mental abilities; patients must be cautioned about performing tasks that require mental alertness (eg, operating machinery, driving).
• Hyperkalemia: Non-steroidal anti-inflammatory drug (NSAID) use may increase the risk of hyperkalemia, particularly in the elderly, diabetics, renal disease, and with concomitant use of other agents capable of inducing hyperkalemia (eg, ACE inhibitors). Monitor potassium closely.
• Ophthalmic effects: Blurred and/or diminished vision has been reported; discontinue use and refer for ophthalmologic evaluation if such symptoms occur.
Disease-related concerns:
• Asthma: Contraindicated in patients with aspirin-sensitive asthma; severe potentially fatal bronchospasm may occur. Use caution in patients with other forms of asthma.
• Bariatric surgery: Gastric ulceration: Avoid chronic use of oral nonselective NSAIDs after bariatric surgery; development of anastomotic ulcerations/perforations may occur (Bhangu 2014; Mechanick 2020). Short-term use of celecoxib or IV ketorolac are recommended as part of a multimodal pain management strategy for postoperative pain (Chou 2016; Horsley 2019; Thorell 2016).
• Hepatic impairment: Use with caution in patients with hepatic impairment; patients with hepatic impairment may require reduced doses due to extensive hepatic metabolism.
• Renal impairment: Use with caution in patients with renal impairment.
Special populations:
• CYP2C9 poor metabolizers: Poor metabolizers of CYP2C9 may require dose reduction.
Dosage form specific issues:
• Injection: Not indicated for long-term use. Onset of pain relief may be delayed up to several hours after administration; use of a non-NSAID analgesic with a rapid onset may be needed. Also, inadequate analgesia for the entire 24-hour dosing interval may be experienced; use of a short-acting, non-NSAID, IR analgesic may be required.
• Phenylalanine: Orally disintegrating tablet: May contain phenylalanine; use is contraindicated in patients with phenylketonuria.
Other warnings/precautions:
• Surgical/dental procedures: Withhold for at least 4 to 6 half-lives prior to surgical or dental procedures.
Qmiiz ODT has been discontinued in the United States for >1 year.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Capsule, Oral:
Vivlodex: 5 mg [DSC] [contains fd&c blue #2 (indigotine,indigo carmine), fd&c red #40 (allura red ac dye), fd&c yellow #6 (sunset yellow)]
Vivlodex: 10 mg [DSC] [contains carmine, fd&c blue #2 (indigotine,indigo carmine), fd&c red #40 (allura red ac dye), fd&c yellow #6 (sunset yellow)]
Generic: 5 mg, 10 mg
Injectable, Intravenous [preservative free]:
Anjeso: 30 mg/mL (1 mL [DSC])
Suspension, Oral:
Generic: 7.5 mg/5 mL (100 mL)
Tablet, Oral:
Mobic: 7.5 mg [DSC], 15 mg [DSC]
Generic: 7.5 mg, 15 mg, 15 mg
Tablet Disintegrating, Oral:
Qmiiz ODT: 7.5 mg [DSC], 15 mg [DSC] [contains aspartame]
May be product dependent
Capsules (Meloxicam Oral)
5 mg (per each): $31.05
10 mg (per each): $31.05
Suspension (Meloxicam Oral)
7.5 mg/5 mL (per mL): $11.31 - $12.58
Tablets (Meloxicam Oral)
7.5 mg (per each): $0.05 - $3.17
15 mg (per each): $0.06 - $4.85
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Generic: 7.5 mg, 15 mg
IV: Administer undiluted as an IV bolus over 15 seconds.
Oral: Administer with or without meals; administer with food or milk to minimize GI irritation.
Orally disintegrating tablet: Do not remove from blister until ready to administer. Using dry hands, peel backing off the blister; do not push tablet through foil. Remove tablet and immediately place in mouth or on tongue and allow to disintegrate. Swallow with saliva (with or without drinking liquid).
Suspension: Shake oral suspension gently prior to use.
Oral: May be taken with or without meals; administer with food or milk to minimize gastrointestinal irritation.
Orally disintegrating tablet (Qmiiz ODT): Children and Adolescents weighing ≥60 kg: Do not remove from blister until ready to administer. Using dry hands, peel backing off the blister; do not push tablet through foil. Remove tablet and immediately place in mouth or on tongue and allow to disintegrate. Swallow with saliva (with or without drinking liquid).
Suspension: Shake gently prior to use. Administer with an accurate measuring device (calibrated oral syringe or measuring cup); do not use a household teaspoon or tablespoon to measure dose (overdosage may occur). Administer with or without food.
An FDA-approved patient medication guide, which is available with the product information and as follows, must be dispensed with this medication:
Mobic oral suspension: https://www.accessdata.fda.gov/drugsatfda_docs/label/2021/021530s017lbl.pdf#page=16
Mobic tablets: https://www.accessdata.fda.gov/drugsatfda_docs/label/2021/020938s028lbl.pdf#page=16
NSAIDs: https://www.fda.gov/media/72932/download
Qmiiz ODT: https://www.accessdata.fda.gov/drugsatfda_docs/label/2021/211210s002lbl.pdf#page=37
IV:
Pain, acute: Management of moderate to severe pain in adults, alone or in combination with non–nonsteroidal anti-inflammatory drug analgesics.
Limitation of use: Because of delayed onset of analgesia, meloxicam alone is not recommended for use when rapid onset of analgesia is required.
Oral:
Osteoarthritis: Relief of the signs and symptoms of osteoarthritis; management of osteoarthritis pain.
Rheumatoid arthritis (orally disintegrating tablet [ODT], tablet, and suspension only): Relief of signs and symptoms of rheumatoid arthritis (RA); relief of the signs and symptoms of pauciarticular or polyarticular course juvenile RA in patients ≥2 years of age (suspension) and in patients weighing ≥60 kg (ODT, tablet).
Gout, treatment, acute flares
Beers Criteria: Meloxicam is identified in the Beers Criteria as a potentially inappropriate medication to be avoided for chronic use in patients 65 years and older (unless alternative agents ineffective and patient can receive concomitant gastroprotective agent) due to increased risk of GI bleeding and peptic ulcer disease in older adults in high risk category (eg, older than 75 years or receiving concomitant oral/parenteral corticosteroids, anticoagulants, or antiplatelet agents). In addition, avoid for short-term scheduled use in combination with oral/parenteral corticosteroids, anticoagulants, or antiplatelet agents unless alternatives are ineffective and patient can receive concomitant gastroprotective agent (Beers Criteria [AGS 2023]).
Substrate of CYP2C9 (major), CYP3A4 (minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
5-Aminosalicylic Acid Derivatives: Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of 5-Aminosalicylic Acid Derivatives. Risk C: Monitor therapy
Abrocitinib: Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the antiplatelet effect of Abrocitinib. Risk X: Avoid combination
Acalabrutinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Acemetacin: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Risk X: Avoid combination
Agents with Antiplatelet Properties (e.g., P2Y12 inhibitors, NSAIDs, SSRIs, etc.): May enhance the antiplatelet effect of other Agents with Antiplatelet Properties. Risk C: Monitor therapy
Alcohol (Ethyl): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Specifically, the risk of GI bleeding may be increased with this combination. Risk C: Monitor therapy
Aliskiren: Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Aliskiren. Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of Aliskiren. Risk C: Monitor therapy
Aminoglycosides: Nonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants. Risk C: Monitor therapy
Aminolevulinic Acid (Systemic): Photosensitizing Agents may enhance the photosensitizing effect of Aminolevulinic Acid (Systemic). Risk X: Avoid combination
Aminolevulinic Acid (Topical): Photosensitizing Agents may enhance the photosensitizing effect of Aminolevulinic Acid (Topical). Risk C: Monitor therapy
Anagrelide: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Angiotensin II Receptor Blockers: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Specifically, the combination may result in a significant decrease in renal function. Nonsteroidal Anti-Inflammatory Agents may diminish the therapeutic effect of Angiotensin II Receptor Blockers. The combination of these two agents may also significantly decrease glomerular filtration and renal function. Risk C: Monitor therapy
Angiotensin-Converting Enzyme Inhibitors: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Specifically, the combination may result in a significant decrease in renal function. Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy
Anticoagulants: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants. Risk C: Monitor therapy
Apixaban: Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the adverse/toxic effect of Apixaban. Specifically, the risk of bleeding may be increased. Management: A comprehensive risk to benefit assessment should be done for all patients before any concurrent use of apixaban and nonsteroidal anti-inflammatory drugs (NSAIDs). If combined, monitor patients extra closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Bemiparin: Nonsteroidal Anti-Inflammatory Agents may enhance the anticoagulant effect of Bemiparin. Management: Avoid concomitant use of bemiparin and nonsteroidal anti-inflammatory agents (NSAIDs) due to the increased risk of bleeding. If concomitant use is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Bemiparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Bemiparin. Management: Avoid concomitant use of bemiparin with antiplatelet agents. If concomitant use is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Beta-Blockers: Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Beta-Blockers. Risk C: Monitor therapy
Bile Acid Sequestrants: May decrease the absorption of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor therapy
Bisphosphonate Derivatives: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Bisphosphonate Derivatives. Both an increased risk of gastrointestinal ulceration and an increased risk of nephrotoxicity are of concern. Risk C: Monitor therapy
Calcium Polystyrene Sulfonate: Meloxicam may enhance the adverse/toxic effect of Calcium Polystyrene Sulfonate. More specifically, concomitant use of meloxicam oral suspension (which contains sorbitol) may increase the risk for intestinal necrosis. Risk X: Avoid combination
Caplacizumab: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Caplacizumab. Specifically, the risk of bleeding may be increased. Management: Avoid coadministration of caplacizumab with antiplatelets if possible. If coadministration is required, monitor closely for signs and symptoms of bleeding. Interrupt use of caplacizumab if clinically significant bleeding occurs. Risk D: Consider therapy modification
Cephalothin: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Cephalothin. Specifically, the risk for bleeding may be increased. Risk C: Monitor therapy
Collagenase (Systemic): Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Collagenase (Systemic). Specifically, the risk of injection site bruising and or bleeding may be increased. Risk C: Monitor therapy
Corticosteroids (Systemic): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Risk C: Monitor therapy
CycloSPORINE (Systemic): Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of CycloSPORINE (Systemic). Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of CycloSPORINE (Systemic). CycloSPORINE (Systemic) may increase the serum concentration of Nonsteroidal Anti-Inflammatory Agents. Management: Consider alternatives to nonsteroidal anti-inflammatory agents (NSAIDs). Monitor for evidence of nephrotoxicity, as well as increased serum cyclosporine concentrations and systemic effects (eg, hypertension) during concomitant therapy with NSAIDs. Risk D: Consider therapy modification
CYP2C9 Inhibitors (Moderate): May increase the serum concentration of Meloxicam. Risk C: Monitor therapy
Dabigatran Etexilate: Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the adverse/toxic effect of Dabigatran Etexilate. Specifically, the risk of bleeding may be increased. Management: A comprehensive risk to benefit assessment should be done for all patients before any concurrent use of dabigatran and nonsteroidal anti-inflammatory drugs (NSAIDs). If combined, monitor patients extra closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Dasatinib: May enhance the anticoagulant effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Deferasirox: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Risk C: Monitor therapy
Deoxycholic Acid: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Deoxycholic Acid. Specifically, the risk for bleeding or bruising in the treatment area may be increased. Risk C: Monitor therapy
Desmopressin: Nonsteroidal Anti-Inflammatory Agents may enhance the hyponatremic effect of Desmopressin. Risk C: Monitor therapy
Digoxin: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Digoxin. Risk C: Monitor therapy
Drospirenone-Containing Products: May enhance the hyperkalemic effect of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor therapy
Edoxaban: Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the adverse/toxic effect of Edoxaban. Specifically, the risk of bleeding may be increased. Management: A comprehensive risk to benefit assessment should be done for all patients before any concurrent use of edoxaban and nonsteroidal anti-inflammatory drugs (NSAIDs). If combined, monitor patients extra closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Enoxaparin: Nonsteroidal Anti-Inflammatory Agents may enhance the anticoagulant effect of Enoxaparin. Management: Discontinue nonsteroidal anti-inflammatory agents (NSAIDs) prior to initiating enoxaparin whenever possible. If concomitant administration is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Enoxaparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Enoxaparin. Management: Discontinue antiplatelet agents prior to initiating enoxaparin whenever possible. If concomitant administration is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Eplerenone: Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Eplerenone. Nonsteroidal Anti-Inflammatory Agents may enhance the hyperkalemic effect of Eplerenone. Risk C: Monitor therapy
Heparin: Nonsteroidal Anti-Inflammatory Agents may enhance the anticoagulant effect of Heparin. Management: Decrease the dose of heparin or nonsteroidal anti-inflammatory agents (NSAIDs) if coadministration is required. Risk D: Consider therapy modification
Heparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Heparin. Management: Decrease the dose of heparin or agents with antiplatelet properties if coadministration is required. Risk D: Consider therapy modification
Herbal Products with Anticoagulant/Antiplatelet Effects (eg, Alfalfa, Anise, Bilberry): May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Bleeding may occur. Risk C: Monitor therapy
Herbal Products with Anticoagulant/Antiplatelet Effects (eg, Alfalfa, Anise, Bilberry): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Bleeding may occur. Risk C: Monitor therapy
HydrALAZINE: Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of HydrALAZINE. Risk C: Monitor therapy
Ibritumomab Tiuxetan: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Ibritumomab Tiuxetan. Both agents may contribute to impaired platelet function and an increased risk of bleeding. Risk C: Monitor therapy
Ibrutinib: May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Icosapent Ethyl: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Inotersen: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Itraconazole: May decrease the serum concentration of Meloxicam. Risk C: Monitor therapy
Ketorolac (Nasal): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Risk X: Avoid combination
Ketorolac (Systemic): Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Ketorolac (Systemic). Risk X: Avoid combination
Lecanemab: May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Specifically, the risk of hemorrhage may be increased. Risk C: Monitor therapy
Limaprost: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Lipid Emulsion (Fish Oil Based): May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Lithium: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Lithium. Management: Consider reducing the lithium dose when initiating a NSAID. Monitor for increased lithium therapeutic/toxic effects if a NSAID is initiated/dose increased, or decreased effects if a NSAID is discontinued/dose decreased. Risk D: Consider therapy modification
Loop Diuretics: Nonsteroidal Anti-Inflammatory Agents may diminish the diuretic effect of Loop Diuretics. Loop Diuretics may enhance the nephrotoxic effect of Nonsteroidal Anti-Inflammatory Agents. Management: Monitor for evidence of kidney injury or decreased therapeutic effects of loop diuretics with concurrent use of an NSAID. Consider avoiding concurrent use in CHF or cirrhosis. Concomitant use of bumetanide with indomethacin is not recommended. Risk D: Consider therapy modification
Lumacaftor and Ivacaftor: May decrease the serum concentration of CYP2C9 Substrates (High Risk with Inhibitors or Inducers). Lumacaftor and Ivacaftor may increase the serum concentration of CYP2C9 Substrates (High Risk with Inhibitors or Inducers). Risk C: Monitor therapy
Macimorelin: Nonsteroidal Anti-Inflammatory Agents may diminish the diagnostic effect of Macimorelin. Risk X: Avoid combination
MetFORMIN: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of MetFORMIN. Risk C: Monitor therapy
Methotrexate: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Methotrexate. Management: Avoid coadministration of higher dose methotrexate (such as that used for the treatment of oncologic conditions) and NSAIDs. Use caution if coadministering lower dose methotrexate and NSAIDs. Risk D: Consider therapy modification
Methoxsalen (Systemic): Photosensitizing Agents may enhance the photosensitizing effect of Methoxsalen (Systemic). Risk C: Monitor therapy
Mifamurtide: Nonsteroidal Anti-Inflammatory Agents may diminish the therapeutic effect of Mifamurtide. Risk X: Avoid combination
Multivitamins/Fluoride (with ADE): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Multivitamins/Minerals (with ADEK, Folate, Iron): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Multivitamins/Minerals (with AE, No Iron): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Naftazone: May enhance the antiplatelet effect of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents: May enhance the adverse/toxic effect of other Nonsteroidal Anti-Inflammatory Agents. Specifically, the risk for gastrointestinal toxicity is increased. Risk X: Avoid combination
Nonsteroidal Anti-Inflammatory Agents (Topical): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Specifically, the risk of gastrointestinal (GI) toxicity is increased. Management: Coadministration of systemic nonsteroidal anti-inflammatory drugs (NSAIDs) and topical NSAIDs is not recommended. If systemic NSAIDs and topical NSAIDs, ensure the benefits outweigh the risks and monitor for increased NSAID toxicities. Risk D: Consider therapy modification
Obinutuzumab: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Obinutuzumab. Specifically, the risk of serious bleeding-related events may be increased. Risk C: Monitor therapy
Omacetaxine: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Omacetaxine. Specifically, the risk for bleeding-related events may be increased. Risk C: Monitor therapy
Omega-3 Fatty Acids: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Pentosan Polysulfate Sodium: May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Specifically, the risk of bleeding may be increased by concurrent use of these agents. Risk C: Monitor therapy
Pentoxifylline: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Phenylbutazone: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Risk X: Avoid combination
Pirtobrutinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Polyethylene Glycol-Electrolyte Solution: Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of Polyethylene Glycol-Electrolyte Solution. Risk C: Monitor therapy
Porfimer: Photosensitizing Agents may enhance the photosensitizing effect of Porfimer. Risk C: Monitor therapy
Potassium Salts: Nonsteroidal Anti-Inflammatory Agents may enhance the hyperkalemic effect of Potassium Salts. Risk C: Monitor therapy
Potassium-Sparing Diuretics: Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Potassium-Sparing Diuretics. Nonsteroidal Anti-Inflammatory Agents may enhance the hyperkalemic effect of Potassium-Sparing Diuretics. Risk C: Monitor therapy
PRALAtrexate: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of PRALAtrexate. More specifically, NSAIDS may decrease the renal excretion of pralatrexate. Management: Avoid coadministration of pralatrexate with nonsteroidal anti-inflammatory drugs (NSAIDs). If coadministration cannot be avoided, closely monitor for increased pralatrexate serum levels or toxicity. Risk D: Consider therapy modification
Probenecid: May increase the serum concentration of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor therapy
Prostacyclin Analogues: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Prostaglandins (Ophthalmic): Nonsteroidal Anti-Inflammatory Agents may diminish the therapeutic effect of Prostaglandins (Ophthalmic). Nonsteroidal Anti-Inflammatory Agents may also enhance the therapeutic effects of Prostaglandins (Ophthalmic). Risk C: Monitor therapy
Quinolones: Nonsteroidal Anti-Inflammatory Agents may enhance the neuroexcitatory and/or seizure-potentiating effect of Quinolones. Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Quinolones. Risk C: Monitor therapy
Rivaroxaban: Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the adverse/toxic effect of Rivaroxaban. Specifically, the risk of bleeding may be increased. Management: A comprehensive risk to benefit assessment should be done for all patients before any concurrent use of rivaroxaban and nonsteroidal anti-inflammatory drugs (NSAIDs). If combined, monitor patients extra closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Salicylates: Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the adverse/toxic effect of Salicylates. An increased risk of bleeding may be associated with use of this combination. Nonsteroidal Anti-Inflammatory Agents (Nonselective) may diminish the cardioprotective effect of Salicylates. Salicylates may decrease the serum concentration of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Management: Nonselective NSAIDs may reduce aspirin's cardioprotective effects. Administer ibuprofen 30-120 minutes after immediate-release aspirin, 2 to 4 hours after extended-release aspirin, or 8 hours before aspirin. Risk D: Consider therapy modification
Selective Serotonin Reuptake Inhibitors: May enhance the antiplatelet effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Nonsteroidal Anti-Inflammatory Agents (Nonselective) may diminish the therapeutic effect of Selective Serotonin Reuptake Inhibitors. Management: Consider alternatives to NSAIDs. Monitor for evidence of bleeding and diminished antidepressant effects. It is unclear whether COX-2-selective NSAIDs reduce risk. Risk D: Consider therapy modification
Selumetinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Serotonin/Norepinephrine Reuptake Inhibitors: May enhance the antiplatelet effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Risk C: Monitor therapy
Sincalide: Drugs that Affect Gallbladder Function may diminish the therapeutic effect of Sincalide. Management: Consider discontinuing drugs that may affect gallbladder motility prior to the use of sincalide to stimulate gallbladder contraction. Risk D: Consider therapy modification
Sodium Phosphates: May enhance the nephrotoxic effect of Nonsteroidal Anti-Inflammatory Agents. Specifically, the risk of acute phosphate nephropathy may be enhanced. Risk C: Monitor therapy
Sodium Polystyrene Sulfonate: Meloxicam may enhance the adverse/toxic effect of Sodium Polystyrene Sulfonate. More specifically, concomitant use of meloxicam oral suspension (which contains sorbitol) may increase the risk for intestinal necrosis. Risk X: Avoid combination
Tacrolimus (Systemic): Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of Tacrolimus (Systemic). Risk C: Monitor therapy
Tenofovir Products: Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of Tenofovir Products. Management: Seek alternatives to these combinations whenever possible. Avoid use of tenofovir with multiple NSAIDs or any NSAID given at a high dose due to a potential risk of acute renal failure. Diclofenac appears to confer the most risk. Risk D: Consider therapy modification
Tenoxicam: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Risk X: Avoid combination
Thiazide and Thiazide-Like Diuretics: May enhance the nephrotoxic effect of Nonsteroidal Anti-Inflammatory Agents. Nonsteroidal Anti-Inflammatory Agents may diminish the therapeutic effect of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor therapy
Thrombolytic Agents: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Thrombolytic Agents. Risk C: Monitor therapy
Tipranavir: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Tolperisone: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Tolperisone. Specifically, the risk of hypersensitivity reactions may be increased. Tolperisone may enhance the therapeutic effect of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor therapy
Tricyclic Antidepressants: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Specifically, the risk of major adverse cardiac events (MACE), hemorrhagic stroke, ischemic stroke, and heart failure may be increased. Tricyclic Antidepressants may enhance the antiplatelet effect of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor therapy
Urokinase: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Urokinase. Risk X: Avoid combination
Vancomycin: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Vancomycin. Risk C: Monitor therapy
Verteporfin: Photosensitizing Agents may enhance the photosensitizing effect of Verteporfin. Risk C: Monitor therapy
Vitamin E (Systemic): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Vitamin K Antagonists (eg, warfarin): Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the anticoagulant effect of Vitamin K Antagonists. Management: Consider alternatives to this combination when possible. If the combination must be used, monitor coagulation status closely and advise patients to promptly report any evidence of bleeding or bruising. Risk D: Consider therapy modification
Zanubrutinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Nonsteroidal anti-inflammatory drugs (NSAIDs) may delay or prevent rupture of ovarian follicles. This may be associated with infertility that is reversible upon discontinuation of the medication. Consider discontinuing use in patients having difficulty conceiving or those undergoing investigation of fertility.
Based on available information, NSAIDs can be continued in males with rheumatic and musculoskeletal diseases who are planning to father a child (ACR [Sammaritano 2020]).
The use of nonsteroidal anti-inflammatory drugs (NSAIDs) close to conception may be associated with an increased risk of miscarriage due to cyclooxygenase-2 inhibition interfering with implantation (Bermas 2014; Bloor 2013).
Birth defects have been observed following in utero NSAID exposure in some studies; however, data are conflicting (Bloor 2013). Nonteratogenic effects, including prenatal constriction of the ductus arteriosus, persistent pulmonary hypertension of the newborn, oligohydramnios, necrotizing enterocolitis, renal dysfunction or failure, and intracranial hemorrhage have been observed in the fetus/neonate following in utero NSAID exposure (Bermas 2014; Bloor 2013). Maternal NSAID use may cause fetal renal dysfunction leading to oligohydramnios. Although rare, this may occur as early as 20 weeks' gestation and is more likely to occur with prolonged maternal use. Oligohydramnios may be reversible following discontinuation of the NSAID (Dathe 2019; FDA 2020). In addition, nonclosure of the ductus arteriosus postnatally may occur and be resistant to medical management (Bermas 2014; Bloor 2013).
Maternal use of NSAIDs should be avoided beginning at 20 weeks' gestation. If NSAID use is necessary between 20 and 30 weeks' gestation, limit use to the lowest effective dose and shortest duration possible; consider ultrasound monitoring of amniotic fluid if treatment extends beyond 48 hours and discontinue the NSAID if oligohydramnios is found (FDA 2020). Because NSAIDs may cause premature closure of the ductus arteriosus, product labeling for meloxicam specifically states use should be avoided starting at 30 weeks' gestation.
Based on available information, NSAIDs can be continued during the first 2 trimesters of pregnancy in patients with rheumatic and musculoskeletal diseases; use in the third trimester is not recommended (ACR [Sammaritano 2020]).
It is not known if meloxicam is present in breast milk.
Nonopioid analgesics, including nonsteroidal anti-inflammatory drugs (NSAIDs), are preferred for breastfeeding patients who require pain control peripartum or for surgery outside of the postpartum period (ABM [Martin 2018]; ABM [Reece-Stremtan 2017]). NSAIDs are considered compatible for the treatment of rheumatic and musculoskeletal diseases in lactating patients; agents with a short half-life and established safety data in infants may be preferred (ACR [Sammaritano 2020]).
The manufacturer recommends that the decision to breastfeed during therapy consider the risk of infant exposure, the benefits of breastfeeding to the infant, and benefits of treatment to the mother. Maternal use of NSAIDs should be avoided if the breastfeeding infant has platelet dysfunction, thrombocytopenia, or a ductal-dependent cardiac lesion (ABM [Martin 2018]; ABM [Reece-Stremtan 2017]; Bloor 2013).
Oral: May be taken with food or milk to minimize GI irritation.
CBC and chemistry profile; periodic LFTs; renal function (urine output, serum BUN and creatinine); BP (baseline and periodically during therapy); signs of bleeding (occult or gross blood loss, especially in patients with coagulation disorders or who are receiving anticoagulants); monitor for anemia with long-term therapy; periodic ophthalmologic exam with long-term therapy; signs/symptoms of immediate or delayed hypersensitivity reactions.
Reversibly inhibits cyclooxygenase-1 and 2 (COX-1 and 2) enzymes, which results in decreased formation of prostaglandin precursors; has antipyretic, analgesic, and anti-inflammatory properties
Other proposed mechanisms not fully elucidated (and possibly contributing to the anti-inflammatory effect to varying degrees), include inhibiting chemotaxis, altering lymphocyte activity, inhibiting neutrophil aggregation/activation, and decreasing proinflammatory cytokine levels.
Distribution:
Children 2 to 6 years (n=7): Oral: Apparent Vd: Mean: 0.19 L/kg (Burgos-Vargas 2004).
Children and Adolescents 7 to 16 years (n=11): Oral: Apparent Vd: Mean: 0.13 L/kg (Burgos-Vargas 2004).
Adults: IV: Vz: 9.63 L; Oral: Vdss~10 L.
Protein binding: ~99%, primarily to albumin; Note: Free fraction was higher in adult patients with renal failure who were receiving chronic dialysis.
Metabolism: Hepatic via CYP2C9 and CYP3A4 (minor); forms 4 metabolites (inactive).
Bioavailability: 89% (capsule).
Half-life elimination:
Children 2 to 6 years (n=7): Oral: Mean: 13.4 hours (Burgos-Vargas 2004).
Children and Adolescents 7 to 16 years (n=11): Oral: Mean: 12.7 hours (Burgos-Vargas 2004).
Adults: IV: ~24 hours; Oral: ~15 to 22 hours.
Time to peak:
IV: 0.12 ± 0.04 hours.
Oral: Initial: Within 2 hours (capsule); 4 to 5 hours (tablet); 4 to 12 hours (orally disintegrating tablet; prolonged with food); ~7 hours (suspension; following a high-fat meal [75 g of fat]); Secondary: ~8 hours (capsule); 12 to 14 hours (tablet).
Excretion: Urine (predominantly as inactive metabolites; <1% unchanged drug); feces (predominantly as inactive metabolites; 1.6% as unchanged drug).
Clearance: Oral:
Children 2 to 6 years (n=7): Mean: 0.17 mL/minute/kg (Burgos-Vargas 2004).
Children and Adolescents 7 to 16 years (n=11): Mean: 0.12 mL/minute/kg (Burgos-Vargas 2004).
Adults: 7 to 9 mL/minute.
Altered kidney function:
IV: Cmax and AUC increased 5% and 7%, respectively, in elderly subjects with mild renal impairment (eGFR 60 to 90 mL/minute/1.73 m2) compared to young healthy controls.
Oral: Meloxicam plasma concentration is decreased and total clearance increased in patients with renal impairment.
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