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Celecoxib

Pronunciation

Pronunciation

(se le KOKS ib)

Dosage Forms

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Capsule, Oral:

CeleBREX: 50 mg, 100 mg, 200 mg, 400 mg

Generic: 50 mg, 100 mg, 200 mg, 400 mg

Brand Names: U.S.

  • CeleBREX

Pharmacologic Category

  • Analgesic, Nonopioid
  • Nonsteroidal Anti-inflammatory Drug (NSAID), COX-2 Selective

Pharmacology

Inhibits prostaglandin synthesis by decreasing the activity of the enzyme, cyclooxygenase-2 (COX-2), which results in decreased formation of prostaglandin precursors; has antipyretic, analgesic, and anti-inflammatory properties. Celecoxib does not inhibit cyclooxygenase-1 (COX-1) at therapeutic concentrations.

Absorption

Prolonged due to low solubility

Distribution

Vd (apparent): Children and Adolescents ~7-16 years (steady-state): 8.3 ± 5.8 L/kg (Stempak 2002); Adults: ~400 L

Metabolism

Hepatic via CYP2C9; forms inactive metabolites (a primary alcohol, corresponding carboxylic acid, and its glucuronide conjugate)

Excretion

Feces (~57% as metabolites, <3% as unchanged drug); urine (27% as metabolites, <3% as unchanged drug); primary metabolites in feces and urine: Carboxylic acid metabolite (73% of dose); low amounts of glucuronide metabolite appear in urine

Time to Peak

Children: Median: 3 hours (range: 1-5.8 hours) (Stempak 2002); Adults: ~3 hours

Half-Life Elimination

Children and Adolescents ~7-16 years (steady-state): 6 ± 2.7 hours (range: 3-10 hours) (Stempak 2002); Adults: ~11 hours (fasted)

Protein Binding

~97% primarily to albumin; binds to alpha1-acid glycoprotein to a lesser extent

Special Populations: Renal Function Impairment

AUC is approximately 40% lower in patients with a CrCl of 35 to 60 mL/minute.

Special Populations: Hepatic Function Impairment

AUC is increased approximately 40% in patients with mild impairment and 180% in patients with moderate impairment.

Special Populations: Elderly

Cmax is 40% higher and AUC is 50% higher.

Special Populations: Children

10 and 25 kg children have 40% and 24% lower clearance, respectively, compared with a 70 kg adult.

Special Populations: Race

AUC is approximately 40% higher in black compared with white patients.

Use: Labeled Indications

Acute pain: Management of acute pain.

Ankylosing spondylitis: Relief of the signs/symptoms of ankylosing spondylitis.

Juvenile idiopathic arthritis: Relief of the signs/symptoms of juvenile idiopathic arthritis (JIA) in patients 2 years and older.

Osteoarthritis: Relief of the signs/symptoms of osteoarthritis.

Primary dysmenorrhea: Treatment of primary dysmenorrhea.

Rheumatoid arthritis: Relief of the signs/symptoms of rheumatoid arthritis.

Use: Unlabeled

Relief of the signs and symptoms of acute gout

Contraindications

Hypersensitivity to celecoxib, sulfonamides, aspirin, other NSAIDs, or any component of the formulation; patients who have experienced asthma, urticaria, or allergic-type reactions after taking aspirin or other NSAIDs; use in the setting of CABG surgery.

Note: Although the FDA approved product labeling states this medication is contraindicated with other sulfonamide-containing drug classes, the scientific basis of this statement has been challenged. See “Warnings/Precautions” for more detail.

Canadian labeling: Additional contraindications (not in US labeling): Pregnancy (third trimester); women who are breast-feeding; severe, uncontrolled heart failure; active gastrointestinal ulcer (gastric, duodenal, peptic); inflammatory bowel disease; cerebrovascular bleeding; severe liver impairment or active hepatic disease; severe renal impairment (CrCl <30 mL/minute) or deteriorating renal disease; known hyperkalemia; use in patients <18 years of age

Dosing: Adult

Note: Use the lowest effective dose for the shortest duration of time, consistent with individual patient treatment goals.

Acute pain or primary dysmenorrhea: Oral: Initial dose: 400 mg, followed by an additional 200 mg if needed on day 1; maintenance dose: 200 mg twice daily as needed

Canadian labeling; Recommended maximum dose for treatment of acute pain: 400 mg/day up to 7 days

Ankylosing spondylitis: Oral: 200 mg once daily or 100 mg twice daily; if no effect after 6 weeks, may increase to 400 mg/day. If no response following 6 weeks of treatment with 400 mg/day, consider discontinuation and alternative treatment.

Canadian labeling; Recommended maximum dose: 200 mg/day

Osteoarthritis: Oral: 200 mg once daily or 100 mg twice daily

Rheumatoid arthritis: Oral: 100 to 200 mg twice daily

Acute gout (off-label use): 800 mg once followed by 400 mg on day 1; then 400 mg twice daily for one week (ACR guidelines [Khanna, 2012]; Schumacker, 2012)

Dosing adjustment in poor CYP2C9 metabolizers (ie, CYP2C9*3/*3): Reduce initial dose by 50%; consider alternative treatment in patients with JIA who are poor CYP2C9 metabolizers.

Canadian labeling: Recommended maximum dose: 100 mg/day.

Dosing: Geriatric

Initiate at the lowest recommended dose. The AUC in elderly patients (especially females and patients weighing <50 kg) may be increased by 50% compared with younger subjects.

Dosing: Pediatric

Note: Use the lowest effective dose for the shortest duration of time, consistent with individual patient treatment goals. Use in patients <18 years of age is not approved in the Canadian labeling.

Juvenile idiopathic arthritis (JIA): Oral: Children ≥2 years:

≥10 kg to ≤25 kg: 50 mg twice daily

>25 kg: 100 mg twice daily

Dosing adjustment in poor CYP2C9 metabolizers (eg, CYP2C9*3/*3): Consider alternative therapy.

Dosing: Renal Impairment

US labeling:

Mild or moderate impairment: There are no dosage adjustments provided in the manufacturer’s labeling; AUC was ~40% lower in patients with chronic renal insufficiency (GFR 35 to 60 mL/minute) compared with subjects with normal renal function.

Severe impairment: Use is not recommended.

Advanced renal disease: Use is not recommended; however, if celecoxib treatment cannot be avoided, monitor renal function closely.

Abnormal renal function tests (persistent or worsening): Discontinue use.

Canadian labeling:

CrCl ≥30 mL/minute: No dosage adjustment necessary.

CrCl <30 mL/minute: Use is contraindicated.

Abnormal renal function tests (persistent or worsening): Discontinue use.

Dosing: Hepatic Impairment

Mild impairment (Child-Pugh class A):

US labeling: No dosage adjustment necessary; AUC increased ~40% in mild hepatic impairment compared with healthy subjects.

Canadian labeling: Initiate at the lowest dose.

Moderate impairment (Child-Pugh class B): Reduce dose by 50%.

Severe impairment (Child-Pugh class C):

US labeling: Use is not recommended.

Canadian labeling: Use is contraindicated.

Abnormal liver function tests (persistent or worsening): Discontinue use.

Administration

May be administered without regard to meals. Capsules may be swallowed whole or the entire contents emptied onto a teaspoon of cool or room temperature applesauce and administered immediately with water. The contents of the capsules sprinkled onto applesauce may be stored under refrigeration for up to 6 hours.

Storage

Store at 20°C to 25°C (68°F to 77°F); excursions permitted to 15°C to 30°C (59°F to 86°F).

Drug Interactions

5-ASA Derivatives: Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of 5-ASA Derivatives. Monitor therapy

ACE 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 ACE Inhibitors. Monitor therapy

Ajmaline: Sulfonamides may enhance the adverse/toxic effect of Ajmaline. Specifically, the risk for cholestasis may be increased. 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. 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. Management: Monitor renal function periodically in patients receiving aliskiren and any nonsteroidal anti-inflammatory agent. Patients at elevated risk of renal dysfunction include those who are elderly, are volume depleted, or have pre-existing renal dysfunction. Monitor therapy

Aminoglycosides: Nonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants. Monitor therapy

Aminolevulinic Acid: Photosensitizing Agents may enhance the photosensitizing effect of Aminolevulinic Acid. Monitor therapy

Amodiaquine: CYP2C8 Inhibitors may increase the serum concentration of Amodiaquine. Avoid combination

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. Monitor therapy

Anticoagulants: Nonsteroidal Anti-Inflammatory Agents may enhance the anticoagulant effect of Anticoagulants. Monitor therapy

Antidepressants (Tricyclic, Tertiary Amine): May enhance the antiplatelet effect of NSAID (COX-2 Inhibitor). Monitor therapy

ARIPiprazole: CYP2D6 Inhibitors (Weak) may increase the serum concentration of ARIPiprazole. Management: Monitor for increased aripiprazole pharmacologic effects. Aripiprazole dose adjustments may or may not be required based on concomitant therapy and/or indication. Consult full interaction monograph for specific recommendations. Monitor therapy

Aspirin: May enhance the adverse/toxic effect of NSAID (COX-2 Inhibitor). Management: Concurrent use of aspirin at doses beyond cardioprotective levels is not recommended. While concurrent use of low-dose aspirin with a COX-2 inhibitor is permissable, patients should be monitored closely for signs/symptoms of GI ulceration/bleeding. Consider therapy modification

Beta-Blockers: Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Beta-Blockers. Exceptions: Levobunolol; Metipranolol. Monitor therapy

Bile Acid Sequestrants: May decrease the absorption of Nonsteroidal Anti-Inflammatory Agents. Consider therapy modification

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. Monitor therapy

Ceritinib: May increase the serum concentration of CYP2C9 Substrates. Management: Concurrent use of ceritinib with a CYP2C9 substrate that has a narrow therapeutic index (e.g., warfarin, phenytoin) should be avoided when possible. Monitor therapy

Corticosteroids (Systemic): May enhance the adverse/toxic effect of NSAID (COX-2 Inhibitor). 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. Specifically, elevated diclofenac concentrations have been reported. Management: Consider alternatives to nonsteroidal anti-inflammatory agents (NSAIDs). Monitor for evidence of nephrotoxicity, as well as increased serum cyclosporine concentrations and systemic effects (e.g., hypertension) during concomitant therapy with NSAIDs. Consider therapy modification

CYP2C8 Substrates: CYP2C8 Inhibitors (Moderate) may decrease the metabolism of CYP2C8 Substrates. Monitor therapy

CYP2C9 Inducers (Strong): May increase the metabolism of CYP2C9 Substrates. Management: Consider an alternative for one of the interacting drugs. Some combinations may be specifically contraindicated. Consult appropriate manufacturer labeling. Consider therapy modification

CYP2C9 Inhibitors (Moderate): May decrease the metabolism of CYP2C9 Substrates. Monitor therapy

CYP2C9 Inhibitors (Strong): May decrease the metabolism of CYP2C9 Substrates. Consider therapy modification

Dabrafenib: May decrease the serum concentration of CYP2C9 Substrates. Management: Seek alternatives to the CYP2C9 substrate when possible. If concomitant therapy cannot be avoided, monitor clinical effects of the substrate closely (particularly therapeutic effects). Consider therapy modification

Dapsone (Topical): May enhance the adverse/toxic effect of Methemoglobinemia Associated Agents. 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. Monitor therapy

Desmopressin: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Desmopressin. Monitor therapy

Dexketoprofen: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Avoid combination

Digoxin: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Digoxin. Monitor therapy

Drospirenone: Nonsteroidal Anti-Inflammatory Agents may enhance the hyperkalemic effect of Drospirenone. Monitor therapy

Enzalutamide: May decrease the serum concentration of CYP2C9 Substrates. Management: Concurrent use of enzalutamide with CYP2C9 substrates that have a narrow therapeutic index should be avoided. Use of enzalutamide and any other CYP2C9 substrate should be performed with caution and close monitoring. 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. Monitor therapy

Estrogen Derivatives: NSAID (COX-2 Inhibitor) may enhance the thrombogenic effect of Estrogen Derivatives. NSAID (COX-2 Inhibitor) may increase the serum concentration of Estrogen Derivatives. Monitor therapy

Floctafenine: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Avoid combination

Haloperidol: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Haloperidol. Specifically including drowsiness and confusion. Monitor therapy

Herbs (Anticoagulant/Antiplatelet Properties) (eg, Alfalfa, Anise, Bilberry): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Bleeding may occur. Management: Concomitant treatment with these agents should generally be avoided. If used concomitantly, increased diligence in monitoring for adverse effects (eg, bleeding, bruising, altered mental status due to CNS bleeds) must be employed. Consider therapy modification

HydrALAZINE: Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of HydrALAZINE. Monitor therapy

Ketorolac (Nasal): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Avoid combination

Ketorolac (Systemic): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Avoid combination

Lithium: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Lithium. 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. Consider therapy modification

Lumacaftor: May decrease the serum concentration of CYP2C9 Substrates. Lumacaftor may increase the serum concentration of CYP2C9 Substrates. Monitor therapy

Mecamylamine: Sulfonamides may enhance the adverse/toxic effect of Mecamylamine. Avoid combination

Methotrexate: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Methotrexate. Management: Alternative anti-inflammatory therapy should be considered whenever possible, especially if the patient is receiving higher, antineoplastic doses of methotrexate. Consider therapy modification

MiFEPRIStone: May increase the serum concentration of CYP2C9 Substrates. Management: Use CYP2C9 substrates at the lowest recommended dose, and monitor closely for adverse effects, during and in the 2 weeks following mifepristone treatment. Consider therapy modification

Morniflumate: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Avoid combination

Naftazone: May enhance the antiplatelet effect of Nonsteroidal Anti-Inflammatory Agents. Monitor therapy

Nitric Oxide: May enhance the adverse/toxic effect of Methemoglobinemia Associated Agents. Combinations of these agents may increase the likelihood of significant methemoglobinemia. Management: Monitor patients for signs of methemoglobinemia (e.g., hypoxia, cyanosis) when nitric oxide is used in combination with other agents associated with development of methemoglobinemia. Avoid lidocaine/prilocaine. Monitor therapy

Nonsteroidal Anti-Inflammatory Agents: May enhance the adverse/toxic effect of NSAID (COX-2 Inhibitor). Avoid combination

NSAID (COX-2 Inhibitor): Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of NSAID (COX-2 Inhibitor). Avoid combination

Omacetaxine: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Omacetaxine. Specifically, the risk for bleeding-related events may be increased. Management: Avoid concurrent use of nonsteroidal antiinflammatory drugs (NSAIDs) with omacetaxine in patients with a platelet count of less than 50,000/uL. Avoid combination

Perhexiline: CYP2D6 Inhibitors (Weak) may increase the serum concentration of Perhexiline. Monitor therapy

Porfimer: Photosensitizing Agents may enhance the photosensitizing effect of Porfimer. 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. 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: Closely monitor for increased pralatrexate serum levels and/or toxicity if used concomitantly with an NSAID. Monitor for decreased pralatrexate serum levels with NSAID discontinuation. Monitor therapy

Prilocaine: Methemoglobinemia Associated Agents may enhance the adverse/toxic effect of Prilocaine. Combinations of these agents may increase the likelihood of significant methemoglobinemia. Management: Monitor patients for signs of methemoglobinemia (e.g., hypoxia, cyanosis) when prilocaine is used in combination with other agents associated with development of methemoglobinemia. Avoid lidocaine/prilocaine in infants receiving such agents. Monitor therapy

Probenecid: May increase the serum concentration of Nonsteroidal Anti-Inflammatory Agents. 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). Monitor therapy

Quinolone Antibiotics: Nonsteroidal Anti-Inflammatory Agents may enhance the neuroexcitatory and/or seizure-potentiating effect of Quinolone Antibiotics. Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Quinolone Antibiotics. Monitor therapy

Selective Serotonin Reuptake Inhibitors: May enhance the antiplatelet effect of NSAID (COX-2 Inhibitor). NSAID (COX-2 Inhibitor) may diminish the therapeutic effect of Selective Serotonin Reuptake Inhibitors. Monitor therapy

Sodium Nitrite: Methemoglobinemia Associated Agents may enhance the adverse/toxic effect of Sodium Nitrite. Combinations of these agents may increase the likelihood of significant methemoglobinemia. Monitor therapy

Sodium Phosphates: May enhance the nephrotoxic effect of Nonsteroidal Anti-Inflammatory Agents. Specifically, the risk of acute phosphate nephropathy may be enhanced. Management: Consider avoiding this combination by temporarily suspending treatment with NSAIDs, or seeking alternatives to oral sodium phosphate bowel preparation. If the combination cannot be avoided, maintain adequate hydration and monitor renal function closely. Consider therapy modification

Tacrolimus (Systemic): Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of Tacrolimus (Systemic). Monitor therapy

Talniflumate: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Avoid combination

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. Consider therapy modification

Tenoxicam: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Avoid combination

Tetracaine (Topical): May enhance the adverse/toxic effect of Methemoglobinemia Associated Agents. Monitor therapy

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. Monitor therapy

Treprostinil: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Bleeding may occur. Monitor therapy

Triflusal: Nonsteroidal Anti-Inflammatory Agents may decrease the protein binding of Triflusal. Specifically, NSAIDs may decrease protein binding of the active Triflusal metabolite. Triflusal may decrease the protein binding of Nonsteroidal Anti-Inflammatory Agents. Monitor therapy

Vancomycin: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Vancomycin. Monitor therapy

Verteporfin: Photosensitizing Agents may enhance the photosensitizing effect of Verteporfin. Monitor therapy

Vitamin K Antagonists (eg, warfarin): NSAID (COX-2 Inhibitor) may enhance the anticoagulant effect of Vitamin K Antagonists. NSAID (COX-2 Inhibitor) may increase the serum concentration of Vitamin K Antagonists. Monitor therapy

Adverse Reactions

≥2%:

Cardiovascular: Peripheral edema

Central nervous system: Dizziness, headache, insomnia

Dermatologic: Skin rash

Gastrointestinal: Abdominal pain, diarrhea, dyspepsia, flatulence, nausea, vomiting

Neuromuscular & skeletal: Arthralgia, back pain

Respiratory: Cough, nasopharyngitis, pharyngitis, rhinitis, sinusitis, upper respiratory tract infection

Miscellaneous: Fever

0.1% to 1.9%:

Cardiovascular: Angina pectoris, aortic insufficiency, chest pain, coronary artery disease, edema, facial edema, hypertension (aggravated), myocardial infarction, palpitations, sinus bradycardia, tachycardia, ventricular hypertrophy

Central nervous system: Anxiety, depression, drowsiness, fatigue, hypertonia, hypoesthesia, migraine, nervousness, pain, paresthesia, vertigo

Dermatologic: Alopecia, cellulitis, dermatitis, diaphoresis, erythematous rash, maculopapular rash, pruritus, skin photosensitivity, urticaria, xeroderma

Endocrine & metabolic: Albuminuria, decreased plasma testosterone, hot flash, hypercholesterolemia, hyperglycemia, hypokalemia, increased nonprotein nitrogen, ovarian cyst, weight gain

Gastrointestinal: Anorexia, constipation, diverticulitis, dysphagia, eructation, esophagitis, gastritis, gastroenteritis, gastroesophageal reflux disease, gastrointestinal ulcer, hemorrhoids, hiatal hernia, increased appetite, melena, stomatitis, tenesmus, xerostomia

Genitourinary: Cystitis, dysuria, hematuria, urinary frequency

Hematologic & oncologic: Anemia, bruise, thrombocythemia

Hepatic: Increased serum alkaline phosphatase, increased serum transaminases

Hypersensitivity: Hypersensitivity exacerbation, hypersensitivity reaction

Neuromuscular & skeletal: Increased creatine phosphokinase, leg cramps, myalgia, osteoarthritis, synovitis, tendonitis

Ophthalmic: Conjunctival hemorrhage, vitreous opacity

Otic: Deafness, labyrinthitis, tinnitus

Renal: Increased blood urea nitrogen, increased serum creatinine, nephrolithiasis

Respiratory: Bronchitis, bronchospasm, dyspnea, epistaxis, flu-like symptoms, laryngitis, pneumonia

Miscellaneous: Cyst

<0.1% (Limited to important or life-threatening): Acute renal failure, agranulocytosis, anaphylactoid reaction, angioedema, anosmia, aplastic anemia, aseptic meningitis, cardiac failure, cerebrovascular accident, cholelithiasis, colitis, deep vein thrombosis, dysgeusia, erythema multiforme, esophageal perforation, exfoliative dermatitis, gangrene of skin or other tissue, gastrointestinal hemorrhage, hepatic failure, hepatic necrosis, hepatitis (including fulminant), hypoglycemia, hyponatremia, interstitial nephritis, intestinal obstruction, intestinal perforation, intracranial hemorrhage, jaundice, leukopenia, pancreatitis, pancytopenia, pulmonary embolism, renal papillary necrosis, sepsis, Stevens-Johnson syndrome, syncope, thrombocytopenia, thrombophlebitis, toxic epidermal necrolysis, vasculitis, ventricular fibrillation

ALERT: U.S. Boxed Warning

Serious cardiovascular risk:

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 the treatment and may increase with duration of use.

Celecoxib is contraindicated in the setting of coronary artery bypass graft (CABG) surgery.

Serious gastrointestinal risk:

NSAIDs cause an increased risk of serious gastrointestinal (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 higher risk for serious GI events.

Warnings/Precautions

Concerns related to adverse effects:

• Anaphylactoid reactions: Even in patients without prior exposure, anaphylactic reactions and angioedema may occur; patients with "aspirin triad" (bronchial asthma, aspirin intolerance, rhinitis) may be at increased risk. Contraindicated in patients who have experienced an anaphylactic reaction with NSAID or aspirin therapy.

• Cardiovascular events: [US Boxed Warning]: NSAIDs cause an increased risk of serious (and potentially fatal) adverse cardiovascular thrombotic events, including MI and stroke. Risk may occur early during treatment and may increase with duration of use. Relative risk appears to be similar in those with and without known cardiovascular disease or risk factors for cardiovascular disease; however, absolute incidence of cardiovascular events (which may occur early during treatment) was higher in patients with known cardiovascular disease or risk factors. New onset hypertension or exacerbation of hypertension may occur (NSAIDs may also impair response to ACE inhibitors, thiazide diuretics, or loop diuretics); may contribute to cardiovascular events; monitor blood pressure; use with caution in patients with hypertension. May cause sodium and fluid retention, use with caution in patients with edema. Avoid use in patients with heart failure (ACCF/AHA [Yancy, 2013]). Avoid use in patients with recent MI unless benefits outweigh risk of cardiovascular thrombotic events. Long-term cardiovascular risk in children has not been evaluated. Use the lowest effective dose for the shortest duration of time, consistent with individual patient goals, to reduce risk of cardiovascular events; alternate therapies should be considered for patients at high risk.

• Gastrointestinal events: [US Boxed Warning]: NSAIDs cause an increased risk of serious gastrointestinal inflammation, ulceration, bleeding, and perforation (may be fatal); elderly patients and patients with history of peptic ulcer disease and/or GI bleeding are at greater risk for serious GI events. These events may occur at any time during therapy and without warning. Avoid use in patients with active GI bleeding. Use caution with a history of GI ulcers, concurrent therapy known to increase the risk of GI bleeding (eg, aspirin, anticoagulants and/or corticosteroids, selective serotonin reuptake inhibitors), smoking, use of alcohol, or in elderly or debilitated patients. Use the lowest effective dose for the shortest duration of time, consistent with individual patient goals, to reduce risk of GI adverse events; alternate therapies should be considered for patients at high risk. When used concomitantly with aspirin, a substantial increase in the risk of gastrointestinal complications (eg, ulcer) occurs; concomitant gastroprotective therapy (eg, proton pump inhibitors) is recommended (Bhatt 2008).

• Hematologic effects: Anemia may occur; monitor hemoglobin or hematocrit in patients on long-term treatment. Celecoxib does not usually affect PT, PTT or platelet counts; does not inhibit platelet aggregation at approved doses.

• Skin reactions: NSAIDs may cause serious skin adverse events including exfoliative dermatitis, Stevens-Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN); may occur without warning and in patients without prior known sulfa allergy; discontinue use at first sign of rash (or any other hypersensitivity).

• Sulfonamide (“sulfa”) allergy: The FDA-approved product labeling for many medications containing a sulfonamide chemical group includes a broad contraindication in patients with a prior allergic reaction to sulfonamides. There is a potential for cross-reactivity between members of a specific class (eg, two antibiotic sulfonamides). However, concerns for cross-reactivity have previously extended to all compounds containing the sulfonamide structure (SO2NH2). An expanded understanding of allergic mechanisms indicates cross-reactivity between antibiotic sulfonamides and nonantibiotic sulfonamides may not occur or at the very least this potential is extremely low (Brackett 2004; Johnson 2005; Slatore 2004; Tornero 2004). In particular, mechanisms of cross-reaction due to antibody production (anaphylaxis) are unlikely to occur with nonantibiotic sulfonamides. T-cell-mediated (type IV) reactions (eg, maculopapular rash) are less well understood and it is not possible to completely exclude this potential based on current insights. In cases where prior reactions were severe (Stevens-Johnson syndrome/TEN), some clinicians choose to avoid exposure to these classes.

Disease-related concerns:

• Asthma: The manufacturer’s labeling states to not administer to patients with aspirin-sensitive asthma due to severe and potentially fatal bronchospasm that has been reported in such patients having received aspirin and the potential for cross reactivity with other NSAIDs. The manufacturer also states to use with caution in patients with other forms of asthma. However, in patients with known aspirin-exacerbated respiratory disease (AERD), the use of celecoxib initiated at a low dose with gradual titration in patients with stable, mild to moderate persistent asthma has been used without incident (Morales, 2013).

• Coronary artery bypass graft surgery: [US Boxed Warning]: Celecoxib is contraindicated in the setting of coronary artery bypass graft surgery (CABG). Risk of MI and stroke may be increased with use following CABG surgery.

• Cytochrome P450 isoenzyme 2C9 deficiency: Use with caution in patients with known or suspected deficiency of cytochrome P450 isoenzyme 2C9; poor metabolizers may have higher plasma levels due to reduced metabolism; consider reduced initial doses. Alternate therapies should be considered in patients with JIA who are poor metabolizers of CYP2C9.

• Hepatic impairment: Use with caution in patients with moderate hepatic impairment; dosage adjustment recommended. Not recommended for patients with severe hepatic impairment. Transaminase elevations have been reported with use; closely monitor patients with any abnormal LFT. Rare (sometimes fatal), severe hepatic reactions (eg, fulminant hepatitis, hepatic necrosis, hepatic failure) have occurred with NSAID use; discontinue if signs or symptoms of liver disease develop, if systemic manifestations occur, or with persistent or worsening abnormal hepatic function tests.

• Renal impairment: NSAID use may compromise existing renal function. Dose-dependent decreases in prostaglandin synthesis may result from NSAID use, causing a reduction in renal blood flow which may cause renal decompensation (usually reversible). Patients with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction, those taking diuretics, ACE inhibitors, angiotensin II receptor blockers, and the elderly are at greater risk for renal toxicity. Rehydrate patient before starting therapy; monitor renal function closely. Avoid use in patients with advanced renal disease; discontinue use with persistent or worsening abnormal renal function tests. Long-term NSAID use may result in renal papillary necrosis.

Concurrent drug therapy issues:

• Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information.

Special populations:

• Pediatric: Use with caution in pediatric patients with systemic-onset juvenile idiopathic arthritis (JIA); serious adverse reactions, including disseminated intravascular coagulation, may occur. The Canadian labeling contraindicates use in patients <18 years of age.

Monitoring Parameters

CBC; hemoglobin/hematocrit (anemic patients); basic metabolic panel; occult blood loss and periodic liver function tests; monitor renal function (urine output, serum BUN and creatinine); monitor response (pain, range of motion, grip strength, mobility, ADL function), inflammation; blood pressure (baseline and during treatment); observe for weight gain, edema; observe for bleeding, bruising; evaluate gastrointestinal effects (abdominal pain, bleeding, dyspepsia)

JIA: Monitor for development of abnormal coagulation tests with systemic onset JIA

Pregnancy Risk Factor

C (prior to 30 weeks gestation)/D (≥30 weeks gestation)

Pregnancy Considerations

Teratogenic effects have been observed in some animal studies; therefore, celecoxib is classified as pregnancy category C. Celecoxib is a NSAID that primarily inhibits COX-2 whereas other currently available NSAIDs are nonselective for COX-1 and COX-2. The effects of this selective inhibition to the fetus have not been well studied and limited information is available specific to celecoxib. NSAID exposure during the first trimester is not strongly associated with congenital malformations; however, cardiovascular anomalies and cleft palate have been observed following NSAID exposure in some studies. The use of a NSAID close to conception may be associated with an increased risk of miscarriage. Nonteratogenic effects have been observed following NSAID administration during the third trimester including: Myocardial degenerative changes, prenatal constriction of the ductus arteriosus, fetal tricuspid regurgitation, failure of the ductus arteriosus to close postnatally; renal dysfunction or failure, oligohydramnios; gastrointestinal bleeding or perforation, increased risk of necrotizing enterocolitis; intracranial bleeding (including intraventricular hemorrhage), platelet dysfunction with resultant bleeding; pulmonary hypertension. Because it may cause premature closure of the ductus arteriosus, the use of celecoxib is not recommended ≥30 weeks gestation. The chronic use of NSAIDs in women of reproductive age may be associated with infertility that is reversible upon discontinuation of the medication. A registry is available for pregnant women exposed to autoimmune medications including celecoxib. For additional information contact the Organization of Teratology Information Specialists, OTIS Autoimmune Diseases Study, at 877-311-8972.

Patient Education

• Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?)

• Patient may experience abdominal pain, heartburn, nausea, vomiting, diarrhea, cough, pharyngitis, rhinitis, or rhinorrhea. Have patient report immediately to prescriber signs of abdominal ulcers (severe abdominal or back pain; black, tarry, or bloody stools; vomiting blood or vomit that looks like coffee grounds; or weight gain or abnormal swelling), signs of bleeding (vomiting blood or vomit that looks like coffee grounds; coughing up blood; blood in the urine; black, red, or tarry stools; bleeding from the gums; abnormal vaginal bleeding; bruises without a reason or that get bigger; or any severe bleeding or persistent bleeding), signs of kidney problems (urinary retention, hematuria, change in amount of urine passed, weight gain), signs of high potassium (abnormal heartbeat, confusion, dizziness, passing out, weakness, shortness of breath, numbness or tingling feeling), signs of liver problems (dark urine, fatigue, lack of appetite, nausea, abdominal pain, light-colored stools, vomiting, or jaundice), signs of severe cerebrovascular disease (change in strength on one side is greater than the other, difficulty speaking or thinking, change in balance, or vision changes), signs of Stevens-Johnson syndrome/toxic epidermal necrolysis (red, swollen, blistered, or peeling skin (with or without fever); red or irritated eyes; or sores in mouth, throat, nose, or eyes), severe headache, vision changes, severe dizziness, passing out, shortness of breath, excessive weight gain, swelling of arm or leg, angina, tachycardia, severe loss of strength and energy, hearing impairment, tinnitus, or depression (HCAHPS).

• Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions.

Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for health care professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience, and judgment in diagnosing, treating, and advising patients.

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