Thủ Thuật Hướng dẫn Which medication classification is known to inhibit prostaglandin synthesis or release? Chi Tiết
Hoàng Trung Dũng đang tìm kiếm từ khóa Which medication classification is known to inhibit prostaglandin synthesis or release? được Update vào lúc : 2022-11-04 21:08:04 . Với phương châm chia sẻ Kinh Nghiệm về trong nội dung bài viết một cách Chi Tiết 2022. Nếu sau khi Read tài liệu vẫn ko hiểu thì hoàn toàn có thể lại phản hồi ở cuối bài để Admin lý giải và hướng dẫn lại nha. Each tablet of ARCOXIA for oral administration contains either 60, 90 or 120 mg of etoricoxib.
Excipients/Inactive Ingredients: Each tablet contains calcium hydrogen phosphate (anhydrous), carnauba wax, croscarmellose sodium, hypromellose, lactose monohydrate, magnesium stearate, microcrystalline cellulose, titanium dioxide, and glycerol triacetate. The 60 mg and 120 mg tablets also contain yellow ferric oxide and FD&C Blue #2 (indigo
carmine lake).
- What are some medications that affect prostaglandins?What drug inhibits the production of prostaglandins in order to reduce fever?What medication inhibits prostaglandin synthesis?Which of the following analgesics acts by inhibiting prostaglandin synthesis?
Therapeutic Class: ARCOXIA (etoricoxib) is a thành viên of a class of arthritis/analgesia medications called Coxibs. ARCOXIA is a highly selective inhibitor of cyclooxygenase-2 (COX-2).
Pharmacology: Mechanism of Action: ARCOXIA is a nonsteroidal anti-inflammatory drug (NSAID) that exhibits anti-inflammatory, analgesic, and antipyretic activities in animal models. ARCOXIA is a potent, orally
active, highly selective cyclooxygenase-2 (COX-2) inhibitor within and above the clinical dose range. Two isoforms of cyclooxygenase have been identified: cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). COX-1 is responsible for prostaglandin-mediated normal physiologic functions such as gastric cytoprotection and platelet aggregation. Inhibition of COX-1 by nonselective NSAIDs has been associated with gastric damage and platelet inhibition. COX-2 has been shown to be primarily responsible
for the synthesis of prostanoid mediators of pain, inflammation, and fever. Selective inhibition of COX-2 by etoricoxib decreases these clinical signs and symptoms with decreased GI toxicity and without effects on platelet function.
Across clinical pharmacology studies, ARCOXIA produced dose-dependent inhibition of COX-2 without inhibition of COX-1 doses up to 150 mg daily.
The influence on gastroprotective COX-1 activity was also assessed in a clinical study where prostaglandin
synthesis was measured in gastric biopsy samples from subjects administered either ARCOXIA 120 mg daily, naproxen 500 mg twice daily, or placebo. ARCOXIA did not inhibit gastric prostaglandin synthesis as compared to placebo. In contrast, naproxen inhibited gastric prostaglandin synthesis by approximately 80% compared with placebo. These data further support the COX-2 selectivity of ARCOXIA.
Platelet Function: Multiple doses of ARCOXIA up to 150 mg administered daily up to nine days had no
effect on bleeding time relative to placebo. Similarly, bleeding time was not altered in a single dose study with ARCOXIA 250 or 500 mg. There was no inhibition of ex vivo arachidonic acid- or collagen-induced platelet aggregation steady state with doses of ARCOXIA up to 150 mg. These findings are consistent with the COX-2 selectivity of etoricoxib.
Pharmacokinetics: Absorption: In studies specifically designated to measure the onset of action
of etoricoxib, the onset of action occurred as early as 24 minutes after dosing.
Orally administered etoricoxib is well absorbed. The mean oral bioavailability is approximately 100%. Following 120 mg once-daily dosing to steady state, the peak plasma concentration (geometric mean Cmax = 3.6 mcg/mL) was observed approximately 1 hour (Tmax) after administration to fasted adults. The geometric mean AUC0-24hr was 37.8 mcg·hr/mL. The pharmacokinetics of
etoricoxib are linear across the clinical dose range.
A standard meal had no clinically meaningful effect on the extent or rate of absorption of a dose of etoricoxib 120 mg. In clinical trials, etoricoxib was administered without regard to food.
The pharmacokinetics of etoricoxib in 12 healthy subjects were similar (comparable AUC, Cmax within approximately 20%) when administered alone, with a magnesium/aluminium hydroxide antacid, or a calcium carbonate antacid (approximately
50 mEq acid-neutralizing capacity).
Distribution: Etoricoxib is approximately 92% bound to human plasma protein over the range of concentrations of 0.05 to 5 mcg/mL. The volume of distribution steady state (Vdss) is approximately 120 L in humans.
Etoricoxib crosses the placenta in rats and rabbits, and the blood-brain barrier in rats.
Metabolism: Etoricoxib is extensively metabolized with <1% of a dose recovered in urine as the parent drug. The
major route of metabolism to form the 6'-hydroxymethyl derivative is catalyzed by cytochrome P450 (CYP) enzymes.
Five metabolites have been identified in man. The principal metabolite is the 6'-carboxylic acid derivative of etoricoxib formed by further oxidation of the 6'-hydroxymethyl derivative. These principal metabolites either demonstrate no measurable activity or are only weakly active as COX-2 inhibitors. None of these metabolites inhibit COX-1.
Elimination: Following
administration of a single 25 mg radiolabeled intravenous dose of etoricoxib to healthy subjects, 70% of radioactivity was recovered in urine and 20% in feces, mostly as metabolites. Less than 2% was recovered as unchanged drug.
Elimination of etoricoxib occurs almost exclusively through metabolism followed by renal excretion. Steady state concentrations of etoricoxib are reached within seven days of once-daily administration of 120 mg, with an accumulation ratio of approximately 2,
corresponding to an accumulation half-life of approximately 22 hours. The plasma clearance is estimated to be approximately 50 mL/min.
ARCOXIA is indicated for: Acute and chronic treatment of the signs and symptoms of osteoarthritis (OA) and rheumatoid arthritis (RA).
Treatment of ankylosing spondylitis (AS).
Treatment of acute gouty arthritis.
Treatment of acute pain, including that related to primary dysmenorrhoea and minor dental procedures.
The decision to prescribe a selective COX-2 inhibitor should be based on an assessment of the individual patient's overall risks (see PRECAUTIONS).
ARCOXIA is administered orally. ARCOXIA may be taken with or without food. ARCOXIA should be administered for the shortest duration possible and the lowest effective daily dose should be used.
Osteoarthritis: The recommended dose is 30 mg or 60 mg once daily.
Rheumatoid Arthritis: The
recommended dose is 60 mg or 90 mg once daily. The minimum effective daily dose is 60 mg once daily. In some patients, 90 mg once daily may provide increased therapeutic benefit.
Ankylosing Spondylitis: The recommended dose is 60 mg or 90 mg once daily. The minimum effective daily dose is 60 mg once daily. In some patients, 90 mg once daily may provide increased therapeutic benefit.
Acute Pain: In the following acute painful conditions, ARCOXIA should be used only for
the acute symptomatic period, limited to a maximum of 8 days treatment: Acute Gouty Arthritis: The recommended dose is 120 mg once daily.
Primary Dysmenorrhea: The recommended dose is 120 mg once daily.
Minor Dental Procedures: The recommended dose is 90 mg once daily.
Doses greater than those recommended for each indication have either not demonstrated additional efficacy or have not been studied. Therefore: The dose for OA should not exceed 60 mg
daily.
The dose for RA should not exceed 90 mg daily.
The dose for ankylosing spondylitis should not exceed 90 mg daily.
The dose for acute gout should not exceed 120 mg daily.
The dose for acute pain and primary dysmenorrhea should not exceed 120 mg daily.
The dose for minor dental procedures should not exceed 90 mg daily.
As the cardiovascular risks of selective COX-2 inhibitors may increase with dose and duration of exposure, the shortest duration possible and the
lowest effective daily dose should be used. The patient's need for symptomatic relief and response to therapy should be re-evaluated periodically (see PRECAUTIONS).
Elderly, Gender, Race: No dosage adjustment in ARCOXIA is necessary for the elderly or based on gender or race.
Hepatic Insufficiency: In patients with mild hepatic insufficiency (Child-Pugh score 5-6), a dose of 60 mg once daily should not be exceeded. In patients with moderate hepatic insufficiency
(Child-Pugh score 7-9), the dose should be reduced; a dose of 60 mg every other day should not be exceeded, administration of 30 mg once daily can also be considered. There are no clinical or pharmacokinetic data in patients with severe hepatic insufficiency (Child-Pugh score >9) (see PRECAUTIONS).
Renal Insufficiency: In patients with advanced renal disease (creatinine clearance <30 mL/min), treatment with ARCOXIA is not recommended. No dosage adjustment is necessary for
patients with lesser degrees of renal insufficiency (creatinine clearance ≥30 mL/min) (see PRECAUTIONS).
In clinical studies, administration of ARCOXIA single doses up to 500 mg and multiple doses up to 150 mg/day for 21 days did not result in significant toxicity. There have been reports of acute overdosage with etoricoxib, although adverse experiences were not reported in the majority of cases. The most frequently observed adverse experience were
consistent with the safety profile for etoricoxib. (e.g. gastrointestinal events, renovascular events).
In the sự kiện of overdose, it is reasonable to employ the usual supportive measures, e.g., remove unabsorbed material from the gastrointestinal tract, employ clinical monitoring, and institute supportive therapy, if required.
Etoricoxib is not dialyzable by hemodialysis; it is not known whether etoricoxib is dialyzable by peritoneal dialysis.
ARCOXIA is contraindicated in patients with: Hypersensitivity to any component of this product.
Congestive heart failure (NYHA II-IV).
Established ischemic heart disease, peripheral arterial disease and/or cerebrovascular disease (including patients who have recently undergone coronary artery bypass graft surgery or angioplasty).
Patients with hypertension whose blood pressure has not been adequately controlled.
Pregnancy.
RISK OF GI
ULCERATION, BLEEDING AND PERFORATION WITH NSAIDs: Serious GI toxicity such as bleeding, ulceration and perforation can occur any time, with or without warning symptoms, in patients treated with NSAIDs therapy. Although minor upper GI problems (e.g. dyspepsia) are common, usually developing early in therapy, prescribers should remain alert for ulceration and bleeding in patients treated with NSAIDs even in the absence of previous GI tract symptoms.
Studies to date have not identified
any subset of patients not risk of developing peptic ulceration and bleeding. Patients with prior history of serious adverse events and other risk factors associated with peptic ulcer disease (e.g. alcoholism, smoking and corticosteroid therapy) are increased risk. Elderly or debilitated patients seem to tolerate ulceration or bleeding less than other individuals and account for most spontaneous reports for fatal GI events.
Clinical trials
suggest that the selective COX-2 inhibitor class of drugs may be associated with an increased risk of thrombotic events (especially MI and stroke), relative to placebo and some NSAIDs (naproxen). As the cardiovascular risks of selective COX-2 inhibitors may increase with dose and duration of exposure, the shortest duration possible and the lowest effective daily dose should be used. The patient's need for symptomatic relief and response to therapy should be re-evaluated periodically.
Patients with significant risk factors for cardiovascular events (e.g. hypertension, hyperlipidaemia, diabetes mellitus, smoking) should only be treated with etoricoxib after careful consideration.
Selective COX-2 inhibitors are not a substitute for aspirin for cardiovascular prophylaxis because of their lack of effect on platelets. Because etoricoxib, a thành viên of this class, does not inhibit platelet aggregation, antiplatelet therapies should not be discontinued.
There is a further
increase in the risk of gastrointestinal adverse effects (gastrointestinal ulceration or other gastrointestinal complications) for etoricoxib, other selective COX-2 inhibitors and NSAIDs, when taken concomitantly with acetylsalicylic acid (even low doses). The relative difference in gastrointestinal safety between selective COX-2 inhibitors + acetylsalicylic acid vs. NSAIDs + acetylsalicylic acid has not been adequately evaluated in long-term clinical trials.
In patients with
advanced renal disease, treatment with ARCOXIA is not recommended. Clinical experience in patients with estimated creatinine clearance of <30 mL/min is very limited. If therapy with ARCOXIA must be initiated in such patients, close monitoring of the patient's renal function is advisable.
Long-term administration of NSAIDs has resulted in renal papillary necrosis and other renal injury. Renal prostaglandins may play a compensatory role in the maintenance of renal perfusion. Therefore,
under conditions of compromised renal perfusion, administration of ARCOXIA may cause a reduction in prostaglandin formation and, secondarily, in renal blood flow, and thereby impair renal function. Patients greatest risk of this response are those with pre-existing significantly impaired renal function, uncompensated heart failure, or cirrhosis. Monitoring of renal function in such patients should be considered.
Caution should be used when initiating treatment with ARCOXIA in patients
with considerable dehydration. It is advisable to rehydrate patients prior to starting therapy with ARCOXIA.
As with other drugs known to inhibit prostaglandin synthesis, fluid retention, edema and hypertension have been observed in some patients taking ARCOXIA. The possibility of fluid retention, edema or hypertension should be taken into consideration when ARCOXIA is used in patients with pre-existing edema, hypertension, or heart failure. All Nonsteroidal Anti-inflammatory Drugs (NSAIDs),
including etoricoxib, can be associated with new onset or recurrent congestive heart failure (see SIDE EFFECTS). Etoricoxib may be associated with more frequent and severe hypertension than some other NSAIDs and selective COX-2 inhibitors, particularly high doses. Therefore, special attention should be paid to blood pressure monitoring during treatment with etoricoxib. If blood pressure rises significantly, alternative treatment should be considered.
Physicians should be aware that
individual patients may develop upper gastrointestinal (GI) ulcers/ulcer complications irrespective of treatment. Although the risk of GI toxicity is not eliminated with ARCOXIA, the results of the MEDAL Program demonstrate that in patients treated with ARCOXIA, the risk of GI toxicity with ARCOXIA 60 mg or 90 mg once daily is significantly less than with diclofenac 150 mg daily. In clinical studies with ibuprofen and naproxen, the risk of endoscopically detected upper GI ulcers was lower in
patients treated with ARCOXIA 120 mg once daily than in patients treated with the non-selective NSAIDs. While the risk of endoscopically detected ulcers was low in patients treated with ARCOXIA 120 mg it was higher than in patients treated with placebo. Upper GI ulcers/ulcer complications have occurred in patients treated with ARCOXIA. These events can occur any time during use and without warning symptoms. Independent of treatment, patients with a prior history of GI perforation, ulcers and
bleeding (PUB) and patients greater than 65 years of age are known to be a higher risk for a PUB.
Elevations of alanine aminotransferase (ALT) and/or aspartate aminotransferase (AST) (approximately three or more times the upper limit of normal) have been reported in approximately 1% of patients in clinical trials treated for up to one year with ARCOXIA 30, 60 and 90 mg daily. In active comparator portions of clinical trials, the incidence of elevated AST and/or ALT in patients treated
with ARCOXIA 60 and 90 mg daily was similar to that of patients treated with naproxen 1000 mg daily, but notably less than the incidence in the diclofenac 150 mg daily group. These elevations resolved in patients treated with ARCOXIA, with approximately half resolving while patients remained on therapy. In controlled clinical trials of ARCOXIA 30 mg daily versus ibuprofen 2400 mg daily or celecoxib 200 mg daily, the incidence of elevations of ALT or AST was similar.
A patient with symptoms
and/or signs suggesting liver dysfunction, or in whom an abnormal liver function test has occurred, should be evaluated for persistently abnormal liver function tests. If persistently abnormal liver function tests (three times the upper limit of normal) are detected, ARCOXIA should be discontinued.
ARCOXIA should be used with caution in patients who have previously experienced acute asthmatic attacks, urticaria, or rhinitis, which were precipitated by salicylates or non-selective
cyclooxygenase inhibitors. Since the pathophysiology of these reactions is unknown, physicians should weigh the potential benefits of prescribing ARCOXIA versus the potential risks.
When using etoricoxib in the elderly and in patients with renal, hepatic, or cardiac dysfunction, medically appropriate supervision should be maintained. If these patients deteriorate during treatment, appropriate measures should be taken, including discontinuation of therapy.
Serious skin reactions, some of
them fatal, including exfoliative dermatitis, Stevens-Johnson syndrome, and toxic epidermal necrolysis, have been reported very rarely in association with the use of NSAIDs and some selective COX-2 inhibitors during post-marketing surveillance (see SIDE EFFECTS). These serious events may occur without warning. Patients appear to be highest risk for these reactions early in the course of therapy: the onset of the reaction occurring in the majority of cases within the first month of treatment.
Serious hypersensitivity reactions (such as anaphylaxis and angioedema) have been reported in patients receiving etoricoxib (see SIDE EFFECTS). Some selective COX-2 inhibitors have been associated with an increased risk of skin reactions in patients with a history of any drug allergy. Etoricoxib should be discontinued the first appearance of skin rash, mucosal lesions, or any other sign of hypersensitivity.
ARCOXIA may mask fever, which is a sign of infection. The physician should be
aware of this when using ARCOXIA in patients being treated for infection.
Use in Children: Safety and effectiveness of etoricoxib in pediatric patients have not been established.
Use in the Elderly: Pharmacokinetics in the elderly (65 years of age and older) are similar to those in the young. In clinical studies, a higher incidence of adverse experiences was seen in older patients compared to younger patients; the relative differences between etoricoxib
and control groups were similar in the elderly and the young. Greater sensitivity of some older individuals cannot be ruled out.
Pregnancy: The use of etoricoxib, as with any drug substance known to inhibit COX-2, is not recommended in women attempting to conceive. No clinical data on exposed pregnancies are available for etoricoxib. Studies in animals have shown reproductive toxicity. The potential for human risk in pregnancy is
unknown. Etoricoxib, as with other medicinal products inhibiting prostaglandin synthesis, may cause uterine inertia and premature closure of the ductus arteriosus during the last trimester. Etoricoxib is contraindicated in pregnancy. If a woman becomes pregnant during treatment, etoricoxib should be discontinued.
Nursing Mothers: Etoricoxib is excreted in the milk of lactating rats. It is not known whether this drug is excreted in human milk. Because many drugs are excreted
in human milk and because of the possible adverse effects of drugs that inhibit prostaglandin synthesis on nursing infants, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
In clinical trials, ARCOXIA was evaluated for safety in 9295 individuals, including 5774 patients with OA, RA or chronic low back pain (approximately 600 patients with OA or RA were treated
for one year or longer).
The following drug-related adverse experiences were reported in clinical studies in patients with OA, RA, or chronic low back pain treated for up to 12 weeks. These occurred in ≥1% of patients treated with ARCOXIA and an incidence greater than placebo: asthenia/fatigue, dizziness, lower extremity edema, hypertension, dyspepsia, heartburn, nausea, headache, ALT increased, AST increased.
The adverse experience profile was similar in patients with OA or RA
treated with ARCOXIA for one year or longer.
In the MEDAL Study, an endpoint driven CV outcomes trial involving 23, 504 patients, the safety of ARCOXIA 60 or 90 mg daily was compared to diclofenac 150 mg daily in patients with OA or RA (mean duration of treatment was 20 months). In this large trial, only serious adverse events and discontinuations due to any adverse events were recorded. The rates of confirmed thrombotic cardiovascular serious adverse events were similar between ARCOXIA and
diclofenac. The incidence of discontinuations for hypertension-related adverse events was less than 3% in each treatment group; however, ARCOXIA 60 and 90 mg demonstrated significantly higher rates of discontinuations for these events than diclofenac. The incidence of congestive heart failure adverse events (discontinuations and serious events) and the incidence of discontinuations due to edema occurred similar rates on ARCOXIA 60 mg compared to diclofenac, however, the incidences for these
events were higher for ARCOXIA 90 mg compared to diclofenac. The incidence of discontinuations due to atrial fibrillation was higher for etoricoxib compared to diclofenac.
The EDGE and EDGE II studies compared the GI tolerability of etoricoxib 90 mg daily (1.5 to 3 times the doses recommended for OA) and diclofenac 150 mg daily in 7111 patients with OA (EDGE Study; mean duration of treatment 9 months) and 4086 patients with RA (EDGE II; mean duration of treatment 19 months). In each of these
studies, the adverse experience profile on ARCOXIA was generally similar to that reported in the phase IIb/III placebo-controlled clinical studies; however, hypertension and edema-related adverse experiences occurred a higher rate on etoricoxib 90 mg than on diclofenac 150 mg daily. The rate of confirmed thrombotic cardiovascular serious adverse events occurring in the two treatment groups was similar.
In a combined analysis of phase IIb to V clinical studies of 4 weeks duration or longer
(excluding the MEDAL PROGRAM Studies), there was no discernible difference in the rate of confirmed thrombotic cardiovascular serious adverse events between patients receiving etoricoxib ≥30 mg or non-naproxen NSAIDs. The rate of these events was higher in patients receiving etoricoxib compared with those receiving naproxen 500 mg twice daily.
In a clinical study for ankylosing spondylitis, patients were treated with ARCOXIA 90 mg once daily for up to 1 year (N=126). In another clinical
study for ankylosing spondylitis (N=857), patients were treated with ARCOXIA 60 mg or 90 mg once daily for up to 26 weeks. The adverse experience profile in these studies was generally similar to that reported in chronic studies in OA, RA and chronic low back pain.
In a clinical study for acute gouty arthritis, patients were treated with ARCOXIA 120 mg once daily for eight days. The adverse experience profile in this study was generally similar to that reported in the combined OA, RA, and
chronic low back pain studies.
In initial clinical studies for acute analgesia, patients were treated with ARCOXIA 120 mg once daily for one to seven days. The adverse experience profile in these studies was generally similar to that reported in the combined OA, RA, and chronic low back pain studies.
Post-marketing experience: The following adverse reactions have been reported in post-marketing experience: Blood and lymphatic system disorders:
thrombocytopenia.
Immune system disorders: hypersensitivity reactions, anaphylactic/anaphylactoid reactions including shock.
Metabolism and nutrition disorders: hyperkalemia.
Psychiatric disorders: anxiety, insomnia, confusion, hallucinations, depression, restlessness.
Nervous system disorders: dysgeusia, somnolence.
Eye disorders: blurred vision.
Cardiac disorders: congestive heart failure, palpitations, angina,
arrhythmia.
Vascular disorders: hypertensive crisis.
Respiratory, thoracic and mediastinal disorders: bronchospasm.
Gastrointestinal disorders: abdominal pain, oral ulcers, peptic ulcers including perforation and bleeding (mainly in elderly patients), vomiting, diarrhea.
Hepatobiliary disorders: hepatitis, jaundice, hepatic failure.
Skin and subcutaneous tissue disorders: angioedema, pruritus, erythema, rash, Stevens-Johnson
syndrome, toxic epidermal necrolysis, urticaria, fixed drug eruption.
Renal and urinary disorders: renal insufficiency, including renal failure (see PRECAUTIONS).
Warfarin: In subjects stabilized on chronic warfarin therapy, the administration of ARCOXIA 120 mg daily was associated with an approximate 13% increase in prothrombin time International Normalized Ratio (INR). Standard monitoring of INR values should be conducted when
therapy with ARCOXIA is initiated or changed, particularly in the first few days, in patients receiving warfarin or similar agents.
Rifampin: Co-administration of ARCOXIA with rifampin, a potent inducer of hepatic metabolism, produced a 65% decrease in etoricoxib plasma area under the curve (AUC). This interaction should be considered when ARCOXIA is co-administered with rifampin.
Methotrexate: Two studies investigated the effects of ARCOXIA 60, 90 or 120 mg
administered once daily for seven days in patients receiving once-weekly methotrexate doses of 7.5 to 20 mg for rheumatoid arthritis. ARCOXIA 60 and 90 mg had no effect on methotrexate plasma concentrations (as measured by AUC) or renal clearance. In one study, ARCOXIA 120 mg had no effect on methotrexate plasma concentrations (as measured by AUC) or renal clearance. In the other study, ARCOXIA 120 mg increased methotrexate plasma concentrations by 28% (as measured by AUC) and reduced renal
clearance of methotrexate by 13%. Monitoring for methotrexate-related toxicity should be considered when ARCOXIA doses greater than 90 mg daily and methotrexate are administered concomitantly.
Diuretics, Angiotensin Converting Enzyme (ACE) Inhibitors and Angiotensin II Antagonists (AIIAs): Reports suggest that NSAIDs including selective COX-2 inhibitors may diminish the antihypertensive effect of diuretics, ACE inhibitors and AIIAs. This interaction should be given consideration
in patients taking ARCOXIA concomitantly with these products.
In some patients with compromised renal function (e.g., elderly patients or patients who are volume-depleted, including those on diuretic therapy) who are being treated with non-steroidal anti-inflammatory drugs, including selective COX-2 inhibitors, the co-administration of ACE inhibitors or AIIAs may result in a further deterioration of renal function, including possible acute renal failure. These effects are usually reversible.
Therefore, the combination should be administered with caution, especially in the elderly.
Lithium: Reports suggest that non-selective NSAIDs and selective COX-2 inhibitors may increase plasma lithium levels. This interaction should be given consideration in patients taking ARCOXIA concomitantly with lithium.
Aspirin: ARCOXIA can be used concomitantly with low-dose aspirin doses for cardiovascular prophylaxis. At steady state, etoricoxib 120 mg once daily had no
effect on the anti-platelet activity of low-dose aspirin (81 mg once daily). However, concomitant administration of low-dose aspirin with ARCOXIA increases the rate of GI ulceration or other complications compared to use of ARCOXIA alone (see PRECAUTIONS).
Oral Contraceptives: ARCOXIA 60 mg given concomitantly with an oral contraceptive containing 35 mcg ethinyl estradiol (EE) and 0.5 to 1 mg norethindrone for 21 days increased the steady state AUC0-24hr of EE by 37%.
ARCOXIA 120 mg given with the same oral contraceptive either concomitantly or separated by 12 hours, increased the steady state AUC0-24hr of EE by 50 to 60%. This increase in EE concentration should be considered when selecting an appropriate oral contraceptive for use with ARCOXIA. An increase in EE exposure can increase the incidence of adverse events associated with oral contraceptives (e.g., venous thrombo-embolic events in women risk).
Hormone Replacement Therapy:
Administration of ARCOXIA 120 mg with hormone replacement therapy consisting of conjugated estrogens (0.625 mg PREMARIN) for 28 days, increased the mean steady state AUC0-24hr of unconjugated estrone (41%), equilin (76%) and 17-β-estradiol (22%). The effect of the recommended chronic doses of ARCOXIA (60 and 90 mg) has not been studied. The effects of ARCOXIA 120 mg on the exposure (AUC0-24hr) to these estrogenic components of PREMARIN were less than half of those observed
when PREMARIN was administered alone and the dose was increased from 0.625 to 1.25 mg. The clinical significance of these increases is unknown, and higher doses of PREMARIN were not studied in combination with ARCOXIA. These increases in estrogenic concentration should be taken into consideration when selecting post-menopausal hormone therapy for use with ARCOXIA.
Other: In drug-interaction studies, ARCOXIA did not have clinically important effects on the pharmacokinetics of
prednisone/prednisolone or digoxin.
Antacids and ketoconazole (a potent inhibitor of CYP3A4) did not have clinically important effects on the pharmacokinetics of ARCOXIA.
Store 30°C (86°F). Protect from moisture and light.
M01AH05 - etoricoxib ; Belongs to the class of non-steroidal antiinflammatory and antirheumatic products, coxibs.
FC tab 60 mg (dark green apple-shape biconvex debossed ARCOXIA 60 on one side and 200 on the other side) x 100's. 90 mg (white apple-shape biconvex debossed ARCOXIA 90 on one side and 202 on the other side) x 30's, 100's. 120 mg (pale green apple-shape biconvex debossed ARCOXIA 120 on one side and 204 on the other side) x 30's.
What are some medications that affect prostaglandins?
Medications. Bimatoprost (Lumigan, Latisse). This is a medication used to treat glaucoma as well as to promote eyelash growth.. Carboprost (Hemabate). This medication produces uterine contractions that may help reduce postpartum bleeding.. Dinoprostone (Cervidil). ... . Misoprostol (Cytotec). ... . Latanoprost (Xalatan)..What drug inhibits the production of prostaglandins in order to reduce fever?
NSAIDs block COX enzymes and reduce production of prostaglandins. Therefore, inflammation, pain, and fever are reduced.What medication inhibits prostaglandin synthesis?
Aspirin and a large number of nonsteroidal anti-inflammatory drugs act primarily through the inhibition of prostaglandin synthesis by inhibiting the enzyme cyclooxygenase.Which of the following analgesics acts by inhibiting prostaglandin synthesis?
Acetaminophen. Acetaminophen inhibits the synthesis of prostaglandins that may serve as mediators of pain and fever primarily in the CNS. Acetaminophen is used to treat mild pain and fever; however, it does not have anti-inflammatory properties. Tải thêm tài liệu liên quan đến nội dung bài viết Which medication classification is known to inhibit prostaglandin synthesis or release?