Adult: 600-900 mg daily in 2-3 divided doses, may be increased up to Max 1,200 mg daily if necessary. Max: 400 mg/dose. Elderly: Use lowest effective dose.
Oral Mild to moderate pain
Adult: 600 mg daily in 2-3 divided doses, may be increased up to Max 1,200 mg daily if necessary. Max: 400 mg/dose. Elderly: Use lowest effective dose.
Mild to moderate: Dose reduction is recommended. Severe (GFR <30 mL/min): Contraindicated.
Mild to moderate: Dose reduction is recommended. Severe: Contraindicated.
Hypersensitivity to NSAIDs. Active or history of recurrent peptic ulcer/haemorrhage, history of gastrointestinal bleeding or perforation associated with previous NSAID therapy; cerebrovascular bleeding or other active bleedings, active Crohn’s disease or ulcerative colitis; severe heart failure. Severe renal (GFR <30 mL/min) and hepatic impairment. Pregnancy (3rd trimester). Concomitant use with NSAIDs including COX2-selective inhibitors.
Patient with allergic disorders, cardiac impairment, cerebrovascular disease, congestive heart failure; history of ulcerative colitis, Crohn’s disease; haemorrhagic diathesis and other coagulation disorders, ischaemic heart disease, peripheral arterial disease, risk factors for CV events, uncontrolled hypertension, bronchial asthma, systemic lupus erythematosus, mixed connective tissue disease. Elderly. Mild to moderate renal and hepatic impairment. Pregnancy (1st and 2nd trimester) and lactation.
Significant: Renal effects (e.g. glomerular nephritis, interstitial nephritis, renal papillary necrosis, nephrotic syndrome, acute renal failure), increase SGOT and SGPT. Ear and labyrinth disorders: Tinnitus. Eye disorders: Visual disturbances. Gastrointestinal disorders: Dyspepsia, abdominal pain, diarrhoea, nausea, vomiting. General disorders and administration site conditions: Fatigue. Immune system disorders: Allergic purpura, angioedema. Nervous system disorders: Drowsiness, headache, dizziness, vertigo, restlessness. Psychiatric disorders: Anxiety, insomnia. Respiratory, thoracic and mediastinal disorders: Rhinitis, bronchospasm. Skin and subcutaneous tissue disorders: Rash, urticaria, pruritus. Potentially Fatal: Gastrointestinal bleeding, ulceration and perforation. Rarely, Stevens-Johnson syndrome and toxic epidermal necrolysis.
Patient Counseling Information
This drug may cause dizziness, fatigue, drowsiness, vertigo or visual disturbances, if affected, do not drive or operate machinery.
Monitor renal, hepatic and haematologic functions in patient receiving long-term therapy. Perform blood coagulation tests (e.g. INR, bleeding time) prior to treatment initiation in patient taking anticoagulants.
Symptoms: Mild symptoms include abdominal pain, nausea, vomiting, lethargy, drowsiness, headache, nystagmus, tinnitus and ataxia. Rarely, moderate or severe symptoms such as gastrointestinal bleeding, hypotension, hypothermia, metabolic acidosis, seizures, impaired kidney function, coma, adult respiratory distress syndrome and transient episodes of apnoea (young children following large ingestions). Management: Symptomatic treatment. Small ingested amounts (<50 mg/kg) may be diluted water to reduce gastrointestinal upset. Consider emesis to empty stomach within 60 minutes of ingestion.
May increase effect of anticoagulants (e.g. warfarin). May increase plasma levels thus increase risk of toxicity of methotrexate, lithium, digoxin and phenytoin. May reduce antihypertensive effect of β-blockers. May increase risk of nephrotoxicity with immunosuppressants (e.g. ciclosporin, tacrolimus, sirolimus) and aminoglycoside antibiotics. Increased risk of gastrointestinal ulceration and bleeding with corticosteroids, antiplatelets and selective serotonin reupdate inhibitors. Reduced effect with CYP2C8 and CYP2C9 inducing agents (e.g. phenytoin, phenobarbital, rifampicin). Potentially Fatal: Increased risk of gastrointestinal bleeding, ulceration or perforation, and renal failure with NSAIDs including selective COX-2 inhibitors.
Increased gastrointestinal adverse effects with alcohol.
Description: Dexibuprofen is the S(+)-enantiomer of ibuprofen, a non-selective NSAID. Its mechanism of action may be due to inhibition of prostaglandin synthesis resulting to reduced pain, inflammation and fever. Pharmacokinetics: Absorption: Well-absorbed mainly from small intestine. Time to peak plasma concentration: Approx 2 hours. Distribution: Plasma protein binding: Approx 99%. Metabolism: Metabolised in the liver via hydroxylation and carboxylation to inactive metabolites. Excretion: Via urine (90%) and faeces. Elimination half-life: 1.8-3.5 hours.