| Indication |
For the acute and chronic treatment of signs and symptoms of osteoarthritis and rheumatoid arthritis. |
| Pharmacodynamics |
Diclofenac is an acetic acid nonsteroidal antiinflammatory drug
(NSAID) with analgesic and antipyretic properties. Diclofenac is used to
treat pain, dysmenorrhea, ocular inflammation, osteoarthritis,
rheumatoid arthritis, ankylosing spondylitis, and actinic keratosis |
| Mechanism of action |
The antiinflammatory effects of diclofenac are believed to be due
to inhibition of both leukocyte migration and the enzyme cylooxygenase
(COX-1 and COX-2), leading to the peripheral inhibition of prostaglandin
synthesis. As prostaglandins sensitize pain receptors, inhibition of
their synthesis is responsible for the analgesic effects of diclofenac.
Antipyretic effects may be due to action on the hypothalamus, resulting
in peripheral dilation, increased cutaneous blood flow, and subsequent
heat dissipation. |
| Absorption |
Completely absorbed from the gastrointestinal tract. |
| Volume of distribution |
|
| Protein binding |
More than 99% |
| Metabolism |
Hepatic |
| Route of elimination |
Diclofenac is eliminated through metabolism and subsequent urinary
and biliary excretion of the glucuronide and the sulfate conjugates of
the metabolites. Little or no free unchanged diclofenac is excreted in
the urine. Approximately 65% of the dose is excreted in the urine and
approximately 35% in the bile as conjugates of unchanged diclofenac plus
metabolites. |
| Half life |
2 hours |
| Clearance |
- oral cl=622 mL/min [healthy]
- renal cl <1 mL/min [healthy]
|
| Toxicity |
Symptoms of overdose include loss of consciousness, increased intracranial pressure, and aspiration pneumonitis. LD50=390mg/kg (orally in mice) |
