Diclofenac¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ 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 ketoprofen. Antipyretic effects may be due to action on the hypothalamus, resulting in peripheral dilation, increased cutaneous blood flow, and subsequent heat dissipation.
Pharmacology
Diclofenac¿¡ ´ëÇÑ Pharmacology Á¤º¸ 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
Diclofenac¿¡ ´ëÇÑ Absorption Á¤º¸ Completely absorbed from the gastrointestinal tract.
Pharmacokinetics
Diclofenac sodiumÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
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Biotransformation
Diclofenac¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hepatic
Toxicity
Diclofenac¿¡ ´ëÇÑ Toxicity Á¤º¸ Symptoms of overdose include loss of consciousness, increased intracranial pressure, and aspiration pneumonitis. LD50=390mg/kg (orally in mice)
Drug Interactions
Diclofenac¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Alendronate Increased risk of gastric toxicityAnisindione The NSAID increases the anticoagulant effectCyclosporine Monitor for nephrotoxicityDicumarol The NSAID increases the anticoagulant effectWarfarin The NSAID increases the anticoagulant effectRifampin Decreased levels/effect of the NSAID
Diclofenac¿¡ ´ëÇÑ Description Á¤º¸ A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt. [PubChem]
The database contains the following fields: The generic name of each chemical For module A10 (liver enzyme composite module): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the number of active and marginally active scores for each compound at the five individual endpoints (see research article for full description of method) Number of endpoints at which each compound is marginally active (M) Number of endpoints at which each compound is active (A) For modules A11 to A15 (alkaline phosphatase increased, SGOT increased, SGPT increased, LDH increased, and GGT increased, respectively): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the RI and ADR values (see the research article for full description of method) Number of ADR reports for each compound, given as <4 or ¡Ã4 Reporting Index value for each compound, except where no shipping units were available (NSU) Group 1 comprises of compounds for which ADR data were available for the first five years of marketing, so when no ADR reports were listed during this period the compounds were evaluated as inactive. Group 2 comprises of compounds for which a 'steady state' period of ADR data were available (1992-1996). In cases where no ADR reports were filed during this period, the compounds were scored as 'NA' (data not available) since they may have had one or more ADR reports during their first five years of marketing which should not be negated by a lack of ADR reports during the steady-state period. DICLOFENAC [GGT Increase] [Composite Activity] (Score)A (Marginal) 1 (Active) 3