Adverse Reaction:
Side effects-
Gastrointestinal effects have occurred in approximately 15% of patients. Pain , nausea,
heartburn and dyspepsia are most common, while diarrhea is uncommon (approximately
1%) .
More serious GI side effects such as peptic ulceration are rare. Carprofen has been used
along with antacids in patients with active peptic ulcer disease and has been well tolerated
Renal or urinary adverse reactions including urinary frequency, dysuria, burning,hematuria,
nephritis, proteinuria and acute renal failure occurred in 3.4% of 1521 patients in premarketing clinical trials
Cutaneous reactions such as eczema, skin rash, urticaria, and photosensitivity have occurred in 6% to 10% of patients
Hepatic enzyme elevation occurred in 1.4% of patients in European trials and in has 14% of
patients in large American trials. Thes enzyme elevations are usually symptomatic
Pharmacology/ Pharmacokinetics:
Pharmacology-
Carprofen (D,L) -6-chloro-alpha-methylcarbazole- 2-acetic acid) is a member of the
arylpropionic class on nonsteroidal anti-ani-inflammatory drugs (NSAIDs), and
posseses analgesic and antipyretic activity.
Although the site and exact mechanism of action of the NSAIDs has not been fully elucidated,most investigators agree that these drugs owe their analgesic and antipyretic anti-inflammatory activity , as well as their gastric irritant properties, to their ability to inhibit prostaglandin synthesase.
Carprofen is considered to be less potent than naproxen or ibuprofen and only 1% to 4% as
potent as indomethicin (eg Indocin)
Considerable evidence suggests that the anti-inflammatory activity of carprofen is due to
primary to the D -isomer , the L--isomer is only about one-seventh as potent.
Pharmacokinetics-
Absorption-Distribution- carprofen is rapidly and extensively absorbed after oral admin.
Peak concentration of approximately 6 to 12mcg/ml are acheived in 1 to 3 hours, absolute
bioavailability is approximately 90%. Ingestion of food results results in a slight reduction in
the rate of absorption as well as peak concentration. However, the total amount of the drug
absorbed is not reduced.
Peak plasma concentrations may be higher in the elderly. Carpofen is highly protein bound
(>98%). In patients with osteoarthiritis (OA) or rheumatoid arthiritis (RA) the drug enters the
synovial fluid rapidly, where it may acheive concentrations in excess of plasma concentrations
Metabolism- Approximately 65% to 70% of an administered dose is metabolized by direct
congugation to an ester glucoronide. The elimination half-life (t 1/2) is between 13 to 25 hours.
Despite the extensive hepatic metabolism no difference has been observed in pharmacokinetics between cirhotics and normal volunteeers. Thus dosage adjustments are unnecessary in patients with renal or hepatic insufficiency
Excretion- Most of an orally administered dose of carpofen (65 to 70% ) is eliminated unchanged The remainder of the drug is excreted in the feaces after undergoing extensive enterohepatic recycling
Clinical trials-
Carpofen is effective in a wide variety of clinical setting including treatment of
rheumatoid arthiritis , osteoarthiritis , ankylosing spondylosis, extra-articular inflammatatory
process (eg tendonitis, bursitis,) , acute pain syndromes (eg.dental and post traumatic pain) and acute gouty arthiritis. Dosages have ranged from 150 to 600 mg/day in two or three divided doses.
The few available comparative studies have usually shown carpofen to be equal to, or superior to, aspirin, up to 3600mg/day. Comparisons with indomethicin 75 to 150mg/day have usually shown the lower doses (up to 300mg/day) of carpofen to be less effective but better tolerated than indomethacin.
Larger doses of carprofen (400 to 600mg/day ) have been used in the treatment of OA , however,the use of larger doses may not produce additional response over lower doses
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