Diclofenac

The obtained analytical forms are used for quantitative determination of both Diclofenac natrium and Ibuprofen content in medicinal forms as well as for the testing uniformity of batching of the basic substance in tableted forms. The relative standard deviation (RSD) were 3,7-4,6 % (n = 5 P = 0,95). 

Less severe pain states (e.g., arthritis, menstruation, headache, minor surgery) are commonly treated with nonselective NSADDs (e.g., aspirin, ibuprofen, indo-methacin, diclofenac). NSAIDs are mostly used orally. 

NSAIDs are of diverse chemical structures salicylates (aspirin, sulphasalazine), indole acetic acids (indomethacin, etodolac), heteroaryl acetic acids (diclofenac), arylpropionic acids (ibuprofen, naproxen), anthranilic acids (mefenamic acid) and enolic acids (piroxicam, meloxicam). 

Celecoxib, which has a low selectivity for COX-2 compared to COX-1, is still available, although its more selective successor, valdecoxib has been withdrawn. Etoricoxib, the successor to rofecoxib, is marketed in Europe but not in the USA. In a large multinational clinical trial, etoricoxib caused no more thromboembolic events than diclofenac, but after 18 months the incidence of gastrointestinal ulcers and bleeding was the same for both drugs [4]. 

Lumiracoxib, which has been approved in the UK but not by the FDA, has a phenyl acetic acid structure resembling diclofenac rather than the other coxibs... 

Cannon CP, Curtis SP, FitzGerald GA et al (2006) Cardiovascular outcomes with etoricoxib and diclofenac in patients with osteoarthritis and rheumatoid arthritis in the Multinational Etoricoxib and Diclofenac Arthritis Long-term (MEDAL) programme a randomised comparison. Lancet 368 1771-1781... 

Diclofenac is an exceedingly potent COX inhibitor slightly more efficacious against COX-2 than COX-1. Its absorption from the gastrointestinal tract varies according to the type of pharmaceutical formulation used. The oral bioavailability is only 30-80% due to a first-pass effect. Diclofenac is rapidly metabolised (hydroxylation and conjugation) and has a plasma half-life of 1.5 h. The metabolites are excreted renally and via the bile. 

Epidemiological studies have demonstrated that diclofenac causes less serious gastrointestinal complications than indomethacin. However, a rise in plasma liver enzymes occurs more frequently with diclofenac than with other NSAIDs. 

The daily oral dose of diclofenac is 50-150 mg. Diclofenac is also available as eye-drops for the treatment of non-specific inflammation of the eye and for the local therapy of eye pain. 

Oxicams, e.g. piroxicam, tenoxicam, meloxicam and lornoxicam are non-specific inhibitors of COX. Like diclofenac, meloxicam inhibits COX-2 ten times more potently than COX-1. This property can be exploited clinically with doses up to 7.5 mg per day, but at higher doses COX-1-inhibition becomes clinically relevant. Since the dose of meloxicam commonly used is 15 mg daily, this agent cannot be regarded as a COX-2-selective NS AID and considerable caution needs to be exercised when making comparisons between the actions of meloxicam and those of other conventional NSAIDs. The average daily dose in anti-rheumatic therapy is 20 mg for piroxicam and tenoxicam, 7.5-15 mg for meloxicam and 12-16 mg for lornoxicam. Oxicams have long elimination half-lives (lornoxicam 3-5 h, meloxicam - 20 h, piroxicam 40 h and tenoxicam 70 h). 

These drug are contraindicated in individuals with known hypersensitivity to an individual drug or any components of the drug. The NSA.ID flurbiprofen is contraindicated in patients with herpes simplex keratitis. Diclofenac and ketorolac are contraindicated in patients who wear soft contact lenses (may cause ocular irritation). 

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