Half‐life of 45 hrs. Once‐daily dosing. Delay onset of  action.

High doses inhibits PMN migration, decrease oxygen  radical production, inhibits lymphocyte function. 

used to relieve the symptoms of  arthritis, primary dysmenorrhoea, pyrexia; and as an analgesic,non-selective  cyclooxygenase (COX) inhibitor

The risk of adverse side efects is nearly ten times higher than with other NSAIDs. Peptic ulcer (9.5 higher)

Related Questions NSAIDS

Mefenamic acid

Analgesic, anti‐inflammatory properties less  effective than aspirin 

Short half‐lives, should not be used for longer  than one week and never in pregnancy and in  children. 

Enhances oral anticoagulants

Used to treat pain, including menstrual pain. It decreases inflammation (swelling) and uterine contractions.


It acts by inhibiting the body's production of prostaglandin.

NSAIDs: Classification by Plasma Elimination Half Lives

Short Half Life (< 6 hours):

more rapid effect and clearance

• Aspirin (0.25-0.33 hrs),

• Diclofenac (1.1 ± 0.2 hrs)

• Ketoprofen (1.8± 0.4 hrs),

• Ibuprofen (2.1 ± 0.3 hrs)

• Indomethacin (4.6 ± 0.7 hrs)

Long Half Life (> 10 hours):

slower onset of effect and slower clearance

• Naproxen (14 ± 2 hrs)

• Sulindac (14 ± 8 hrs),

• Piroxicam (57 ± 22 hrs)

Pharmacodynamic Effects of NSAIDs

A. Positive

analgesic - refers to the relief of pain by a mechanism other than the reduction of inflammation (for example, headache);

- produce a mild degree of analgesia which is much less than the analgesia produced by opioid analgesics such as morphine

anti-inflammatory - these drugs are used to treat inflammatory diseases and injuries, and with larger doses - rheumatoid disorders

antipyretic - reduce fever; lower elevated body temperature by their action on the hypothalamus; normal body temperature is not reduced

Anti-platelet - inhibit platelet aggregation, prolong bleeding time; have anticoagulant effects

B. Negative

Gastric irritant

Decreased renal perfusion


(CNS effects)

Adverse effects

The two main adverse drug reactions (ADRs) associated with NSAIDs relate to gastrointestinal (GI) effects and renal effects of the agents.

Gastrointestinal ADRs

The main ADRs associated with use of NSAIDs relate to direct and indirect irritation of the gastrointestinal tract (GIT). NSAIDs cause a dual insult on the GIT - the acidic molecules directly irritate the gastric mucosa; and inhibition of COX-1 reduces the levels of protective prostaglandins.

Common gastrointestinal ADRs include:

Nausea, dyspepsia, ulceration/bleeding, diarrhoea


Risk of ulceration increases with duration of therapy, and with higher doses. In attempting to minimise GI ADRs, it is prudent to use the lowest effective dose for the shortest period of time..

 Ketoprofen and piroxicam appear to have the highest prevalence of gastric ADRs, while ibuprofen (lower doses) and diclofenac appear to have lower rates.

Commonly, gastrointestinal adverse effects can be reduced through suppressing acid production, by concomitant use of a proton pump inhibitor, e.g. omeprazole

Renal ADRs

NSAIDs are also associated with a relatively high incidence of renal ADRs. The mechanism of these renal ADRs is probably due to changes in renal haemodynamics (bloodflow), ordinarily mediated by prostaglandins, which are affected by NSAIDs.

Common ADRs associated with altered renal function include:

salt and fluid retention,hypertension

These agents may also cause renal impairment, especially in combination with other nephrotoxic agents. Renal failure is especially a risk if the patient is also concomitantly taking an ACE inhibitor and a diuretic - the so-called "triple whammy" effect.

In rarer instances NSAIDs may also cause more severe renal conditions.

interstitial nephritis, nephrotic syndrome, acute renal failure


Photosensitivity is a commonly overlooked adverse effect of many of the NSAIDs. These antiinflammatory agents may themselves produce inflammation in combination with exposure to sunlight. The 2-arylpropionic acids have proven to be the most likely to produce photosensitivity reactions, but other NSAIDs have also been implicated including piroxicam, diclofenac and benzydamine.

ibuprofen having weak absorption, it has been reported to be a weak photosensitising agent.

Other ADRs

Common ADRs, other than listed above, include: raised liver enzymes, headache, dizziness.

Uncommon ADRs include: heart failure, hyperkalaemia, confusion, bronchospasm, rash.

The COX-2 paradigm

It was thought that selective inhibition of COX-2 would result in anti-inflammatory action without disrupting gastroprotective prostaglandins.

The relatively selective COX-2 oxicam, meloxicam, was the first step towards developing a true COX-2 selective inhibitor. Coxibs, the newest class of NSAIDs, can be considered as true COX-2 selective inhibitors and include celecoxib, rofecoxib, valdecoxib, parecoxib and etoricoxib.


is a highly selective COX-2 inhibitor and primarily inhibits this isoform of cyclooxygenase, whereas traditional NSAIDs inhibit both COX-1 and COX-2. Celecoxib is approximately 10-20 times more selective for COX-2 inhibition over COX-1.

Being a sulphonamide can cause skin rash &  hypersensitivity rxn., occasional oedema& HT.


Osteoarthritis ( 100‐200mg BID ) , rheumatoid  arthritis, dysmenorrhea, acute gouty attacks,  acute musculoskeletal pain.