Non-steroidal anti-inflammatory drugs,
usually abbreviated to NSAIDs, are drugs with analgesic,
antipyretic and anti-inflammatory effects - they reduce
pain, fever and inflammation. The term "non-steroidal"
is used to distinguish these drugs from steroids, which
(amongst a broad range of other effects) have a similar
eicosanoid depressing anti-inflammatory action. NSAIDs
are sometimes also referred to as non-steroidal anti-inflammatory
agents/analgesics (NSAIAs). The most prominent members
of this group of drugs are aspirin and ibuprofen. Paracetamol,
or acetaminophen, has little anti-inflammatory activity,
and is not an NSAID.
Beginning in 1829, with the isolation of salicylic
acid from the folk remedy willow bark, NSAIDs have become
an important part of the pharmaceutical treatment of
pain (at low doses) and inflammation (at higher doses).
Part of the popularity of NSAIDs is that, unlike opioids,
they do not produce sedation, respiratory depression,
or addiction. NSAIDs, however, are not without their
own problems. Certain NSAIDs have become accepted as
relatively safe, resulting in the rescheduling of these
agents, e.g. ibuprofen, to allow availability over-the-counter.
The widespread use of NSAIDs has meant that the adverse
effects of these relatively safe drugs have become increasingly
prevalent. The two main adverse drug reactions (ADRs)
associated with NSAIDs relate to gastrointestinal (GI)
effects and renal effects of the agents.
GI effects or Adverse Drug Reactions (ADRs)
Common gastrointestinal adverse reactions iinclude:
- dyspepsia (constant pain in the stomach)
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, a practice which studies
show is not often followed.
There are also some differences in the propensity of
individual agents to cause gastrointestinal ADRs. Ketoprofen
and piroxicam appear to have the highest prevalence
of gastric ADRs, while ibuprofen (lower doses) and diclofenac
appear to have lower rates.
Certain NSAIDs, such as aspirin, have been marketed
in enteric-coated formulations which are claimed to
reduce the incidence of gastrointestinal ADRs. Similarly,
there is a belief that rectal formulations may reduce
gastrointestinal ADRs. However, in consideration of
the mechanism of such ADRs and indeed in clinical practice,
these formulations have not been shown to have a reduced
risk of GI ulceration.
Commonly, gastrointestinal adverse effects can be reduced
through suppressing acid production, by concomitant
use of a proton pump inhibitor, e.g. omeprazole; or
the prostaglandin analogue misoprostol. Misoprostol
is itself associated with a high incidence of gastrointestinal
ADRs (diarrhoea). While these techniques may be effective,
they prove to be expensive for maintenance therapy.
Renal (Kidney) Adverse Drug Reactions (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
Common ADRs associated with altered renal function include:
- Salt and fluid retention
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, such as:
- Interstitial nephritis
- Nephrotic syndrome
- Acute renal failure
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