Non-steroidal anti-inflammatory drugs (NSAIDs)
NSAIDs, including aspirin, are the most widely used analgesics. Traditionally these medications are considered to be weak analgesics and have been used extensively for headaches, arthritis and a wide range of minor aches and post-surgical conditions.
NSAIDs are powerful inhibitors of prostaglandin synthesis through the effect on cyclooxygenase (COX). Prostaglandins are not thought to be important pain mediators, but they do cause hyperalgesia by sensitizing peripheral nociceptors to the effects of various mediators of pain and inflammation, such as somatostatin, bradykinin, and histamine. Thus, NSAIDs are used primarily to treat pain that results from inflammation and hyperalgesia. The table below presents the most commonly used NSAIDs.
| Acetaminophen | Tylenol | 500-1000 mg q4h |
| Acetylsalicylic Acid |
Aspirin | 325-650 mg q4h |
| Celecoxib | Celebrex | 200 mg q12hr |
| Choline Magnesium Trisalicylate |
Trilisate |
500-750 mg q8-12h |
| Diclofenal Sodium | Voltaren | 25-75 mg q8-12h |
| Diflusinal |
Dolobid |
250-500 mg q8-12h |
| Etodolic Acid | Lodine | 200-400 mg q6 |
| Fenoprofen calcium |
Nalfon |
200 mg q4-6h |
| Flurbiprofen | Ansaid | 100 mg q8-12h |
| Ibuprofen |
Motrin |
400-800 mg q6-8h |
| Indomethacin | Indocin | 25-50 mg q8--12h |
| Ketoprofen |
Orudis |
25-75 mg q6-8h |
| Ketorolac | Toradol | 10 mg q6-8h |
| Meclofenamate sodium |
Meclomen |
50 mg q4-6h |
| Naproxen | Naprosyn | 275-500 mg q8-12 h |
| Phenylbutazone |
Butazolidin |
100 mg q6-8h |
| Piroxicam | Feldene | 10-20 mg qd |
| Salsalate |
Disalcid |
500 mg q4h |
| Sulindac | Clinoril | 150-200 mg q12h |
| Tolmetin |
Tolectin |
200-600 mg q8h |
| Table 1. Commonly Used Oral NSAIDs |
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Acetaminophen is not strictly an anti-inflammatory medication. Its peripheral and antiinflammatory effects are weak. However, it shares many properties of NSAIDs.
The medication readily crosses the blood-brain barrier. Its action resides primarily in the central nervous system, where prostaglandin inhibition produces analgesia and antipyresis.
Common side effects of NSAIDs include gastrointestinal toxicity, stomach ulcers, and gastric bleeding. Inhibition of platelet cyclooxygenase can result in decreased hemostasis and surgical bleeding. Renal dysfunction can occur with prolonged and excessive use of NSAIDs. Particularly at risk from excessive use of NSAIDs are the elderly, patients with renal dysfunction, congestive heart failure, ascites, or hypovolemia. Patients treated with nephrotoxic drugs such as aminoglycosides are also at significant risk. Other adverse effects of NSAIDs include hepatic dysfunction or necrosis, asthma, vasomotor rhinitis, angioneurotic edema, urticaria, laryngeal edema or even cardiovascular collapse.
Cardiovascular risks of NSAIDs, especially COX2 inhibitors, have become a major focus of attention recently. Suggestions that the use of COX2 inhibitors may decrease prostacyclin (PGI2) levels with relatively unopposed platelet thromboxane A2 generation may lead to increased thrombotic risk have cautioned against the use of such agents. There is strong clinical evidence that rofecoxib (Vioxx) is associated with increased cardiovascular risks, which resulted in the withdrawal of this medication from market. Recent studies show inconsistent results with regards to the cardiovascular risks for celecoxib(2;3). Until now the experimental and clinical data are quite discordant regarding the cardiovascular hazard from the administration of naproxen and other NSAIDs (4;5). In the absence of clear-cut data, physicians will have to use traditional NSAIDs (or coxibs) in patients with high cardiovascular risks on the basis of their common sense rather than on evidence-based medicine.
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