Iliotibial Band Syndrome Medication
- Author: Jerold M Stirling, MD; Chief Editor: Craig C Young, MD more...
NSAIDs are often incorporated into the medical management of overuse injuries such as ITBS because of these agents' analgesic and anti-inflammatory effects. All NSAIDs share a common mechanism of action, inhibition of prostaglandins. Many types of NSAIDs are available for treatment of overuse injuries, but these drugs vary primarily in their onset of effectiveness and duration of action.
To some degree, all NSAIDs share a common side effect of irritation of the gastrointestinal (GI) tract. Patients who take NSAIDs may experience symptoms of flatulence, abdominal cramping, and diarrhea. The more serious GI side effects include esophageal reflux, gastritis, acid reflux, peptic disease, and ulcer formation. NSAIDs as a group may also produce renal side effects (interstitial nephritis, vasomotor nephropathy), dermatologic reactions (rashes), and central nervous system (CNS) symptoms (eg, headache, dizziness, mood change, confusion), but these are much less common than GI side effects.
The ideal NSAID for treatment of an overuse injury is one that combines several properties. The drug should act quickly, have good penetration into synovial tissues, and produce few or no side effects. Unfortunately, no NSAID exists that fulfills all these criteria. The following list indicates only a few of the NSAIDs that are commonly prescribed for overuse injuries.
Nonsteroidal anti-inflammatory drugs
NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action of these agents is not known, but NSAIDs may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.
For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Designated chemically as 2-[(2,6-dichlorophenyl) amino] benzeneacetic acid, monosodium salt, with an empirical formula of C14 H10 Cl2 NO2 NA.
One of a series of phenylacetic acids that has demonstrated anti-inflammatory and analgesic properties in pharmacologic studies. Believed to inhibit the enzyme cyclooxygenase, which is essential in the biosynthesis of prostaglandins. Can cause hepatotoxicity; hence, liver enzymes should be monitored in the first 8 weeks of treatment.
Rapidly absorbed; metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation.
The delayed-release, enteric-coated form is diclofenac sodium, and the immediate-release form is diclofenac potassium. Has relatively low risk for bleeding GI ulcers. Available in extended-relief dosage of 75 mg or 100 mg (Voltaren SR) am or hs.
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