Patellofemoral Syndrome Medication

Updated: Nov 01, 2018
  • Author: Noel F So, MD, FAAPMR; Chief Editor: Consuelo T Lorenzo, MD  more...
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Medication

Medication Summary

Two approaches to medicating symptoms of patellofemoral syndrome are recognized. These approaches are administration of analgesic medication and administration of nonsteroidal anti-inflammatory drugs (NSAIDs). Analgesics commonly are restricted to acetaminophen or aspirin. The choices of NSAIDs available for management of joint pain are expanding continuously. Consider tolerance of medication (which may result in epigastric distress), prior history of gastric ulceration, renal disease, possible interaction with other medications, and cost. The NSAIDs all have similar efficacy, but changes in formulation have been made to reduce the frequency of adverse effects. Selective cyclooxygenase 2 (COX-2) inhibitors have fewer gastrointestinal adverse effects.

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Nonsteroidal anti-inflammatory drugs

Class Summary

No NSAID has been found to be more effective in treating symptoms of patellofemoral syndrome than any other, although tolerances of NSAIDs vary between individuals. Listed below are the commonly used NSAIDs. These NSAIDs are used predominantly in the adult population. Except for the COX-2 NSAIDs, most have similar adverse effect profiles, and most have the same effect on prostaglandins.

Diclofenac (Cataflam, Voltaren)

Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclo-oxygenase, which in turn decreases formation of prostaglandin precursors.

Etodolac (Lodine, Lodine XL)

Inhibits prostaglandin synthesis by decreasing activity of the enzyme cyclo-oxygenase.

The decreased activity of cyclo-oxygenase results in decreased formation of prostaglandin precursors, which in turn results in reduced inflammation.

Flurbiprofen (Ansaid)

May inhibit cyclo-oxygenase enzyme, which in turn inhibits prostaglandin biosynthesis.

These effects may result in analgesic, antipyretic, and anti-inflammatory activities.

Ibuprofen (Motrin, Ibuprin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Indomethacin (Indocin, Indochron ER)

Rapidly absorbed. Inhibits prostaglandin synthesis. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation.

Ketoprofen (Actron, Orudis, Oruvail)

For relief of mild to moderate pain and inflammation. Small dosages initially are indicated in small and elderly patients and in those with renal or liver disease.

Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.

Nabumetone (Relafen)

Nonacidic NSAID rapidly metabolized after absorption to a major active metabolite that inhibits cyclo-oxygenase enzyme, which in turn inhibits pain and inflammation.

Naproxen (Aleve, Naprelan, Anaprox, Naprosyn)

For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.

Oxaprozin (Daypro)

For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which is responsible for prostaglandin synthesis.

Piroxicam (Feldene)

Decreases activity of cyclo-oxygenase, which in turn inhibits prostaglandin synthesis. These effects decrease formation of inflammatory mediators.

Sulindac (Clinoril)

Decreases activity of cyclo-oxygenase, which in turn inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators.

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Cyclo-oxygenase-2 (COX-2) inhibitors

Class Summary

Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.

Celecoxib (Celebrex)

Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient.

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