Patellofemoral Syndrome Medication

  • Author: Patrick J Potter, MD, FRCP(C); Chief Editor: Consuelo T Lorenzo, MD   more...
 
Updated: Feb 16, 2012
 

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.

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Diclofenac (Cataflam, Voltaren)

 

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

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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.

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Flurbiprofen (Ansaid)

 

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

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

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Ibuprofen (Motrin, Ibuprin)

 

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

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Indomethacin (Indocin, Indochron ER)

 

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

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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.

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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.

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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.

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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.

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Piroxicam (Feldene)

 

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

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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.

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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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Contributor Information and Disclosures
Author

Patrick J Potter, MD, FRCP(C)  Associate Professor, Department of Physical Medicine and Rehabilitation, University of Western Ontario School of Medicine; Consulting Staff, Department of Physical Medicine and Rehabilitation, St Joseph's Health Care Centre

Patrick J Potter, MD, FRCP(C) is a member of the following medical societies: American Paraplegia Society, Canadian Association of Physical Medicine and Rehabilitation, Canadian Medical Association, College of Physicians and Surgeons of Ontario, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Keith Aj Sequeira  MD, FRCPC, Associate Professor, Director of Education, Department of Physical Medicine and Rehabilitation, Parkwood Hospistal, University of Western Ontario

Disclosure: Nothing to disclose.

Specialty Editor Board

Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM  President and Director, Georgia Pain Physicians, PC; Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Emory University School of Medicine

Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, American Medical Association, International Association for the Study of Pain, and Texas Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Patrick M Foye, MD  Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society

Disclosure: Nothing to disclose.

Kelly L Allen, MD  Medical Director, Medevals

Disclosure: Nothing to disclose.

Chief Editor

Consuelo T Lorenzo, MD  Physiatrist, Department of Physical Medicine and Rehabilitation, Alegent Health Immanuel Rehabilitation Center

Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

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