Supraspinatus Tendonitis Medication
- Author: Thomas M DeBerardino, MD; Chief Editor: Sherwin SW Ho, MD more...
During the acute to subacute phases of shoulder impingement syndrome, a short course of nonsteroidal anti-inflammatory drugs (NSAIDs) is appropriate as an adjunct to the therapy program and other treatment modalities because of their analgesic and anti-inflammatory effects. Choices in this drug classification are extensive; only selected examples are discussed. Patient responses to different NSAIDs may vary. For information on the full array of NSAIDs, their dose, and their schedule, refer to the latest edition of the Physician's Desk Reference.
NSAIDs mechanism of action
The major mechanism of action of NSAIDs is inhibition of the synthesis of prostaglandin (PG), specifically PGE2, via blocking cyclooxygenase (COX), which is the enzyme that converts arachidonic acid into PG. PGs lower the threshold to noxious stimuli by sensitizing the nociceptors to the actions of other noxious endogenous substances (eg, bradykinin, histamine, substance P, serotonin). In soft tissue, PGE2 causes pain and inflammation. In the GI tract, it is cytoprotective and increases the secretion of mucus and bicarbonates and decreases the secretion of gastric acids and digestive enzymes. In the renal system, PGE2 enhances renal salt and water excretion by acting as a vasodilator of small arterial blood vessels.
The COX pathway is subdivided into COX-1, which is responsible for PGE2 production in the GI tract and kidneys, and COX-2, which is responsible for inflammatory PG synthesis during soft tissue injury. NSAIDs serve as competitive inhibitors of COX activity and either selectively inhibit the COX-2 enzymes or nonselectively inhibit both the COX-1 and the COX-2 enzymes, making the nonselective NSAIDs a higher risk for potential ulcerogenic and other adverse effects.
Adverse drug reactions
All NSAIDs have similar adverse drug reactions. The first is hepatotoxicity. The liver function profile should be monitored periodically, especially in high-risk individuals. The second is renal toxicity. The renal function profile should be monitored periodically, especially in high-risk individuals. The third is GI toxicity. Symptoms may include nausea, diarrhea, acid reflux, and periumbilical cramping. Consider administering NSAIDs in conjunction with GI protective medications (eg, misoprostol, omeprazole, H2 blockers), and instruct patients to take NSAIDs with food. If GI symptoms persist for more than 2 weeks or if patients have evidence of complications (eg, iron deficiency anemia, GI bleeding, unexplained weight loss, dysphagia), an endoscopic evaluation is indicated. The fourth is aplastic anemia. Monitor the complete blood count, especially platelets, periodically for 1-2 months. The fifth is anaphylaxis. Inquire about and check medical records for a history of allergic reactions.
Nonsteroidal anti-inflammatory drugs
Most widely used drugs in the world, exhibiting anti-inflammatory, antipyretic, and analgesic activities. They are primarily used for treating inflammatory conditions that are musculoskeletal in origin. Numerous drugs are available in this category, and they all have similar drug profiles.
Arylpropionic acid prototypical NSAID that has the advantage of causing less epigastric pain, GI occult blood loss, and less hepatotoxicity. Mostly indicated for rheumatoid arthritis and osteoarthritis for mild to moderate pain. Compared with other available NSAIDs, it has a short half-life.
Chemical composition is heteroaryl acetic acid with a short half-life. Delayed-release enteric-coated form is diclofenac sodium, and immediate-release form is diclofenac potassium. Both are primarily indicated for rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis. Diclofenac can cause hepatotoxicity; hence, monitor liver enzymes in the first 8 wk of treatment. Diclofenac has a relatively low risk for bleeding GI ulcers.
Indole NSAID with an intermediate half-life, indicated for rheumatoid arthritis and osteoarthritis. Short-acting form is approved for analgesic use, comparable to aspirin/acetaminophen with codeine. Etodolac has a lower risk of producing GI complications and, as a result, is especially well tolerated in elderly patients.
Probably the most potent of the arylpropionic acids, with a long half-life. Indicated for rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, juvenile arthritis, acute gout, and mild to moderate pain. Available in a controlled-release form, which is also used for acute pain, and an enteric-coated form, which is not used for acute pain.
An arylpropionic acid with a 40-50 h half-life and can be given once daily. Used for relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of COX, which results in a decrease in PG synthesis.
Alkanone NSAID with a long (24 h) half-life and can be given once daily. Has a lower risk of producing GI complications and is indicated for rheumatoid arthritis and osteoarthritis.
Enolic acid, piroxicam with long half-life (50 h) that can be given once daily. Indicated for use in rheumatoid arthritis and osteoarthritis. Has high GI toxicity (greater than aspirin).
Selective COX-2 inhibitor NSAID. Approved by FDA on December 31, 1998 and indicated for use in osteoarthritis and rheumatoid arthritis and for moderate to severe pain. Potentially presents less GI complications and platelet aggregation problems than the nonselective COX-inhibitor NSAIDs. Renal complications are comparable. Has a sulfonamide chain and is primarily dependent on cytochrome P-450 enzymes (a hepatic enzyme) for metabolism.
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