Which medications in the drug class Analgesics are used in the treatment of Guillain-Barre Syndrome?

Updated: Jun 24, 2020
  • Author: Michael T Andary, MD, MS; Chief Editor: Milton J Klein, DO, MBA  more...
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Answer

Analgesics

Pain medications may be required in inpatient and outpatient settings. A tiered pharmacologic approach that starts with nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen, with narcotic agents added as needed, is usually recommended.

Acetaminophen (Tylenol, AspirinFree Anacin, Cetafen, Feverall, Mapap Extra Strength)

Acetaminophen is the drug of choice for the treatment of pain in patients with documented hypersensitivity to aspirin or NSAIDs, as well as in those with upper GI disease or who are taking oral anticoagulants.

Ibuprofen (Motrin, Advil, Neoprofen, Provil)

Ibuprofen inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. It is used to provide relief of cervical myofascial pain.

Indomethacin (Indocin)

Indomethacin is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.

Naproxen (Naprosyn, Naprelan, Aleve, Anaprox)

Naproxen is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.

Diclofenac (Voltaren-XR, Cataflam, Zipsor, Cambia)

Diclofenac inhibits prostaglandin synthesis by decreasing COX enzyme activity, which, in turn, decreases formation of prostaglandin precursors.

Ketoprofen

Ketoprofen is used for relief of mild to moderate pain and inflammation. Small dosages are indicated initially in small patients, elderly patients, and patients with renal or liver disease. Doses higher than 75 mg do not increase the therapeutic effects. Administer high doses with caution, and closely observe the patient's response.

Celecoxib (Celebrex)

Celecoxib primarily inhibits 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 the lowest dose of celecoxib for each patient. It is extensively metabolized in liver primarily via cytochrome P450 2C9.

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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