The essential guide to anti inflammatory drugs
by Nathan Wei, MD, FACP, FACR
Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.
Click here: Second Opinion Arthritis Treatment Kit
Non Steroidal Anti Inflammatory Drugs (NSAIDS) are among the most commonly prescribed drugs for arthritis.
The prototype of all NSAIDS is aspirin. Other NSAIDS include ibuprofen (Motrin, Advil), naproxen (Naprosyn, Aleve), sulindac (Clinoril), oxaprozin (Daypro), fenoprofen (Nalfon), etodolac (Lodine), piroxicam (Feldene), nabumetone (Relafen), indomethicin (Indocin), ketoprofen (Orudis), meclofenamate (Meclomen), tolmetin (Tolectin), diflunisal (Dolobid), diclofenac (Voltaren, and meloxicam (Mobic).
Another type of NSAID, a COX-2 inhibitor that has fewer gastrointestinal side effects is Celebrex. A combination of naproxen adn a proton pump inhibitor to protect the stomach is Vimovo. A food-based NSAID is Limbrel. Topical NSAIDS include Voltaren gel and Pennsaid. NSAIDS help reduce signs and symptoms of inflammation. They do not eliminate it because they have no significant effect on the underlying disease process.
NSAIDS are organic acids that are highly protein bound in the blood. These properties allow them to penetrate into inflamed tissue which have a lower pH.
NSAIDS work by blocking cyclooxygenase, the enzyme that helps with production of prostaglandins, and thromboxane- key factors in the initiation of inflammation.
Prostaglandins also are responsible for a multitude of normal functions in the body including maintenance of kidney blood flow, secretion of the protective mucus lining in the stomach, and enhancing the attraction of platelets (a blood cell responsible for clotting) to each other.
Besides inhibiting inflammation, NSAIDS also decrease pain, suppress fever, and decrease the stickiness of platelets.
As mentioned earlier, more recently, specific COX 2 inhibitory NSAIDS have been developed. These block the branch of the cyclooxygenase system that causes inhibition of inflammation without inhibiting the prostaglandins that protect the stomach. Theoretically, these are safer anti inflammatory drugs.
An example is celecoxib (Celebrex.
Because of their mechanism of action, NSAIDS have many potential side effects.
In the gastrointestinal (GI) system, NSAIDS cause stomach irritation and ulcer. Stomach acid is increased and the protective mucus lining and bicarbonate buffer is decreased. Gastrointestinal bleeding and ulcer risk is increased.
NSAIDS also cause an anticoagulant effect. Platelet adhesiveness is decreased. Aspirin will cause long-term irreversible platelet effects that last the lifetime of the platelet (about 10 days), while other NSAIDS have a reversible effect that lasts as long as the drug is in the system. NSAIDS appear to inhibit the anti-platelet effect of aspirin and should not be taken at the same time.
Another anticoagulant effect occurs in patients who are taking the blood-thinner, warfarin. NSAIDS, because they are so highly protein bound, displace warfarin from plasma proteins and as a result there is more warfarin available to cause more anticoagulant effect.
NSAIDS can cause liver toxicity. Up to 15 per cent of patients will have elevations in liver enzymes. While severe toxicity is unusual, life-threatening hepatitis has been reported. Regular monitoring of liver function is advised for patients who take anti inflammatory drugs regularly.
NSAIDS can have a negative effect on kidney function. They reduce blood flow to the kidney. In elderly patients and in patients who already have reduced kidney blood flow (dehydrated, congestive heart failure), these effects can be substantial leading to the possibility of kidney failure.
Patients with arthritis conditions like systemic lupus erythematosus and progressive systemic sclerosis also are increased risk for this problem. NSAIDS may cause inflammation of kidney tissue and severe protein leakage in the urine.
Other potential side effects include rashes, allergic reactions (asthma), anaphylactic shock, blood cell disorders, ringing in the ears headaches, and meningitis (particularly in patients with SLE).
More recently, all NSAIDS have been associated with an increased risk of cardiovascular side-effects (hypertension, edema, heart attack and stroke).
Virtually all NSAIDS are converted to inactive metabolites in the liver and excreted by the kidney. Dose reduction and careful monitoring are required in the elderly and in other patients where kidney blood flow may be compromised.
The treatment of a disorder is dependent on the auteness or chronicity of the disorder. For instance a headache may require a single or perhaps two doses of NSAID for its analgesic effect. Arthritis, on the other hand, will generally require a chronic anti-inflammatory effect which indicates constant and regular dosing.
Patients who do not respond to one NSAID are often switched to another. While going to an NSAID of a different chemical class may make sense, this is not always effective.
Combining NSAIDS is not advised since toxicity is enhanced. Many patients take aspirin for cardiovascular prophylaxis. Adding an aspirin to COX 2 therapy essentially converts COX 2 therapy to NSAID therapy.
While anti inflammatory drugs are helpful for many patients, they are not a panacea and are capable of causing many potential side effects. They should only be used with the advice of a knowledgeable physician.
More recently there has been a trend away from using oral NSAIDS in favor of topical ones.
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