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Inflammation & Anti-Inflammatory Medications - by James Tippett, MD


Anti-Inflammatory Medication


Inflammation is one of the earliest disease states recognized and defined by medical scientist. The inflammatory response is a physiologic defense mechanism mediated by our immune system in response to many potential insults in our environment including physical (trauma, injury), chemical (burns, toxins), and biologic (infection) agents. It can be localized, confined to a specific area or organ system of our body, or generalize, affecting our entire body and multiple organ systems. In acute inflammation, the defense involves walling-off or isolating the offending agent, removing it and any damaged tissue from the area, followed by reconstitution of the damaged area with normal cells/tissue. There are also diseases of chronic inflammation whereby the pathological process is long-standing and in some of these diseases, our immune system becomes faulty and attacks normal tissue as if it were foreign matter (as in rheumatoid arthritis, RA).


This is called autoimmunity.


The immune process begins with dilatation of arteries and increased blood flow to the inflamed area, then serum from the vessels leaks out into the soft tissue space. White blood cells are recruited to the area (like soldiers going to battle) and this results in exudative fluid (pus). This vascular and cellular response accounts for the classic signs and symptoms of inflammation: redness, swelling, heat, pain, and loss of function. There are also biochemical reactions that occur through enzyme catalyst. Remember from previous articles that enzymes are proteins that control biochemical reactions and thus the product(s) that are formed from that particular reaction. The mechanism of action of many medications involves either inhibiting or stimulating enzymes, the former decreasing and the later increasing the amount of product produced. Two enzymes important in the inflammatory process are known as cyclooxygenase-1 and -2, abbreviated Cox-1 and Cox-2. Attempts to modify the inflammatory symptoms with drug therapy that inhibits these enzymes have been occurring for many years and are known as anti-inflammatory agents.


Centuries ago scientists discovered that the bark from various trees and plants, when applied topically to inflamed tissue, had anti-inflammatory properties removing the redness, heat, swelling, and pain from the area. The Willow tree bark was noted to have strong therapeutic benefits and eventually the specific substance that had these properties was isolated and found to be salicylic acid. The acid was crystallized into a powder and administered orally to patients resulting in improvement in symptoms of systemic inflammation such as fever, headache, muscle and joint pain, and malaise. However, the compound was a very strong acid and, in many patients, had severe side effects of abdominal pain, nausea, and vomiting. Around the beginning of the 20th century, a German chemist was able perform a simple chemical reaction that esterified salicylic acid to acetylsalicylic acid, a much weaker acid with less gastrointestinal side effects. The drug was mass produced by, guess who? Bayer Corporation. It became known as Aspirin (ASA), the first anti-inflammatory drug.


ASA was recommended world- wide for many illnesses, but particularly for most forms of arthritis. It was noted in the treatment of rheumatoid arthritis that relatively small doses improved symptoms, but to truly impact the severe deforming symptomatology, very large doses were required. In the 1970’s, the ability to measure therapeutic blood levels of Aspirin was not readily available but it was determined that when these necessary levels were obtained, patients would experience ringing in their ears (tinnitus). In the rheumatology clinic, after starting a patient on ASA, I recall instructing them to increase the dose each week by 2-4 tablets daily until they experienced tinnitus, then decrease the dose back by 2-3 tablets. We had some patients taking up to 40 tablets daily!


Around 1950, an astute physician noted that when patients with rheumatoid developed a new illness, particularly an infection, their arthritis pain improved. He concluded that this occurred because in response to the new stress, the patient’s adrenal glands produced more of the stress hormone, cortisone. Researchers harvested many pounds of animal adrenal glands, extracted the cortisone, and physicians began administering it to rheumatoid patients at the Mayo Clinic. An almost immediate and miraculous response was noted. Patients who had been wheelchair bound for years were walking without assistance in a matter of weeks. Physicians nationwide began using adrenal steroids indiscriminately for a host of diseases including allergies and asthma, but the results for rheumatoid disease were spectacular. In a few short years, however, physicians began to observe a growing list of increasingly severe side effects: skin damage with the occurrence of poorly healing wounds, osteoporosis with spontaneous fractures, infections from compromised immunity, diabetes mellitus, hypertension, and dense cataracts. Gradually, the relationship between the steroid use and the damages was established and cortisone treatments had to be stopped or tapered.

Researchers embarked on developing new anti-inflammatory drugs based on the chemical structure of ASA and distanced them from the steroid catastrophe by calling them Non-Steroidal Anti-Inflammatory Drugs, NSAIDs. There are over 20 NSAIDs now available with the most widely recognized being ibuprofen (Advil, Motrin, Nuprin) and naproxen (Alleve, Naproxen).


Grab a copy of the Herald Journal next week to read about the effectiveness and safety profile of the different NSAIDs.


Dr. Tippett is the founder of Comprehensive Quality Healthcare Providers located at 1210 Commerce Dr. Suite 106 Greensboro, Ga 30642. He can be reached at 706-510-3659. Visit his webpage at www.drrtippett.com

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