Non-steroidal anti-inflammatory drugs and the continuum of renal dysfunction

NSAIDs may be grouped according to their preference for COX-1 and COX-2 enzymes. Those that favor COX-1 are more likely to cause gastrointestinal side effects. Those that favor COX-2 have a higher risk of cardiovascular effects but less gastrointestinal effects. Higher dosages of NSAIDs tend to result in more COX-2 enzyme inhibition (and more cardiovascular side effects), even in those NSAIDs traditionally seen as low risk (such as ibuprofen). NSAIDs with higher activity against COX-2 enzymes should be used with caution in people with cardiovascular disease or at increased risk of cardiovascular disease.

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Early pilot studies have revealed that when injured football players were treated following competition with the conventional methods of ice or NSAIDs versus Cytolyse and Life Force Super Antioxidant, they returned to play with more vigor when treated with the latter combination. In a clinical setting, Dr. Tris Trethart, a family physician who uses a complementary nutritional approach, found that anti-oxidants ( Life Force ) and proteolytic enzymes ( Cytolyse ) "were extremely useful in the early stages after a sports injury, or for persons recovering from surgical procedures. Also, our preliminary experience indicates that the combination of Life Force Super Antioxidant and Cytolyse have benefited some athersclerosis conditions. NSAIDs are incapable of this type of effect. We have also seen some promising work by Dr. William Donald Kelly, who has worked with cancer patients using proteolytic enzymes and anti-oxidants. We've had good success with conditions such as back strain, disc pain, sciatica and whip lash. With these conditions, the management of the anti-inflammatory process by the proteolytic enzymes and anti-oxidants may well be why we are seeing a positive response."

A variety of allergic or allergic-like NSAID hypersensitivity reactions follow the ingestion of NSAIDs. These hypersensitivity reactions differ from the other adverse reactions listed here which are toxicity reactions, . unwanted reactions that result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual; hypersensitivity reactions are idiosyncratic reactions to a drug. [67] Some NSAID hypersensitivity reactions are truly allergic in origin: 1) repetitive IgE -mediated urticarial skin eruptions, angioedema , and anaphylaxis following immediately to hours after ingesting one structural type of NSAID but not after ingesting structurally unrelated NSAIDs; and 2) Comparatively mild to moderately severe T cell -mediated delayed onset (usually more than 24 hour), skin reactions such as maculopapular rash , fixed drug eruptions , photosensitivity reactions , delayed urticaria , and contact dermatitis ; or 3) far more severe and potentially life-threatening t-cell-mediated delayed systemic reactions such as the DRESS syndrome , acute generalized exanthematous pustulosis , the Stevens–Johnson syndrome , and toxic epidermal necrolysis . Other NSAID hypersensitivity reactions are allergy-like symptoms but do not involve true allergic mechanisms; rather, they appear due to the ability of NSAIDs to alter the metabolism of arachidonic acid in favor of forming metabolites that promote allergic symptoms. Afflicted individuals may be abnormally sensitive to these provocative metabolites or overproduce them and typically are susceptible to a wide range of structurally dissimilar NSAIDs, particularly those that inhibit COX1. Symptoms, which develop immediately to hours after ingesting any of various NSAIDs that inhibit COX-1, are: 1) exacerbations of asthmatic and rhinitis (see aspirin-induced asthma ) symptoms in individuals with a history of asthma or rhinitis and 2) exacerbation or first-time development of wheals or angioedema in individuals with or without a history of chronic urticarial lesions or angioedema. [26]

Non-steroidal anti-inflammatory drugs and the continuum of renal dysfunction

non-steroidal anti-inflammatory drugs and the continuum of renal dysfunction

A variety of allergic or allergic-like NSAID hypersensitivity reactions follow the ingestion of NSAIDs. These hypersensitivity reactions differ from the other adverse reactions listed here which are toxicity reactions, . unwanted reactions that result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual; hypersensitivity reactions are idiosyncratic reactions to a drug. [67] Some NSAID hypersensitivity reactions are truly allergic in origin: 1) repetitive IgE -mediated urticarial skin eruptions, angioedema , and anaphylaxis following immediately to hours after ingesting one structural type of NSAID but not after ingesting structurally unrelated NSAIDs; and 2) Comparatively mild to moderately severe T cell -mediated delayed onset (usually more than 24 hour), skin reactions such as maculopapular rash , fixed drug eruptions , photosensitivity reactions , delayed urticaria , and contact dermatitis ; or 3) far more severe and potentially life-threatening t-cell-mediated delayed systemic reactions such as the DRESS syndrome , acute generalized exanthematous pustulosis , the Stevens–Johnson syndrome , and toxic epidermal necrolysis . Other NSAID hypersensitivity reactions are allergy-like symptoms but do not involve true allergic mechanisms; rather, they appear due to the ability of NSAIDs to alter the metabolism of arachidonic acid in favor of forming metabolites that promote allergic symptoms. Afflicted individuals may be abnormally sensitive to these provocative metabolites or overproduce them and typically are susceptible to a wide range of structurally dissimilar NSAIDs, particularly those that inhibit COX1. Symptoms, which develop immediately to hours after ingesting any of various NSAIDs that inhibit COX-1, are: 1) exacerbations of asthmatic and rhinitis (see aspirin-induced asthma ) symptoms in individuals with a history of asthma or rhinitis and 2) exacerbation or first-time development of wheals or angioedema in individuals with or without a history of chronic urticarial lesions or angioedema. [26]

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