The side-effects of NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) are not appreciated by the average consumer. A review by Wolfe et. al. (1999) helps put the problem in perspective for one of the problems, i.e. gastrointestinal toxicity. On the basis of conservative figures "...the annual number of hospitalizations in the United States for serious gastrointestinal complications is estimated to be at least 103,000.
At an estimated cost of $15,000 to $20,000 per hospitalization, the annual direct costs of such complications exceed $2 billion." The emphasis of cost fails to recognize the more important mortality rate for patients hospitalized for NSAID-induced upper gastrointestinal bleeding which is reported by Wolfe et. al. as about 5 to 10 percent.
They further report, "It has been estimated conservatively that 16,500 NSAID-related deaths occur among patients with rheumatoid arthritis or osteoarthritis every year in the United States. This figure is similar to the number of deaths from the acquired immunodeficiency syndrome [AIDS] and considerable greater than the number of deaths from multiple myeloma, asthma, cervical cancer, or Hodgkin's disease."
NSAIDs cause problems in the entire gastrointestinal tract,
(Roth, 1988) ranging from peptic ulcers
(Gabriel et al., 1991; Griffin et al., 1991; Langman et al, 1994) to small intestine
(Melo Gomes et al., 1993) and colon problems. In a study to determine the safety of low-dose daily aspirin therapy in the gastrointestinal tract, it was concluded that the safety of even 10 mg of daily aspirin is questionable
,(Cryer & Feldman, 1999) which is way below the typical baby aspirin dosage of 80 mg. The problems do not stop in the gut; the breakdown of the gut mucous membranes leads to leaky gut syndrome with all of its ramifications, including liver toxicity.
One of the most common reasons for taking NSAIDs is to relieve joint pain. Unfortunately the very thing that is expected to gain relief often makes the condition worse by blocking glycosaminoglycans (GAGS) production necessary for repair,
(Dekel et al., 1980; de Vries et al., 1985; Hugenberg et al., 1993) in one in vitro study by as much as 60-70%.
(Yoo et al., 1992) Therapeutic levels of aspirin in vitro have effects of suppressing proteoglycan biosynthesis in normal and degenerating articular cartilage similar to several other NSAIDs
(Brandt & Palmoski, 1984) and permeate osteoarthritic cartilage 35% more than in normal cartilage.
(Palmoski et al., 1984) Glucosamine is in the popular press as an aid to improve the symptoms of osteoarthritis or joint pain. It is one of the glycosamionglycans.and the more NSAIDs are taken to control joint pain the more the very thing that repairs the joints is destroyed. It is a vicious circle.
References
- Wolfe, Michael M., et al, "Gastrointestinal Toxicity of Nonsteroidal Antiinfammatory Drugs" New Eng Jn of Med Vol 340, No 24 (Jun 17, 1999)
- Roth, S.H., “Nonsteroidal anti-inflammatory drugs: Gastropathy, deaths, and medical practice,” Ann Intern Med, Vol 109, No 5 (Sep 1, 1988).
- Gabriel, S.E., L. Jaakkimainen, & C. Bombardier, “Risk for serious gastrointestinal complications related to use of nonsteroidal anti-inflammatory drugs. A meta-analysis,” Ann Intern Med, Vol 115, No 10 (Nov 15, 1991).
- Griffin, M.R. et al., “Nonsteroidal anti-inflammatory drug use and increased risk for peptic ulcer disease in elderly persons,” Ann Intern Med, Vol 114, No 4 (Feb 15, 1991).
- Langman, M.J. et al., “Risks of bleeding peptic ulcer associated with individual non-steroidal anti-inflammatory drugs,” Lancet, Vol 343 (Apr 30, 1994).
- Melo Gomes, J.A. et al., “Double-blind comparison of efficacy and gastroduodenal safety of diclofenac/misoprostol, piroxicam, and naproxen in the treatment of osteoarthritis,” Ann Rheum Dis, Vol 52, No 12 (Dec 1993).
- Cryer, B., & M. Feldman, “Effects of very low dose daily, long-term aspirin therapy on gastric, duodenal, and rectal prostaglandin levels and on mucosal injury,” Gastroenterology, Vol 117, No 1 (Jul 1999).
- Dekel, S., J. Falconer, & M.J. Francis, “The effect of anti-inflammatory drugs on glycosaminoglycan sulphation in pig cartilage,” Prostaglandins Med, Vol 4, No 3 (Mar 1980).
- de Vries, B.J., W.B. van den Berg, & L.B. van de Putte, “Salicylate-induced depletion of endogenous inorganic sulfate. Potential role in the suppression of sulfated glycosaminoglycan synthesis in murine articular cartilage,” Arthritis Rheum, Vol 28, No 8 (Aug 1985).
- Hugenberg, S.T., K.D. Brandt, & C.A. Cole, “Effect of sodium salicylate, aspirin, and ibuprofen on enzymes required by the chondrocyte for synthesis of chondroitin sulfate,” J Rheumatol, Vol 20, No 12 (Dec 1993).
- Yoo, J.U., R.S. Papay, & C.J. Malemud, “Suppression of proteoglycan synthesis in chondrocyte cultures derived from canine intervertebral disc,” Spine, Vol 17, No 2 (Feb 1992).
- Brandt, K.D., & M.J. Palmoski, “Effects of salicylates and other nonsteroidal anti-inflammatory drugs on articular cartilage,” Am J Med, Vol 77, No 1A (Jul 13, 1984).
- Brandt, K.D., “Effects of nonsteroidal antiinflammatory drugs on chondrocyte metabolism in vitro and in vivo,” Am J Med, Vol 83, No 5A (Nov 20, 1987).
- Palmoski, M.J., R.A. Colyer, & K.D. Brandt, “Marked suppression by salicylate of the augmented proteoglycan synthesis in osteoarthritis cartilage,” Arthritis Rheum, Vol 23, No 1 (Jan 1980).
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