Even before aspirin was developed, people with arthritis used willow bark to ease their pain and inflammation. By the 1850s, natural derivatives of the bark were widely used in Germany.
But even then people recognized that these salicylates were tough on the tummy. Taking these products was described as “having fire ants in the stomach.”
When aspirin came along in 1899, it was supposed to be easier on the digestive tract. We now know, however, that aspirin can cause heartburn, nausea, stomach pain and even ulcers.
Over the last 100 years the pharmaceutical industry has developed many more nonsteroidal anti-inflammatory drugs (NSAIDs) to alleviate pain. Drugs like ibuprofen, naproxen, diclofenac and piroxicam were all immensely popular as prescription drugs when they were first introduced.
Yet each one shares the same complication as aspirin or salicylic acid derived from willow bark. They can all cause digestive tract distress or worse. Experts have estimated that more than 100,000 people are hospitalized annually and over 16,000 die because of complications caused by NSAIDs (New England Journal of Medicine, June 17, 1999).
What makes this especially troubling is that bleeding or perforated ulcers can occur without warning at any time. Just being vigilant may not be enough to prevent a fatal reaction.
With such a sword of Damocles hanging over patients’ heads, it is hardly surprising that physicians eagerly embraced a new class of NSAIDs called COX-2 inhibitors. Drugs like Vioxx, Celebrex and Bextra were supposed to ease pain without causing the gastrointestinal problems associated with traditional NSAIDs.
Despite the reputation these drugs enjoyed, however, it is not clear that they delivered on the promise. Canadian researchers tracked hospital admissions due to GI bleeding following the introduction of the COX-2 inhibitors (British Medical Journal, June 12, 2004). Instead of dropping, as investigators expected, the rate of this serious problem paradoxically rose 10 percent.
A recent study from Great Britain compared COX-2 inhibitors with conventional NSAIDs (British Medical Journal, Dec. 3, 2005). The researchers concluded that the new COX-2 inhibitors did not offer a significant GI safety advantage over drugs like diclofenac or naproxen.
This revelation is especially disheartening in light of the additional risk COX-2 inhibitors pose for heart attacks and strokes. Vioxx and Bextra were both removed from the market because the cardiovascular risks outweighed the benefits.
Even more alarming is a recent study from the Netherlands suggesting that the NSAID “diclofenac may not be harmless and may induce accelerated progression of hip and knee OA” [osteoarthritis] (Arthritis and Rheumatism, Oct. 2005). Scientists don’t know whether other prescription arthritis drugs might also accelerate joint deterioration.
If there is a lesson to be learned from the COX-2 catastrophe, it is that we need to be more cautious before adopting new medications. Ideally they should be safer and more effective than those they replace. It now appears that the COX-2 inhibitors were neither.
