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Potential Arthritis Drug Falls Short
FRIDAY, Sept. 30 (HealthDay News) -- Efforts to develop a new class of chronic arthritis medications using a painkiller compound naturally produced by the body have fallen short, researchers say. A new animal-based study has shown that endomorphin, the morphine-like pain control agent in question, does not have any "observable effect" on reducing the sensitivity of arthritic joint nerves in the long run. The therapy did, however, provoke a dramatic reduction -- upwards of 75 percent -- in short-term joint hypersensitivity. "I don''t think it''s all negative news," said study co-author Jason J. McDougall, an associate professor in the department of physiology and biophysics at the University of Calgary in Alberta, Canada. "We were able to block pain responses in normal joints and also in the early stages of arthritis. But clearly arthritis is a chronic long-term disease, so we were obviously disappointed that we weren''t able to block the pain of long-term inflammation." The mixed findings come against the backdrop of last year''s ban by the U.S. Food and Drug Administration on sales of the popular cox-2 inhibitors Vioxx and Bextra due to an increased risk for cardiovascular complications associated with long-term use. The removal of the drugs has limited pain management options for millions of Americans, although a third cox-2 drug -- Celebrex -- has been allowed to remain on the market with new packaging that highlights potential risks. In this context, the authors described the excitement that has recently greeted the identification of two forms of endomorphin, a painkiller, or analgesic, naturally produced by the body. Scientists have agreed that endomorphins are, theoretically, at least as powerful a tool for pain management as morphine, a problematic narcotic derived from the opium poppy. The authors stressed that morphine is notoriously difficult to administer with precision -- provoking a wide range of side-effects like cardio-respiratory depression, severe constipation, nausea, and a manic-depressive disorder known as dysphoria. On the other hand, researchers have previously found that endomorphins are able to sidestep such concerns by virtue of their hard-wired relationship to the body''s own pain control receptors. Such receptors, known as u-opioids, appear to be highly sensitized to endomorphins, selectively drawing the natural analgesic to their target spots throughout the peripheral tissue of joints. In the October issue of Arthritis and Rheumatism, the researchers say these findings have raised hopes that the body''s home-made painkiller might be the most beneficial means for helping the one-third of the world''s adult population who suffer from some form of arthritic pain. To explore their potential, McDougall and his colleagues looked at the effect of "endomorphin 1" -- the most common and potent of the two known endomorphins-- on both acute and chronic arthritis in male lab rats. After inducing inflammation in their right knee joints, the researchers treated the rats with endomorphin 1 at various points following the onset of knee arthritis -- either 48 hours post-inflammation during the acute stage of joint pain, or at the one-week or three-week point during the chronic stage. At all stages of treatment, the authors measured the electrical activity, or firings, of knee nerve-endings in response to an exaggerated rotation of the joint. Nerve-ending readings were also taken among rats that did not have arthritic knees but were nonetheless also treated with endomorphin. The researchers found that endomorphin treatment caused nerve activity -- and presumably any related pain -- to drop off by approximately 75 percent in both normal rats and those with acute arthritis of the knee. However, when injected one or three weeks after the onset of arthritis, endomorphin had no effect on nerve activity. Subsequent autopsies further revealed that beginning one week after induced knee joint inflammation, the numbers and activity levels of some local u-opioid receptors had dropped below normal. At three weeks, all receptor activity levels dropped off significantly. The Canadian team concluded that both the presence and activity levels of the endomorphin receptors do not appear sustainable over the long haul, decreasing in effectiveness as arthritis pain continues into its long-term chronic phase. Nevertheless, the researchers said, future study might lead to a better understanding of exactly how receptor activity works, and how to perhaps alter this naturally occurring process to better control chronic pain. "An inflamed joint is obviously not a normal joint, so there are mechanisms in these joints that are preventing endomorphins from addressing these analgesic effects," McDougall said. "So the next question is: what can we do to improve that?" Dr. Brennan Spiegel, an assistant professor of medicine at the David Geffen School of Medicine at the University of California in Los Angeles, isn''t sure if endomorphin will ever fit the bill. "For a while, it looked like the cox-2 drugs were manna from heaven, but clearly they''re not," Spiegel said. "So now we know that we''re basically out at sea again groping for another island of safety." "But, clinically, we have not had much success at all with morphine-like substances," Spiegel added. "They''re useful for other pains but not for this sort of chronic arthritis pain, so you could argue it''s a groundless pursuit." Spiegel stressed that arthritis sufferers need not despair, and noted that his own research has highlighted many pain management routines that are effective, safe, inexpensive and widely available. "Just using an over-the-counter NSAID like Aleve or Advil plus a proton-pump inhibitor such as Prilosec or Nexium is a very effective combo that appears to be a very safe in minimizing GI side-effects," he said. "And it''s the safest on the heart compared to cox-2 inhibitors . . . It may not be manna from heaven, but it''s the closest we''ve got." More information For more on arthritis medications, check out the Arthritis Foundation. .
Last Updated: Sept. 30, 2005 |