Trying to unravel 'The Great Imitator.' (systemic lupus erythematosus)
For many allergy sufferers, the answer seems obvious--avoid the substance that causes the allergies. But for people with systemic lupus erythematosus (SLE), the answer isn't quite so simple: They are, in a sense, allergic to themselves because their immune system attacks healthy cells. Advances in
treating the disease, which used to claim the lives of most of its victims, have dramatically lowered the fatality rate and paved inroads for patients to lead normal lifestyles. Last week, researchers added pinpoints to mapping the disease's cause and its treatment.
Like other inflammatory forms of arthritis, such as rheumatoidarthritis, SLE has a propensity to attack the lining of joints and other tissues. Known best for the butterfly-shaped facial rash it sometimes creates, SLE causes the body to produce excess antibodies, called autoantibodies, that target healthy cells. Production of these by B cells is either helped or suppressed by T cells; both B and T cells are immune system components that researchers believe may be part of the disease's etiology. In addition, because the body fails to clear all of these excess autoantibodies, they may lodge in and damage such vital organs as the kidneys, brain, heart and lungs.
Causing an estimated 16,000 new cases in the United Statesannually, SLE has a predilection for women, who are infected some nine times more than men. Symptoms include fever, appetite loss, fatigue and joint pain and swelling, although these vary in each individual by severity and frequency. The disease, often referred to as "The Great Imitator,' is commonly misdiagnosed as fibrositis, skin photosensitivity and even psychosomatic illness. In addition, there are drugs that either induce SLE or exacerbate current symptoms, including hydralazine, an antihypertensive drug, and procainamide, a drug used to control irregular heartbeats.
But one group of researchers is using those drugs to try to getat the heart of what causes SLE. Bruce C. Richardson and his colleagues at the University of Michigan in Ann Arbor previously found that in a process called autoreactivity, some chemicals induce T cells to produce autoantibodies, suggesting that normal T cells may contain suppressed genes that are triggered by some mechanism to become autoreactive. The group last week presented research showing that hydralazine and procainamide produced the same effects in T cells as previously tested chemicals, including altering T cell DNA. This finding represents one more step in unraveling the complex mechanism of what activates the disease, says Gale McCarty, a rheumatologist with Georgetown University Hospital in Washington, D.C. "Once you understand the mechanism,' she says, "you understand the disease.'
Yet since the mechanism still is not fully understood,emphasis on treatment continues. In San Francisco, researchers at the Veterans Administration Medical Center at the University of California successfully used monoclonal antibodies to extend the life of mice with a lupus-like disease. Although David Wofsy and his colleagues previously showed they could retard progress of the disease in mice, this is the first time they actually tried to reverse advanced cases of the disease. Using the antibodies, researchers slowed the functions of helper T cells that normally aid in production of antibodies but may "overhelp' in the case of SLE. Mice more than 7 months old that were injected with the monoclonal antibodies lived 1 year past their expected death at 9 months. Untreated mice lived only about 1 more month. But because the antibodies also diminished helper T cells that might be needed for future normal immune responses, Wofsy now is looking into using just fragments of the monoclonal antibody to combat this problem.
Photo: Karen Hartley reports from Washington, D.C., at the 51st annual scientific meeting of the American Rheumatism Association
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|Date:||Jun 20, 1987|
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