Rituxamab, a drug that treats lymphoma and rheumatoid arthritis, may soon be used to help combat the destruction of pancreatic beta cells in newly diagnosed cases of type 1 diabetes. Researchers at Indiana University have found that the drug, originally developed and sold by Genentech as Rituxan, temporarily slows or stops the destruction of the 10 or 20 percent of beta cells that type 1s typically have remaining when they are first diagnosed.
Rituxan works to wipe out B lymphocytes, immune cells that grow out of control in lymphatic cancer and begin destroying healthy tissue. The same cells are at work in rheumatoid arthritis. Because both illnesses are autoimmune diseases, scientists theorized that the drug might work to counter the autoimmune destruction of remaining insulin-producing beta cells in recently diagnosed type 1s. One reason behind their thinking was that B cells have been shown to modulate T cell behavior. Rogue T cells are the prime culprit in the body’s destruction of beta cells in type 1s.
The team recruited 87 recently diagnosed type 1 patients, ranging in age from 8 to 40 years old. The patients were divided into two groups, with one receiving four 375 mg/m2 doses of rituxamab and the other receiving four doses of placebo over a three-week period.
Rituxamab worked well at first, halting the destruction of beta cells and even allowing the pancreas to begin producing more insulin. Over the course of a year, however, the effects lessened and insulin production declined at the same rate as in the type 1s who were receiving a placebo. The scientists said that rituxamab, to remain effective, may have to be administered at regular intervals, as it is in cancer and rheumatoid arthritis treatments. Redosing in the treatment of those diseases typically occurs at four- to six-month intervals. Because the research team did not pursue the study beyond a one-time administration of the drug to test its usefulness in treating diabetes, nobody will know the long-term effects of rituxamab until a more comprehensive study is done.
The study opens to door to focusing on rogue B cells, as well as out-of-control T cells, as a prime element in therapies designed to make the body stop destroying its own beta cells.
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