Cancer drug could help lupus patients, German researchers confirm
Hamburg - A drug used to treat a form of blood cancer could also be helpful in the treatment of lupus, according to a team of German researchers.
The drug, marketed under the brand name Velcade (bortezomib), is called a proteasome inhibitor and laboratory experiments with mice indicate it is effective against the auto-immune disease lupus," says lead researcher Dr. Reinhard Voll, of the University of Erlangen- Nuremberg.
"Autoantibody-mediated diseases such as autoimmune hemolytic anemia, immune thrombocytopenia, myasthenia gravis and systemic lupus erythematosus are often difficult to treat," Voll says in a report by HealthDay.
"A big problem is that plasma cells, which are the predominant producers of the disease-causing autoantibodies, can't be efficiently attacked with current treatments," Voll says.
Systemic lupus erythematosus (SLE or lupus) is a chronic autoimmune disease that can be fatal, though with recent medical advances, fatalities are becoming increasingly rare.
As with other auto-immune diseases, the immune system attacks the body's cells and tissue, resulting in inflammation and tissue damage.
Lupus can affect any part of the body, but most often harms the heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system.
The course of the disease is unpredictable, with periods of illness (called flares) alternating with remission. Lupus can occur at any age, and is most common in women, particularly of non-European descent.
Lupus is treatable symptomatically, mainly with corticosteroids and immunosuppressants, though there is currently no cure.
For the new study, Voll's team found that bortezomib efficiently eliminated the plasma cells in the mice, leading to a drastic decrease in autoantibodies and prolonged survival. In addition, the drug had no effect on other cells, he says.
"Proteasome inhibitors may be beneficial in refractory human diseases caused predominantly by autoantibodies," Voll says. "Proteasome inhibitors can selectively deplete plasma cells, which are resistant to current treatments."
The findings were published in the latest online edition of Nature Medicine. (dpa)