Patients receiving thalidomide for treatment of multiple myeloma may be at an increased risk of developing deep vein thrombosis, according to a recent article published in the journal Blood.
There are approximately 40,000 people in the United States living with multiple myeloma, with 14,000 new cases of multiple myeloma diagnosed each year in the U.S., making it the second most common blood cancer. Multiple myeloma is a cancer involving important immune (infection-fighting) cells called plasma cells. Plasma cells aid the body in fighting infection by producing specialized proteins called antibodies that have the ability to target and/or kill foreign cells. In multiple myeloma, cancerous plasma cells produce abnormal and excessive antibodies that do not have the ability to properly fight infection. In addition, the cancerous plasma cells accumulate in the bone marrow, suppressing the normal formation and function of other cells that are necessary for normal production of blood cells and immune functions. The excessive accumulation of cancer cells in the bone marrow ultimately leads to the formation of tumors in the bone and to the breakdown of bone. Standard treatment for multiple myeloma is chemotherapy.
Thalidomide is a substance known for its anti-angiogenesis properties. Angiogenesis is the formation of new blood vessels in the body and is a crucial component for the development of cancer. Blood vessels are needed to supply cancer cells with essential nutrients from the blood. Anti-angiogenesis is the inhibition of the formation of new blood vessels. By stopping blood vessels from forming, cancer cells are “starved” of nutrients, ultimately inhibiting cancer development and growth. Previous clinical studies have demonstrated that thalidomide achieves significant anti-cancer responses in patients with recurrent multiple myeloma.
Researchers from the University of Arkansas recently conducted a clinical trial further evaluating thalidomide in the treatment of multiple myeloma. In this study, 100 patients with multiple myeloma received combination chemotherapy and dexamethasone (steroid). Fifty of these patients were also treated with thalidomide. Following treatment, nearly 30% of patients who received thalidomide developed deep vein thrombosis (DVT), compared with only 4% not given the agent. DVT is the accumulation of cellular elements, platelets, fibrin and clotting proteins which develop into a thrombus (clot) on the inside of a deep blood vein. DVT can be life threatening as it can develop in major veins or dislodge and travel to the lungs, blocking necessary blood flow and oxygen exchange. Patients who developed DVT in this trial were treated with anticoagulants, which resolved the problem in 75% of patients and allowed them to continue treatment with thalidomide.
These findings suggest that the addition of thalidomide to combination chemotherapy and dexamethasone in patients with multiple myeloma increases the risk of the development of DVT. However, treatment with anticoagulants appear to resolve this complication in the majority of patients and allow continued treatment. Future clinical trials will help determine the timing for which anticoagulants may be utilized in order to prevent DVT in patients receiving thalidomide. Patients with multiple myeloma receiving thalidomide may wish to speak with their physician about monitoring for DVT and/or the use of anticoagulants. (Blood, Vol 98, No. 5, pp. 1614-1615, 2001)