Acute Pulmonary Toxicity from Thalidomide in a Patient with Multiple Myeloma

There are many factors which determine the drug combination a patient is prescribed when diagnosed with multiple myeloma. Some of these factors include the patient’s age, level of abnormal serum proteins, abnormal metaphase cytogenetics, and whether or not a patient is a candidate for autologous stem cell transplant (1). Thalidomide is a chemotherapeutic drug that acts by inhibiting angiogenesis. It is used alone or in combination with dexamethasone to treat recurrent or resistant multiple myeloma. Thalidomide is an immunomodulator as well as anti-angiogenic, is a known teratogen, and can increase the risk of thromboembolic events, such as deep venous thrombosis (DVT) and pulmonary embolus (PE) (2). Although many other classes of chemotherapeutic drugs have been known to cause pulmonary disease, thalidomide as the inciting agent has been reported only once in the English literature (3) and twice in the world literature (4-5).