Reply to Hattori et al: Thalidomide and pulmonary hypertension. A causal or casual relationship?

amyloid protein. The aetiology of PH in this patient is still unclear. She was sero-negative for human immunodeficiency virus, and lacked the clinical symptoms that would indicate systemic sclerosis and systemic lupus erythematosus. She did not have preexisting chronic lung and liver disease or congestive heart disease. Direct association of MM with PH is unlikely in this case because dyspnoea progressed when MM was well controlled by thalidomide. In addition, there was no evidence for plasma cell invasion or amyloidosis in the lungs and heart. Thus, a coincidental occurrence of primary PH in MM is one explanation; however, this disease is usually diagnosed before 40 years of age (Peacock, 1999). In this case, plasma concentration of vascular endothelial growth factor (VEGF) was persistently elevated; 110 pg/ml in May 2000, 75 pg/ml in September 2000, 62 pg/ml in March 2001 and 80 pg/ml in July 2001 (control level is less than 35 pg/ml). Continuous elevation of VEGF may augment the proliferation of pulmonary arteries (Farber & Loscaizo, 2004). Alternatively, an adverse effect of thalidomide should be considered because symptoms for PH appeared and gradually progressed after the use of this drug. Although pulmonary complications of this drug are rare, in the absence of PE, drug-induced PH has been reported, for example by appetite suppressants (Peacock, 1999; Farber & Loscaizo, 2004). Although the precise mechanism remains to be elucidated, PH should be taken into consideration when thalidomide is used in MM patients. Yutaka Hattori Masayuki Shimoda Shinichiro Okamoto Toru Satoh Tsunayuki Kakimoto Yasuo Ikeda Division of Haematology, Department of Pathology, and Division of Cardiology, Department of Medicine, Keio University School of Medicine, Tokyo, Japan. E-mail: [email protected]