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Journal of Clinical Oncology, Vol 23, No 10 (April 1), 2005: pp. 2425-2426 © 2005 American Society of Clinical Oncology. DOI: 10.1200/JCO.2005.04.054
Side Effects and Good Effects from New Chemotherapeutic AgentsCASE 2. Thalidomide-Induced Interstitial PneumonitisHokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Japan
A 65-year-old woman with multiple myeloma (immunoglobulin G-
Thalidomide, which was originally produced in Germany, was used as a sedative and hypnotic drug from the 1950s but was withdrawn from the market in the 1960s due to its teratogenic effects in the fetus when administered to pregnant women. However, thalidomide has been used in recent years after having shown to be of great value in the treatment of inflammatory manifestations of leprosy, multiple myeloma, and other malignancies, owing to its immunomodulating and antiangiogenetic effects.1 The common adverse effects of thalidomide are constipation, dizziness, edema, fatigue, mood changes, and peripheral neuropathy.2 Thalidomide-induced pulmonary toxicity is rare. The only previously reported significant pulmonary toxicity associated with thalidomide is pulmonary emboli.3 Only one case with lung toxicity due to thalidomide has previously been reported.4 That patient developed respiratory insufficiency with a right-sided interstitial and alveolar pattern on chest x-ray that was normalized after discontinuation of treatment with thalidomide. However, this was not a definite case because computed tomography data or data on bronchoscopy or BAL were not presented. Three cases of pulmonary toxicity during prostate cancer treatment with docetaxel and thalidomide, including one case of IP, have been reported.5 It was concluded that lung toxicity was mainly caused by docetaxel. Our case is therefore the first definite case of thalidomide-induced IP. BAL revealed markedly increased cell counts with preponderance of lymphocytes, suggesting a hypersensitivity phenomenon.6 We postulate that allergic reaction is the mechanism by which IP developed in our case. The earlier recurrence of respiratory insufficiency following readministration of thalidomide at a smaller dose supports the speculation of allergic etiology. The possibility of relapse of sarcoidosis was ruled out because of the normal angiotensin I-converting enzyme level and benign clinical course without steroid use. Since thalidomide is being prescribed with increasing frequency for hematological and nonhematological malignancies, we believe that physicians should be aware of this rare but serious complication. Authors' Disclosures of Potential Conflicts of Interest The authors indicated no potential conflicts of interest.
REFERENCES
1. Raje N, Anderson K: Thalidomide: A revival story. N Engl J Med 341:1606-1609, 1999
2. Figg WD, Dahut W, Duray P, et al: A randomized phase II trial of thalidomide, an angiogenesis inhibitor, in patients with androgen-independent prostate cancer. Clin Cancer Res 7:1888-1893, 2001
3. Osman K, Comenzo R, Rajkumar SV: Deep venous thrombosis and thalidomide therapy for multiple myeloma. N Engl J Med 344:1951-1952, 2001 4. Carrion Valero F, Bertomeu Gonzalez V: Lung toxicity due to thalidomide [in Spanish]. Arch Bronconeumol 38:492-494, 2002[Medline] 5. Behrens RJ, Gulley JL, Dahut WL: Pulmonary toxicity during prostate cancer treatment with docetaxel and thalidomide. Am J Ther 10:228-232, 2003[CrossRef][Medline] 6. Akoun GM, Cadranel J, Rosenow EC 3rd, et al: Bronchoalveolar lavage cell data in drug-induced pneumonitis. Allerg Immunol 23:245-252, 1991 This article has been cited by other articles:
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Copyright © 2005 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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) was admitted to our hospital because of back pain and an increased level of M-protein. She had a history of pulmonary sarcoidosis in 1984, which was treated with steroids. She had no history of drug allergy. She was diagnosed as having multiple myeloma in 1994. Her myeloma cells had already become resistant to conventional chemotherapies, including MP (melphalan and prednisolone) and VAD (vincristine, doxorubicin, and dexamathasone). Treatment with thalidomide was started initially at 100 mg/d, and then increased by 100 mg every 3 days. On the eighth day, when thalidomide was administered at a dose of 300 mg, the patient suffered from fever and dyspnea on effort. Physical examinations revealed fine crackles in the bilateral lower lung fields. Her ambulatory pulse oximetry on room air was decreased to less than 90%, and she received oxygen by a nasal cannula. Her arterial blood gas analysis showed severe hypoxia (PO2, 59.8 mmHg; PCO2, 47.5 mmHg; nasal cannula O2 2 L/min). She had no chest pain. A chest x-ray film showed bilateral mild interstitial and reticular opacities, and high-resolution lung computed tomography (CT) confirmed diffuse interstitial changes in both lungs with a ground glass appearance (
