Publication details
Lenalidomid als neue Therapie-Option fur Castleman-Krankheit: erste Erfahrungen
| Title in English | Lenalidomide as a new treatment option for Castleman disease: first experience |
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| Authors | |
| Year of publication | 2011 |
| Type | Conference abstract |
| MU Faculty or unit | |
| Citation | |
| Description | Introduction: Castleman disease is a rare idiopathic non-neoplastic disease characterized by enlargement of lymph nodes. Clinically unicentric or multicentric and histopathologically hyaline-vascular, plasmocellular or mixed forms are recognized. Herein, using radiological (PET/CT scanning), laboratory (cytokine analysis, measurement of blood inflammatory markers) and clinical (relief of fatigue and paresthesia) data, we are the first to report on a therapy effect of lenalidomide (Revlimid) in a patient with Castleman disease. Materials and Methods: Based on repeated lymph node biopsies and CT scan examination showing generalized lymphadenopathy and a mild splenomegaly, a male, born 1961, was diagnosed with plazmocellular multicentric Castleman disease in 2008. First line treatment (rituximab, cyclophosphamide, vincristine, doxorubicin, prednisone, 3 cycles) remained without any treatment response. In March 2009, a second line treatment (thalidomide, cyclophosphamide, dexamethazone) leading to a significant clinical and radiological (size reduction of lymph nodes on CT and PET/CT examinations) therapy effect was started. However, after 12 cycles the thalidomide based regimen was stopped due to progressive adverse effects of thalidomide (neuropathy) and glucocorticoids (Cushing’s syndrome). After signing an inform consent, the patient was started on lenalidomide monotherapy (25 mg orally days 1-21 of a 28-day cycle) in October 2010. Results: Gradual decrease of elevated C-reactive protein was evident after the first dose of lenalidomide. Interleukin-6 levels were oscillating between 3.1 and 10.7 pg/ml during the 1st cycle and were below detection limit from the 2nd cycle on. The laboratory response was paralleled by general clinical improvement with relief of chronic fatigue and paresthesia of the lower limbs. A restaging PET/CT examination after 4 cycles of lenalidomide regimen showed a clear regression of metabolic activity in the affected lymph nodes (from SUVmax = 5.61 in 09/2010 to SUVmax = 2.57 in 02/2011). Tolerability of this treatment was excellent with no signs of myelotoxicity. Conclusions: Lenalidomide therapy proved effective in a patient with pretreated multicentric Castleman disease. Based on our experience, we propose further investigation of therapeutic potential of this new drug in Castleman disease. Moreover, we suggest cytokine analysis and PET/CT scanning to be standard parts of therapy response monitoring in these patients. |