%0 Journal Article
%T Intrapleural Bortezomib for the Therapy of Myelomatous Pleural Effusion: A Case Report
%A Magdalena Klanova
%A Pavel Klener
%A Marek Trneny
%A Jan Straub
%A Ivan Spicka
%J Case Reports in Immunology
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/978479
%X Myelomatous pleural effusion (MPE) is an extremely rare manifestation of multiple myeloma (MM). We present a case of MPE in a patient with IgG-百 MM treated with intrapleural bortezomib with systemic bortezomib-based therapy. Although we observed good local response, the patient succumbed due to systemic myeloma progression. 1. Introduction Myelomatous pleural effusion is an extremely rare manifestation of multiple myeloma and only a few cases have been reported to date [1]. MPE in patients with MM is often associated with high-risk disease and poor prognosis despite aggressive treatment. There is no standard treatment strategy for MPE and the majority of cases of MM presenting with MPE were associated with resistance to therapy [2]. Bortezomib (the dipeptidylboronic acid analogue, proteasome inhibitor) belongs now to backbone antimyeloma drugs. The data concerning intrapleural administration of bortezomib is scarce. We present a case of MPE in a patient with IgG-百 MM treated with intrapleural bortezomib and concomitantly with systemic bortezomib-based-combined therapy. 2. Case History A 43-year-old female initially presented to the hospital in November 2009 with a dry cough, dyspnea, and left chest pain. The chest X-ray showed bilateral pneumonia. The computer tomography demonstrated a massive tumor involving the left breast and chest cavity, a tumor in the uterus and right ovary, multiple osteolytic lesions in the skull and ribs, and bilateral axillar lymphadenopathy. Immunohistochemical analysis of the breast tumor biopsy revealed plasmacytoma/multiple myeloma. Bone marrow examination by trephine biopsy revealed 30% infiltration with atypical plasma cells. Cytogenetic studies including FISH showed a deletion of chromosome 13 and amplification of 1q21 and 1q26 genomic regions. On admission the total plasma protein was 106ˋg/L, albumin 40ˋg/L, urea 5.7ˋmmol/L, creatinine 74ˋumol/L, calcium 2.12ˋmmol/L, LDH 3.7ˋukat/L (normal values 2,2每3,75ˋukat/L), and 汕-2 microglobulin 3.0ˋmg/L (normal values 1.0每2,4ˋmg/L). The international staging system (ISS) score was 1. Serum protein electrophoresis with immunofixation confirmed monoclonal gammopathy IgG-百 44ˋg/L. Initially, the patient was treated with cyclophosphamide, thalidomide, and dexamethasone (CTD), but achieved no objective response (stable disease). In the second line therapy bortezomib (Velcade) was added (VTD combination) but due to side effects (severe myopathy) dexamethasone had to be shortly discontinued. In July 2010, after 2 VT cycles, the CT scan showed a progression of extranodal masses with
%U http://www.hindawi.com/journals/crii/2012/978479/