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Hepatic Plasmacytosis as a Manifestation of Relapse in Multiple Myeloma Treated With Thalidomide

Auro del Giglio, MD, FACP, Patricia Weinschenker, MD, Ana Rita de Araújo Burgos Manhani, MD, Ana Lucia Ippolito Carbonell, MD, Cristina A.T.S. Mitteldorf, MD
Volume: 98 Issue: 2 February, 2005

Abstract:

Thalidomide and its analogs have been extensively studied in patients with multiple myeloma. We present the case of a 58-year-old female patient with immunoglobulin GA-κ multiple myeloma who was receiving thalidomide after failing an autologous transplant. She presented with profound asthenia and several space-occupying hepatic lesions, one of which was shown by a CT-guided percutaneous biopsy to be plasmacytoma. The patient then received bortezomib and had a transient response. Because thalidomide may also increase the expression of cytoadhesion molecules in myeloma cells and in the bone marrow microenvironment, it is possible that some patients with multiple myeloma who relapse on thalidomide may present with extramedullary plasmacytomas, as seen in this case. Therefore, whenever symptoms arise in patients with multiple myeloma who are receiving thalidomide, extramedullary plasmacytomas should be considered.


Key Points


* Patients with multiple myeloma who are receiving thalidomide may progress to extramedullary plasmacytomas.


* Multiple space-occupying lesions in the liver of such patients may represent plasmacytomas.


* Bortezomib may be a therapeutic option for these patients.

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References:

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13. Richardson PG, Barlogie B, Berenson J, et al. A phase 2 study of bortezomib in relapsed, refractory myeloma. N Engl J Med 2003;348:2609–2617.
 

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