Plasmablastic lymphoma of the lung: Report of a unique case and review of the literature

Archives of Pathology & Laboratory Medicine, Feb 2001 by Lin, Yuan, Rodrigues, Gilberto D, Turner, John F, Vasef, Mohammad A

* Non-Hodgkin lymphomas associated with acquired immunodeficiency syndrome are heterogeneous. Recently, a novel subtype of non-Hodgkin lymphoma occurring mostly in patients with acquired immunodeficiency syndrome has been described and designated as plasmablastic lymphoma. The histomorphologic and immunophenotypic findings of this distinct subtype of non-Hodgkin lymphoma have been characterized previously. Most patients present with oral cavity involvement. We report a case of plasmablastic lymphoma presenting as a lung tumor. To our knowledge, this is the first case report of this unusual subtype of diffuse large B-cell lymphoma in this location.

(Arch Pathol Lab Med 2001;125:282-285)

Non-Hodgkin lymphoma is the second most common malignancy in patients with acquired immunodeficiency syndrome (AIDS). The majority of the AIDS-related non-Hodgkin lymphomas are high grade with frequent extranodal presentation and aggressive clinical behavior. Acquired immunodeficiency syndrome-related lymphomas are a heterogeneous group of tumors. Recently, a distinct AIDS-related lymphoma with unique immunohistologic features has been described and designated as plasmablastic lymphoma (PBL).1 This subtype of lymphoma typically occurs in the oral cavity. The morphologic and immunophenotypic features of this unusual subtype of AIDS-related lymphoma have been previously studied and characterized.1

All previously reported cases of PBL have been localized to the oral cavity,1-3 with the exception of a single case in which the stomach was the primary site of involvement.4 Involvement of other sites by PBL has not been reported previously.

We report an unusual example of PBL presenting in the lung. In our review of the English literature, we found no previously reported PBLs in this location; therefore, to the best of our knowledge, this case represents the first reported example of AIDS-related PBL occurring in the lung. The histomorphologic, immunophenotypic, and molecular genetic findings are reviewed.

REPORT OF A CASE

A 47-year-old man was diagnosed with human immunodeficiency virus (HIV) infection in 1986. A diagnosis of AIDS was made in 1994 after the patient developed Pneumocystis carinii pneumonia, as well as pulmonary Mycobacterium kansasii infection. In 1996 he developed hemoptysis. A computed tomographic scan showed a 2.5-cm nodule in right lower lobe of the lung. A transbronchial biopsy and culture revealed pulmonary aspergillosis. He was treated with oral itraconazole. Hemoptysis and radiological abnormalities improved. However, follow-up computed tomographic scans revealed an increase in the size of the lung nodule, as well as new satellite nodules that were 1 to 2 cm in diameter. A single enlarged anterior mediastinal lymph node was also identified. The patient presented with worsening chest pain in the summer of 1999.

Physical examination revealed 2- to 3-mm pitting edema and digital clubbing. No peripheral lymphadenopathy was detected. Laboratory examination showed a CD4 count of 105 cell/mm and a normal lactase dehydrogenase level. No HIV RNA copies were detected using polymerase chain reaction. The right lower lobe mass was excised for pathologic examination.

MATERIALS AND METHODS

The excised portion of right lower lobe of the lung was cut fresh, fixed in 10% buffered formalin, and representative blocks were processed routinely. Paraffin-embedded tissue sections were stained with hematoxylin-eosin for microscopic evaluation.

Immunohistochemical Studies

Immunohistochemical studies were performed using formalinfixed, paraffin-embedded tissue sections and previously described methods.5 The following antibodies were used: CD3, L26 (CD20), leukocyte common antigen (CD45), CD45RA, CD79a, immunoglobulin (Ig) kappa and lambda light chains, IgG, IgM, IgA, IgD, Bcl-2, VS38c, epithelial membrane antigen (Dako, Carpinteria, Calif), Leu-22 (CD43) (Becton-Dickinson, San Jose, Calif), UCHL1 (CD45RO) (Ventana Medical Systems, Tucson, Ariz), Bcl-1/cyclin D1 (P2D11F11, Novocastra/Vector, Burlingame, Calif), syndecan-1 (CD138) (MCA681, SeroTec, Raleigh, NC), and cytokeratin (AE1/AE3) (Boehringer Mannheim, Indianapolis, Ind). A heat-induced epitope-retrieval method was used for CD20, CD45, CD45RA, CD45RO, CD79a, CD138, VS38c, Bcl-2, and cyclin Dl. The antibodies were used at the following dilutions: CD3 and CD20, 1:200; CD45, 1:100; CD45RA, 1:20; CD79a, 1:50; CD138, 1: 5; VS38c, 1:25; IgK, 1:3200; IgX, 1:12800; IgG and IgA, 1:6400; IgM, 1:3200; IgD, 1:800; Bcl-2, 1:20; cyclin Dl, 1:10; AE1/AE3, 1:400; and epithelial membrane antigen, 1:25. The anti-CD45RO antibody was used as a ready-made dispenser. Reactivity was detected using avidin-biotin technique and 3',3'-diaminobenzidine tetrahydrochloride dehydrate as the chromogen. The secondary antibody was polyvalent, reactive with both polyclonal (rabbit) and monoclonal (mouse IgG and IgM and rat IgG) primary antibodies. Sections of multitissue control blocks were used as positive and negative external controls.