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A 59-year-old man presented with accumulation of pleural fluid. As reported previously in detail, the patient first presented with gastric mucosa-associated lymphoid tissue (MALT) lymphoma eight years earlier, which responded to antibiotic therapy for the eradication of Helicobacter pylori (H. pylori). Three years before the current presentation, however, he underwent subtotal gastrectomy due to gastric perforation. The excised stomach showed transmural infiltrates of MALT lymphoma and regional lymph nodes showed the histopathology of marginal zone B-cell lymphoma. The patient was further treated with six cycles of chemotherapy consisting of rituximab, vincristine, cyclophosphamide, and prednisolone, and was subsequently lost to follow-up. Computer-assisted tomography of the chest at this presentation revealed a large amount of pleural fluid within the left thoracic cavity. Although mediastinal adenopathy was identified, no primary tumor was apparent within the lung field. Endoscopic examination of the upper gastrointestinal tract revealed no recurrent disease at the site of anastomosis. Laboratory data included a hemoglobin level of 11.3 g/dL, white blood cell count of 8,100/mL with 7% plasmacytoid cells, and platelet count of 379,000/mL. Blood chemistry was unremarkable except for a total protein level of 8.4 g/dL and albumin of 3.6 g/dL. Protein electrophoresis revealed an Mspike, which migrated in the fast g-globulin region ; immunoelectrophoresis confirmed that monoclonal immunoglobulin (Ig) in the serum was labeled by IgA as well as IgM and klight chain anti-sera, and the k chain was excreted in the urine. The serum level of IgA was 1,677 mg/dL, that of IgG was 981 mg/dL, and IgM was 241 mg/dL. Thoracocentesis yielded exudative fluids containing monoclonal Ig identical to that found in the serum ; the levels of Ig were 1,030 mg/dL IgA, 652 mg/dL IgG, and 132 mg/dL IgM. Cytologic examination of the fluids demonstrated lymphoplasmacytoid cells (Fig. 1A), and flow cytometry of the mononuclear cell fraction confirmed a monoclonal B-cell population with plasma cell differentiation ; i.e., the cells were CD10, CD19, CD20, CD38, CD138, and surfacemembrane and cytoplasmic Ig k-light chain (Fig. 2) ; the predominant heavy chain was a. On the other hand, the pleural fluid contained large clumps of atypical epithelial cells (Fig. 1A, B). Some cells showed a signet ring cell morphology (Fig. 1, inset) and were positive for periodic acid-Schiff (PAS) staining (Fig. 1C). The cells corresponded to the class V category of the cytopathological grading. Prominent values of tumor markers in the fluids included 8,540 U/mL CA19-9 and 27,500 U/mL CA125, and their serum levels were 433 U/mL CA19-9 (normal level in serum, C 37 U/mL) and 317.4 U/mL CA125 (C 35.0 U/mL). Cytogenetic analysis was performed after short-term culture of the pleural fluid cells. The G-banded karyotype of 6 out of 20 metaphase spreads analyzed was 46, XY, t(11;18) (q21;q21). The chromosome number of the remaining 14 metaphases ranged from 71 to 81, with many unidentified marker chromosomes. Fluorescence in situ hybridization using a kit confirming t(11;18) detected a fusion signal on the der (11) t(11;18) chromosome, corresponding to the production of the API2/MALT1 chimeric protein, and interphase cells carrying one fusion signal (Fig. 3). As the der (18) t(11;18) chromosome lacked the expected fusion signal, a part of the reciprocal MALT1/ API2 fusion gene may have been deleted. On the other hand, the majority of interphase nuclei showed multiple hybridization signals ; 3 green and 4 orange signals in 37% of nuclei, and 4 green and 4 orange signals in 28% of nuclei (Fig. 3).

Coexistence of Mucosa-associated Lymphoid Tissue Lymphoma with Plasma Cell Features and Adenocarcinoma Cells in Pleural Fluid