Reed–Sternberg Cells in Pleural Effusion

Dear Editor,

Pleural effusion in Hodgkin lymphoma (HL) is a very common presentation constituting 20%–30% of cases, however, Reed–Sternberg (R–S) cells in effusion cytology of HL are very rarely seen.[1] The mechanisms suggested for pleural effusion include thoracic duct compression/rupture, or increased capillary permeability from inflammation or overt endothelial damage.[2]

A 10-year-old male child presented with a complaint of shortness of breath and chest pain for the past 15 days. X-ray examination showed the presence of slight mediastinal widening and bilateral pleural effusion. He also complained of axillary and cervical swelling of size 3 and 1 cm, respectively. History revealed the patient to be a known case of classic HL diagnosed 2 years back on cervical lymph node swelling on biopsy. He was then lost to follow-up.

We received 2 mL of yellow-colored pleural fluid for cytological examination. Direct and cytospin smears were made by cytospin centrifugation method and slides were stained with May–Grunwald Giemsa (MGG) stain. Smears showed the presence of large, atypical cells with abundant cytoplasm and bi and multinucleated cells with prominent nucleoli suspicious of R–S cells. The background cells included numerous eosinophils, few plasma cells, lymphocytes, and neutrophils [Figure 1a and b]. Fine needle aspiration cytology (FNAC) was also done from the axillary lymph node with a 23-G needle and Giemsa-stained slides also showed similar findings as in pleural fluid [Figure 1a]. The lymph node was excised and also showed the presence of classical and mononuclear R–S cells with a mixed population of reactive lymphoid cells, eosinophils, and plasma cells. Immunohistochemistry (IHC) with cluster of differentiation 15 (CD15), cluster of differentiation 30 (CD30), and leucocyte common antigen (LCA) were performed. The R–S cells were positive for CD15 and CD30 and negative for LCA [Figure 2a–c]. Thus, a final diagnosis of HL was made.

About 25% of cases of HL present with pleural effusions and it is associated with poor prognosis and a median survival of 3 months.[3] It is more common in adults compared with children.

The pattern of spread may be from the anterior mediastinal/paratracheal area to other mediastinal lymph nodes and then into the lung by direct extension or separate nodules.[2] In pleural effusions, R–S cells and R–S-like cells can be confused with atypical cells of non-HL and pleomorphic carcinomas. Sometimes reactive mesothelial cells and histiocytes are binucleated and have atypical morphological features which can be easily confused with R–S cells. In addition, the presence of megakaryocytes in pleural fluid associated with extramedullary hematopoiesis also resembles R–S cells. Background cells include mixed inflammatory cells including eosinophils, plasma cells, histocytes, and lymphocytes and they often mislead the diagnosis toward benign inflammatory and infectious diseases.[4] The presence of an isolated R–S-like cell in a pleural fluid along with correlation with biopsy/FNAC of the primary lymph node needs to be done for diagnosis of HL, therefore, a combined approach of clinical and cytomorphological features should be present to make a diagnosis of HL in effusion cytology.

To conclude, pleural effusion is not a rare presentation in HL but the presence of R–S cells is rare and difficult to find so, both clinical and cyto-morphological features are very important to diagnose such cases in effusion cytology.