Head and Neck Classic Hodgkin, T and NK Lymphomas with Eosinophilia

Abstract

Eosinophilia is a notable feature in various hematological malignancies, including specific types of leukemias and lymphomas that may occur in the head and neck. In hematologic malignancies, eosinophilia can be primary, driven by genetic abnormalities, or secondary, resulting from cytokine and chemokine production by the neoplastic cells or the tumor microenvironment. This review examines the association between eosinophilia and head and neck hematolymphoid malignancies including Classic Hodgkin lymphoma, T-cell lymphoblastic leukemia, mature T and NK-cell lymphomas, and Langerhans cell histiocytosis. It explores the underlying mechanisms of eosinophilia in these malignancies, highlighting the role of chemokines and cytokines such as IL-5, TARC, and eotaxin. Recognition of eosinophilia may aid in the diagnosis of these conditions and understanding the mechanisms of eosinophilia may provide insights into potential prognostic implications and treatment strategies.

Keywords: Eosinophilia; Head and neck Pathology; Hematopathology; Leukemia; Lymphoma.

Fig. 1

Classic Hodgkin lymphoma with numerous eosinophils. (A) Low power showing the architectural features of sclerosis and a nodular proliferation of hematolymphoid cells (2X). (B) Hodgkin-Reed-Sternberg (HRS) cells in a polymorphous background of lymphocytes (40X), eosinophils, plasma cells, and histiocytes. C, D, E, and F. High power of an HRS cell showing positive staining for CD30 (100X) (D) and CD15 (40X) (E) and weak PAX5 positivity (40X) (F)

Fig. 2

Peripheral T cell lymphoma with numerous eosinophils. (A) Effacement of the architecture by small to intermediate atypical lymphocytes (10X). (B) Intermediate power of the atypical lymphocytes and numerous eosinophils (20X)

Fig. 3

Anaplastic large cell lymphoma with numerous eosinophils in the upper airway. (A) Low power image of effaced lymphoid tissue (2X). (B) High power showing large atypical cells with neutrophils and numerous eosinophils (40X). C, D, E, and F. The tumor cells show uniform, strong expression of CD30 (20X) (C), are positive for ALK1 (20X) (D) and CD2 (20X) (F), and negative for CD3 (20X) (F)

Fig. 4

NK/T cell lymphoma of the hard palate. A. Low power showing architectural effacement (2X). B, C, D, E, and F. High power images showing large atypical cells with abundant cytoplasm (40X) (B), which show cytoplasmic CD3 expression (40X) (C), are positive for CD56 (40X) (D), granzyme (40X) (E), and EBV RNA (40X) (F). The cells are also positive for TIA1 and CD2 and are negative for CD5 (not shown)

Fig. 5

CD30 mucocutaneous lesion in the mouth. (A) Low power image of oral mucosa with necrosis and an atypical large cell infiltrate (2X). (B) Large cells are scattered in the tissue and perivascular (20X). C, D, E, F, G, and H. The majority of large atypical cells are positive for CD30 (20X) (C), CD2 (20X) (D), CD7 (20X) (G), and granzyme (20X) (H) and subset positive for CD3 (20X) (E) and CD56 (20X) (F). The cells were negative for CD5, TCRBF1, TCR delta, CD8, CD4, CD56, perforin EBV and ALK (not shown). The lesion was indolent and resolved

Fig. 6

Langerhans cell histiocytosis in an 11 year old with an ear mass. (A) Low power showing large, atypical cells with numerous eosinophils (2X). (B) High power image showing large cells with indentations and abundant cytoplasm with background eosinophils (40X). C, D, E, and F. The neoplastic cells are positive for CD163 (20X) (C), S100 (20X) (D), and CD1a (20X) (E) and a subset of cells is positive for Langerin (20X) (F).Factor XIII and BRAF are negative (not shown)