Hodgkin lymphoma is a neoplastic proliferation
of lymphoid cells predominantly involving lymphoid tissues.
The malignant cell is the Reed-Sternberg cell.
Reed-Sternberg (R-S) cells are essential to the diagnosis
of Hodgkin lymphoma. The presence of R-S cells is necessary,
but as R-S cells are not unique to HD, R-S cells alone
are not sufficient for the diagnosis.
The Reed-Sternberg cell is a lymphoid cell and in most cases,
is a B cell, and clonal. R-S cells are very large with abundant
pale cytoplasm and two or more oval lobulated nuclei containing
large nucleoli (red on H & E).
Hodgkin lymphoma was first described by Thomas Hodgkin
in an 1832 series of tumors of the absorbent (lymph) glands.
The characteristic Reed-Sternberg cell was decribed by Carl
Sternberg (l898) and Dorothy Reed (l902).
Hodgkin lymphoma repesents about 30% of all lymphoma
or almost 10,000 cases per year (2-3 /100,000/year)
in the United States.
Hodgkin lymphoma is separated from non-Hodgkin lymphoma not
only by a unique histologic appearance, but also because the
systemic manifestations (such as fever) and the clinical presentation
Hodgkin lymphoma generally presents as regional enlargement
of a single group of peripheral lymph nodes, as opposed
to non-Hodgkin lymphoma in which nodal involvement is more
Hodgkin lymphoma generally involves contiguous
Non-Hodgkin lymphoma is noncontiguous.
In addition, Hodgkin lymphoma is rarely extranodal
whereas extranodal involvement is frequent in non-Hodgkin
lymphomas. At presentation, bone marrow involvement by HD
is highly unusual (< 5%).
When Hodgkin lymphoma involves the spleen or liver it generally
presents as a mass lesion rather than as diffuse involvement.
The etiology of HD
is unknown. Possible etiologic factors associated with
the development of Hodgkin lymphoma (no conclusive evidence
supporting any factor) include: prior EBV infection and frequent
bcl-2 translocations. Epstein-Barr virus has been detected
in approximately 40% of the cases of classical HL, and it
is clonal; suggesting that EBV might play a role in the pathogenesis
of at least some types of HL.
Rearrangements of immunoglobulin genes are found
in Hodgkin lymphoma. Most cases are B-cell derived and the
Hodgkin cells are clonal.
Abnormal cellular immunity is a feature
of HD. Combined with chemotherapy it may lead to infectious
complications. Further evidence of an immune defect is the
lymphopenia seen in 40-50% of people with HD and which is
more common in late stages.
Classic Reed-Sternberg cells are large (15-45 m)
with abundant pale cytoplasm and two or more oval lobulated
nuclei containing prominent "owl-eye" eosinophilic (H&E)
In some R-S cell variants the cytoplasm shrinks during
formalin fixation and processing of tissue, leaving an empty
space around the nucleus. Such R-S variants are known as "lacunar
Another R-S variant is the "L&H" or "popcorn"
cell with a fluffy, lobulated nucleus having fine chromatin
and small nucleoli.
Other common R-S variants are mononuclear Hodgkin cells and
The frequency and character of the Reed-Sternberg cells
ie., mononuclear R-S variants (Hodgkin cells), lacunar cells
or so-called "popcorn" cells are features contributing to
the histopathologic classification.
The accompanying cellular background of lymphocytes, plasma
cells, eosinophils, histiocytes, and stromal cells is variable
and is reactive to the neoplastic R-S cells.
Numerous eosinophils & plasma cells in MC, Hodgkin
The relative frequency of lymphocytes, eosinophils, and plasma
cells and the character and amount of fibrosis in lymph
nodes, are further clues as to the diagnosis and classification
of Hodgkin lymphoma.
The primary diagnosis of Hodgkin lymphoma from the
histopathologic examination of a lymph node requires the
identification of Reed-Sternberg cells in an appropriate,
reactive cellular background.
If a diagnosis of HD has been established on lymph
node biopsy, the criteria for diagnosis of extranodal sites
can be relaxed - requiring only mononuclear R-S cells and
their variants in an appropriate background- not classic bilobed
Of course, benign reactive disorders must be ruled out by
an experienced hematopathologist (see Reactive Lymphadenopathy).
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