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Coexistence of a primary immunodeficiency disorder and hodgkin's disease: Evidence against a B‐Lymphocyte origin for the reed‐sternberg cell
Author(s) -
Bobrove Arthur M.,
Onder Oguz,
Myers Thomas J.,
Rickles Frederick R.,
Pastuszak William T.,
Martin Robert S.,
Hild David H.
Publication year - 1981
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19811215)48:12<2624::aid-cncr2820481214>3.0.co;2-h
Subject(s) - hypogammaglobulinemia , medicine , lymphocyte , pokeweed mitogen , immunodeficiency , primary immunodeficiency , immunology , immune system , lymph node , lymph node biopsy , pathology , antibody , biology , in vitro , peripheral blood mononuclear cell , biochemistry
A 44‐year‐old woman with a life‐long history of recurrent sinopulmonary infections developed Hodgkin's disease with characteristic Reed‐Sternberg cells in a biopsy specimen of a mediastinal lymph node. Hypogammaglobulinemia was documented on several serum determinations and plasma cells were absent from biopsy specimens of the lymph node and bone marrow. Immunochemical studies failed to demonstrate any B lymphocytes bearing surface immunoglobulin or Fc‐receptors for IgG in the peripheral blood. Pokeweed mitogen stimulation of the patient's peripheral blood lymphocytes in vitro resulted in the development of virtually no plasma cells. Peripheral blood T‐lymphocyte number and function were defective initially. Following chemotherapy and radiotherapy, peripheral blood E‐rosette‐forming cells returned to normal, but T‐cell function remained defective and B lymphocytes remained undetectable. These findings are compatible with the presence of two separate immune disorders: a primary hypogammaglobulinemia and Hodgkin's disease. The absence of lymphocytes bearing surface Ig or Fcreceptors for IgG in this patient adds further support against a B‐lymphocyte origin for the Reed‐Sternberg cell.