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Decreased adenosine deaminase (ADA) and 5′nucleotidase (5NT) activity in peripheral blood T cells in hodgkin disease
Author(s) -
Murray James L.,
PerezSoler Roman,
Bywaters Daniel,
Hersh Evan M.
Publication year - 1986
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830210108
Subject(s) - adenosine deaminase , 5' nucleotidase , medicine , peripheral blood , nucleotidase , adenosine , adenosine deaminase deficiency , disease , immunology
The purine metabolic enzymes adenosine deaminase (ADA), purine nucleoside phosphorylase (PNP), and 5′nucleotidase (5NT) play an important role in normal lymphocyte differentiation. Abnormal levels of one or all of these enzymes have been associated with immunodeficiency diseases and lymphoproliferative disorders. ADA, PNP, and 5NT activity was measured in peripheral blood T cells from 24 patients with Hodgkin disease (HD) (12 in complete remission and 12 with active disease) to determine whether an association existed between enzyme abnormalities and the decreased cellular immune function previously described in this disorder. HD patients had a significantly decreased absolute lymphocyte count (1,618 ± 1107/mm 3 ; mean ± SD) compared to controls (2,320 ± 980; p <.001). ADA, PNP, and NT activity was assessed in lymphocyte extracts by measuring the conversion of radiolabeled substrates to products over time. ADA activity expressed as mean ± SEM nanomoles/10 6 lymphocytes/hr was significantly decreased in T cells from HD patients (84.6 ± 7.5) compared to controls (128 ± 12.3; p < 0.025). Likewise, 5NT was significantly decreased in HD patients (12.7 ± 1.3) compared to controls (24.0 ± 3.6; p <.005). There was not a significant difference in PNP activity between both groups. Low 5NT activity was present irrespective of whether patients had active disease (12.1 ± 1.5) or were in unmaintained complete remission (14.5 ± 2.4). These findings suggest that biochemical abnormalities may be responsible for or related to the persistent abnormalities in T‐cell function noted throughout the clinical course of HD.