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Clinical course of human T-lymphotropic virus type I carriers with
molecularly detectable monoclonal proliferation of T lymphocytes: defining
a low- and high-risk population
S Ikeda, S Momita, K Kinoshita, S Kamihira, Y Moriuchi, K Tsukasaki, M Ito, T Kanda, R Moriuchi and T Nakamura
Department of Hematology, Nagasaki University School of Medicine, Japan.
To characterize the prodromal phase of adult T-cell leukemia (ATL), a
prospective follow-up study was conducted on 50 carriers in a putative
pre-ATL state. This state was defined by the presence of molecularly-
detectable monoclonal proliferation of human T-lymphotropic virus type I
(HTLV-I)-infected T lymphocytes, and the absence of clinical symptoms of
leukemia. The median observation time was 50 months. The pre-ATL subjects
were divided into two groups according to initial white blood cell (WBC)
counts: group A, those with a normal WBC count (9,000/microL) (n = 30), and
group B, those with an increased WBC count (9,000 to 15,000) (n = 20).
Comparisons were made between the two groups and with a group of 25
patients with chronic ATL (group C) who had WBC counts of more than 15,000.
Significant differences in survival rate were found between groups A and B
(10-year survival 65.7%) and group C (32.8%) (P < .01), and between
group A (10-year survival 90.0%) and group B (52.1%) (P < .05). The
incidence of transformation to overt ATL was 10% (3 of 30) in group A and
50% (10 of 20) in group B (P < .01). In six transformed cases (one in A
and five in B) we found exactly the same integration sites in pre-ATL and
overt ATL phases, confirming the multistep leukemogenesis hypothesized for
this disease. However, the pre-ATL subjects could be divided into two
distinct prognostic groups based on the initial WBC count; those with good
and those with poor prognosis. Although the 10% transformation rate (2.5%
annually) in group A seemed to be extremely high compared with that in the
general population of HTLV-I carriers (around 0.06% to 0.4% annually), the
majority of group A subjects and some in group B showed stable clinical
courses without transformation. Further, development of ATL was not
observed in four group A subjects with HTLV-I-associated myelopathy (HAM),
which is rarely associated with ATL. We propose to call this group of
rather benign HTLV-I carriers "HTLV-I carriers with monoclonal
proliferation of T lymphocytes (HCMPT)." Thus far we have been unable to
identify reliable parameters other than WBC counts that prospectively
distinguish HCMPT from the true pre-ATL state, in which there is a high
probability of developing ATL. Further clinical and biologic approaches
should elucidate the natural history of the HTLV-I carrier state and early
events in ATL leukemogenesis.
Volume 82,
Issue 7,
pp. 2017-2024,
10/01/1993
Copyright © 1993 by The American Society of Hematology
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