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Chronic lymphatic leukemia evolving into chronic myelocytic leukemia
Author(s) -
Faguet Guy B.,
Little Thomas,
Agee Julia F.,
Garver Fred A.
Publication year - 1983
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(19831101)52:9<1647::aid-cncr2820520917>3.0.co;2-4
Subject(s) - lymphocytosis , chronic lymphocytic leukemia , medicine , chronic myelogenous leukemia , lymphatic system , leukemia , pathology , immunology
A diagnosis of chronic lymphatic leukemia (CLL) was made in an 83‐year‐old man on the basis of marked lymphocytosis (131.1 × 10 9 /L) and infiltration of the marrow (77%) by small lymphoid cells. The hemoglobin was 11.8 g/dL and the platelet count was 427.5 × 10 9 /L. With minimal and unsustained treatment, abrupt resolution of the lymphocytosis occurred with reciprocal emergence of a classic picture of chronic myelogenous leukemia (CML). During the hematologic evolution, blood lymphoid cells were isolated for surface marker, cytogenetic, and functional studies. E‐rosette receptors, Fcreceptors, and membrane immunoglobulins were found on only 7.5%, 7.4%, and 10.0% of these cells. These cells also failed to express a CLL‐associated antigen we have detected on ≈ 95% of the cells of all CLL patients studied, regardless of cell phenotype. In addition, the patient's lymphoid cells responded poorly to leucoagglutinin (LPHA) stimulation, showed increased spontaneous metabolic activity and exhibited the Philadelphia chromosome. These observations suggest that the patient's transient initial lymphocytosis was not due to CLL, but perhaps represented myeloid precursors in circulation prior to terminal differentiation.