[Clinical study on prognosis of acute leukemia subtypes Ly + AML and My + ALL].
The purpose of this study was to investigate the prognosis of acute myelogenous leukemia (AML), acute lymphoblastic leukemia (ALL), lymphoid antigen-positive acute myeloid leukemia (Ly + AML), myeloid antigen-positive acute leukemia (My + ALL) and biphenotypic acute leukemia (BAL). Immunophenotyping was performed on medullary specimens of 197 acute leukemia (AL) patients by using three-color flow cytometry analysis and CD45/SSC gating. The scoring systems proposed by EGIL was adopted to classify the AL patients into five groups: 43 of ALL, 53 of AML, 53 of My + ALL, 39 of Ly + AML and 9 of BAL patients. The results showed that in Ly + AML, CD7 was the most common (53.8%) as compared to other lymphoid markers, however, in My + ALL CD13 was the most common (47.2%) as compared to other myeloid markers. Compared with Ly + AML, My + ALL had higher incidences of enlargement of liver, spleen and lymphnodes significantly (P<0.05). As for the case numbers of WBC counts > 100 x 10(9)/L, the positive rate of CD34 and the complete remission rate there was no obvious difference between groups of Ly + AML and My + ALL (P>0.05). As for incidences of enlargement of liver, spleen and lymphnodes, the case numbers of WBC counts > 100 x 10(9)/L, the positive rate of CD34 and complete remission rate, no obvious difference was found between ALL and My + ALL (P>0.05). Compared with AML, Ly + AML had lower complete remission rate significantly (P<0.05). As for incidences of enlargement of liver, spleen and lymphnodes, the case numbers of WBC counts > 100 x 10(9)/L and the positive rate of CD34, no obvious difference was found between AML and Ly + AML (P>0.05). Compared with Ly + AML and My + ALL, BAL showed no significant difference in complete remission rate (P>0.05) because the number of BAL patients was too small. It is concluded that since Ly + AML has lymphoid markers, and the prognosis of Ly + AML is worse than AML, the clinical therapy for Ly + AML should contain both AML and ALL. Though My + ALL had myeloid markers, no significant difference was found between My + ALL and ALL, it might be supposed that their therapy could be the same.
Liu
Bin
B
Department of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Li
Rui
R
Wu
Hui-Jing
HJ
Chen
Yan
Y
D000293:Adolescent; D000328:Adult; D000368:Aged; D018952:Antigens, CD34 / Q000096:biosynthesis; D019011:Antigens, CD7 / Q000096:biosynthesis; D018826:CD13 Antigens / Q000096:biosynthesis; D002648:Child; D002675:Child, Preschool; D005260:Female; D006801:Humans; D016130:Immunophenotyping; D015470:Leukemia, Myeloid, Acute / Q000145:classification / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000145:classification / Q000276:immunology*; D011379:Prognosis
D018952:Antigens, CD34; D019011:Antigens, CD7; D018826:CD13 Antigens