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<p>The incidence of leukemic conversion during the clinical course of paroxysmal nocturnal hemoglobinuria (PNH) has been reported to be 0.6–2.9%. Such an association is logically linked to the progression of PNH to acute leukemia, especially the M6 subtype of acute myeloid leukemia (AML-M6). In many of these cases (11/26, 42%), leukemic conversion from PNH is associated with development of AML-M6. A literature review including our cases showed that this leukemic conversion from PNH has two distinct development patterns. In type 1, leukemic clones were derived from non-PNH clones in most cases, and the PNH phenotype of erythrocytes disappeared with progression. In one of our cases, however, the patient was diagnosed with concomitant PNH and AML-M6, and leukemic cells were observed alongside CD55-negative and CD59-negative PNH clones. In Type 2 cases such as this one, conversion of PNH is characterized by the coexistence of leukemic cells with PNH clones. Flow cytometry revealed that CD34-positive blast cells were deficient in CD55 and CD59. In Type 2, PNH clones do progress into malignancies, albeit rarely, demonstrating a distinct second development pattern of leukemic conversion from PNH.</p>

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Discovery of a second, distinct development pattern of leukemic conversion from paroxysmal nocturnal hemoglobinuria

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  • 发表日期：

    2025年2月6日

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  • Junji Tokushige,
  • Kazuki Taoka,
  • Masako Nishikawa,
  • Masahiro Jona,
  • Kumi Nakazaki,
  • Yutaka Yatomi,
  • Mineo Kurokawa

摘要

The incidence of leukemic conversion during the clinical course of paroxysmal nocturnal hemoglobinuria (PNH) has been reported to be 0.6–2.9%. Such an association is logically linked to the progression of PNH to acute leukemia, especially the M6 subtype of acute myeloid leukemia (AML-M6). In many of these cases (11/26, 42%), leukemic conversion from PNH is associated with development of AML-M6. A literature review including our cases showed that this leukemic conversion from PNH has two distinct development patterns. In type 1, leukemic clones were derived from non-PNH clones in most cases, and the PNH phenotype of erythrocytes disappeared with progression. In one of our cases, however, the patient was diagnosed with concomitant PNH and AML-M6, and leukemic cells were observed alongside CD55-negative and CD59-negative PNH clones. In Type 2 cases such as this one, conversion of PNH is characterized by the coexistence of leukemic cells with PNH clones. Flow cytometry revealed that CD34-positive blast cells were deficient in CD55 and CD59. In Type 2, PNH clones do progress into malignancies, albeit rarely, demonstrating a distinct second development pattern of leukemic conversion from PNH.