Study of bone marrow microvessel density is one of the diagnostic approaches in patients with Ph-negative chronic myeloproliferative diseases


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Abstract

Aim. To define an association of bone marrow microvessel density (MVD) with histological properties (the magnitude of fibrosis and quantification of megakaryocytes (MGKC)) in patients with Ph-negative chronic myeloproliferative diseases (CMPD).
Subjects and methods. MVD was analyzed in 93 patients with different forms of CMPD, by estimating histological parameters. True polycythemia (TP) was present in 28 patients; 20 patients had essential thrombocythemia (ET), 36 had subleukemic myelosis, out them 6 were in a prefibrotic stage, and 9 with diagnosed post-TP(ET) myelofibrosis. The grade of myelofibrosis was estimated from the degree of bone marrow fibrosis as 0, 1, 2, and 3 and the clusters of MGKC were in accordance with degrees: 0, 1, and 2. MVD was studied from the absolute number of CD34-positive vascular structures.
Results. In patients with TP, fibrosis was defined as grade 0 and 1 in 23 (82%) and 5 (18%) cases, respectively. The content of reticulin fiber was in the normal range in 19 (95%) of the 20 patients with ET. The clusters of MGKC of grades 1 and 2 showed an even distribution among patients with ET and those with TP. Fibrosis was absent in all the patients (n = 6) with prefibrotic-stage primary myelofibrosis (PMF). The patients with PMF had high MVD values [6.5 (range 2.8-22)] than those with TP [4.0 (range 1.76-10.2)] or ET [3.7 (range 2-8.5)] and the controls [3.2 (range 2-4.1)] (p < 0.001) confirming that angiogenesis is uninvolved at the onset of disease in patients with ET and those with TP. The patients with prefibrotic-stage PMF had higher values [6.0 (range 4.8-10.6)] than those with ET [3.7 (range 2-8.5)] (p < 0.001). This suggests that angiogenesis is an early sign preceding the development of fibrosis.
Conclusion. Bone marrow angiogenesis assessment (from MVD measurements) may be an additional criterion for the diagnosis of disease evolution and an additional criterion between ET and PMF in a prefibrotic stage.

About the authors

Manana Aleksandrovna Sokolova

Email: s_manana@mail.ru

Nina Dmitrievna Khoroshko

Nina Valentinovna Tsvetaeva

Elena Aleksandrovna Semenova

Irina Borisovna Kaplanskaya

Georgiy Avraamovich Frank

Andrey Vital'evich Misyurin

M A Sokolova

Hematology Research Center, Russian Academy of Medical Sciences

Hematology Research Center, Russian Academy of Medical Sciences

N D Khoroshko

Hematology Research Center, Russian Academy of Medical Sciences

Hematology Research Center, Russian Academy of Medical Sciences

N V Tsvetayeva

Hematology Research Center, Russian Academy of Medical Sciences

Hematology Research Center, Russian Academy of Medical Sciences

E A Semenova

Hematology Research Center, Russian Academy of Medical Sciences

Hematology Research Center, Russian Academy of Medical Sciences

I B Kaplanskaya

Hematology Research Center, Russian Academy of Medical Sciences

Hematology Research Center, Russian Academy of Medical Sciences

G A Frank

Hematology Research Center, Russian Academy of Medical Sciences

Hematology Research Center, Russian Academy of Medical Sciences

A V Misyurin

Hematology Research Center, Russian Academy of Medical Sciences

Hematology Research Center, Russian Academy of Medical Sciences

References

  1. Mesa R. A., Hanson C. A., Rajkumar S. V. et al. Evaluation and clinical correlations of bone marrow angiogenesis in myelofibrosis with myeloid metaplasia. Blood 2000; 96: 3374-3380.
  2. Ponzoni M., Savage D. G., Ferreri A. J. et al. Chronic idiopathic myelofibrosis: independent prognostic importance of bone marrow microvascular density evaluated by CD105 (endoglin) immunostaining. Modern Pathol. 2004; 17: 1513-1520.
  3. Mesa R. A., Steensma D. P., Pardanini A. et al. A phase 2 trial of combination low-dose thalidomide and prednisolone for the treatment of myelofibrosis with myeloid metaplasia. Blood 2003; 101: 2534-2541.
  4. Elliot M. A., Mesa R. A., Li C. Y. et al. Thalidomide treatment in myelofibrosis with myeloid metaplasia. Br. J. Haematol. 2002; 117: 288-296.
  5. Tefferi A., Cortes J., Verstovsek S. et al. Lenalidomide therapy in myelofibrosis with myeloid metaplasia. Blood 2006; 108: 1158-1164.
  6. Arora B., Ho C. L., Hoyer I. D. et al. Bone marrow angiogenesis and its clinical correlates in myelofibrosis with myeloid metaplasia. Haematologica 2004; 89: 1454-1458.
  7. Panteli K., Zagorianakou N., Agnantis N. J. et al. Clinical correlation of bone marrow microvessel density in essential thrombocytemia. Acta Haematol. 2005; 114: 99-103.
  8. Weidner N. Tumor angiogenesis: review of current applications in tumor prognostication. Semin. Diagn. Pathol. 1993; 10: 302-313.
  9. Aguayo A., Kantarjian H., Manshouri T. et al. Angiogenesis in acute and chronic leukemias and myelodysplastic syndromes. Blood 2000; 96: 2240-2245.
  10. Keith T., Araki Y., Ohyagi M. et al. Regulation of angiogenesis in the bone marrow of myelodysplastic syndromes transforming to overt leukemia. Br. J. Haematol. 2007; 137: 206-215.
  11. Marchetti M., Barosi G., Balestri F. et al. Low-dose thalidomide ameliorates cytopenias and splenomegaly in myelofibrosis with myeloid metaplasia: a phase 2 trial. J. Clin. Oncol. 2004; 22: 424-431.

Copyright (c) 2010 Sokolova M.A., Khoroshko N.D., Tsvetaeva N.V., Semenova E.A., Kaplanskaya I.B., Frank G.A., Misyurin A.V., Sokolova M.A., Khoroshko N.D., Tsvetayeva N.V., Semenova E.A., Kaplanskaya I.B., Frank G.A., Misyurin A.V.

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