A A Correlative Study on Bone Marrow Angiogenesis with Bone Marrow Fibrosis and Splenomegaly
Keywords:
Myelofibrosis, Reticulin fibrosis, Splenomegaly, CD34, Mean Vessel Density
Abstract
Background: Myelofibrosis is characterised by increased deposition of collagen type I and III in the bone marrow. Fibroplasia is associated with increased blood flow through marrow substance. Fibrosis occurs in variety of haematological and non haematological disorders. The present study was conducted to study the pattern of mean vessel density in various pathological disorders presenting with marrow fibrosis and to correlate it with spleen size. Methods: This is one year observational study undertaken in Department of pathology, Coimbatore medical college hospital, Coimbatore. A total of 25 cases presented with bone marrow fibrosis were taken and correlative study was done with mean vessel density and splenomegaly. Result: Of a total 25 Patients, 17 were secondary myelofibrosis and 8were Primary myelofibrosis. Patient from 18 to 80years were encountered in the study. Total of 13males and 12 females were included. Among Primary myelofibrosis 6 were males and 2 were females. Most of the cases of secondary myelofibrosis (11 out of 18) were Hematological malignancies which included AML(3), CML(2), CLL(1), MDS(1), NHL(3), MM(1).CD34 Immunostaining showed increased mean vessel density among all the cases of primary myelofibrosis. Conclusion: Reticulin fibrosis occurs in variety of Hematological, Non Hematological Malignancies and Non neoplastic disorders including Tuberculosis, SLE and post radiotherapy accompanied by various degree of mean vessel density. Increase in MVD is considered as mother event in causing fibrosis and splenomegaly. Hence studying MVD and correlating it with fibrosis and splenomegaly will be helpful in evaluating the disease progression.References
1. Hotta T , Utsumi M , Katoh T ,et al: Granulocytic and stromal progenitors in the bone marrow of patient with primary myelofibrosis. Scand J Haematol 34:251,1985.
2. Folkman J, Seminars in Medicine of the Beth Isreal Hospital, Boston: Clinical applications of research on angiogenesis. N Engl J Med.1995;333:1757-1763.
3.Perez-Atayde AR, Sallan SE, Tedrow U, Connors S, Allred E, Folkman J: Spectrum of tumor angiogenesis in the bone marrow of children with acute lymphoblastic leukemia. Am J Pathol. 1997;150:815-821.
4.Hussong JW, Rodgers GM, Shami PJ: Evidence of increased angiogenesis in patients with acute myeloid leukemia. Blood. 2000;95:309-313.
5.Pruneri G, Bertolini F, Soligo D, et al: Angiogenesis in myelodysplastic syndromes. Br J Cancer. 1999;81:1398-1401.
6.Aguayo A, Kantargian H, Talpaz M,et al: Increased angiogenesis in chronic myeloid leukemia and myelodysplastic syndromes(abstract).Blood. 1998;92(suppl 1):607a.
7.Vacca A, Ribatti D, Presta M, et al: Bone marrow neovascularisation, plasma cell angiogenic potential, and matrix metalloproteinase-2 secretion parallel progression of human multiple myeloma. Blood. 1999;93:3064-73.
8.Weidner, N. Tumor angiogenesis: Review of current applications in tumor prognostication. Seminars in Diagnostic Pathology,1993; 10, 302-313.
9. Mesa, R.A., Hanson, C.A., Rajkumar, S.V., Schroeder, G. & Tefferi, A. Evaluation and clinical correlation of bone marrow angiogenesis in myelofibrosis with myeloid metaplasia. Blood, 2000;96, 3374-80.
10.Soini Y, Kamel D , Apaja-Sarkkinen M, et al : Tenascin immunoreactivity in normal and pathological bone marrow. J Clin Pathol 1993;46 ;218
11. Reily JT , Nash JRG: Vitronectin (serum spreading factor): Its localization in normal and fibrotic tissue . J Clin Pathol 1988;41 : 1269
12.Le Bousse-Kerdiles MC, Martyre MC, et al : Involement of the fibrogenic cytokines , TGF-b and bFGf , in the pathogenesis of idiopathic myelofibrosis. Pathol Biol 2001;49 :153.
13.Barosi G: Myelofibrosis with myeloid metaplasia. Hematol Clin North Am 2003;17:1211.
14. Ozen S, Ferhanoglu B, Senocak M, Tuzuner N: Idiopathic myelofibrosis (agnogenic myeloid metaplasia). Leuk Res 1997;21:125.
15.Okamura T, Kinukawa N, Niho Y, Mizoguichi H: Primary chronic myelofibrosis: Clinical and prognostic evaluation in 336 japanese patients Int J Hematol 2001;73:194.
16.Wolf BC, Neiman RS: Myelofibrosis with myeloid metaplasia: Pathophysiological implications between bone marrow changes and progression of splenomegaly. Blood 1985:65:803.
17.Panteli, K., Zagorianakou, N.,Bai, M., Katsaraki, A., Agnantis, N.J., Bourantas, K. Angiogenesis in chronic myeloproliferative diseases detected by CD34 expression. European Journal of Haematology, 2004:72,410-415.
18.Varki A, Lottenberg R, Griffin R, Reinhard E: The syndrome of idiopathic myelofibrosis: Clinicopathologic review with emphasis on the prognostic variables predicting survival. Medicine (Baltimore) 1983:62:353.
2. Folkman J, Seminars in Medicine of the Beth Isreal Hospital, Boston: Clinical applications of research on angiogenesis. N Engl J Med.1995;333:1757-1763.
3.Perez-Atayde AR, Sallan SE, Tedrow U, Connors S, Allred E, Folkman J: Spectrum of tumor angiogenesis in the bone marrow of children with acute lymphoblastic leukemia. Am J Pathol. 1997;150:815-821.
4.Hussong JW, Rodgers GM, Shami PJ: Evidence of increased angiogenesis in patients with acute myeloid leukemia. Blood. 2000;95:309-313.
5.Pruneri G, Bertolini F, Soligo D, et al: Angiogenesis in myelodysplastic syndromes. Br J Cancer. 1999;81:1398-1401.
6.Aguayo A, Kantargian H, Talpaz M,et al: Increased angiogenesis in chronic myeloid leukemia and myelodysplastic syndromes(abstract).Blood. 1998;92(suppl 1):607a.
7.Vacca A, Ribatti D, Presta M, et al: Bone marrow neovascularisation, plasma cell angiogenic potential, and matrix metalloproteinase-2 secretion parallel progression of human multiple myeloma. Blood. 1999;93:3064-73.
8.Weidner, N. Tumor angiogenesis: Review of current applications in tumor prognostication. Seminars in Diagnostic Pathology,1993; 10, 302-313.
9. Mesa, R.A., Hanson, C.A., Rajkumar, S.V., Schroeder, G. & Tefferi, A. Evaluation and clinical correlation of bone marrow angiogenesis in myelofibrosis with myeloid metaplasia. Blood, 2000;96, 3374-80.
10.Soini Y, Kamel D , Apaja-Sarkkinen M, et al : Tenascin immunoreactivity in normal and pathological bone marrow. J Clin Pathol 1993;46 ;218
11. Reily JT , Nash JRG: Vitronectin (serum spreading factor): Its localization in normal and fibrotic tissue . J Clin Pathol 1988;41 : 1269
12.Le Bousse-Kerdiles MC, Martyre MC, et al : Involement of the fibrogenic cytokines , TGF-b and bFGf , in the pathogenesis of idiopathic myelofibrosis. Pathol Biol 2001;49 :153.
13.Barosi G: Myelofibrosis with myeloid metaplasia. Hematol Clin North Am 2003;17:1211.
14. Ozen S, Ferhanoglu B, Senocak M, Tuzuner N: Idiopathic myelofibrosis (agnogenic myeloid metaplasia). Leuk Res 1997;21:125.
15.Okamura T, Kinukawa N, Niho Y, Mizoguichi H: Primary chronic myelofibrosis: Clinical and prognostic evaluation in 336 japanese patients Int J Hematol 2001;73:194.
16.Wolf BC, Neiman RS: Myelofibrosis with myeloid metaplasia: Pathophysiological implications between bone marrow changes and progression of splenomegaly. Blood 1985:65:803.
17.Panteli, K., Zagorianakou, N.,Bai, M., Katsaraki, A., Agnantis, N.J., Bourantas, K. Angiogenesis in chronic myeloproliferative diseases detected by CD34 expression. European Journal of Haematology, 2004:72,410-415.
18.Varki A, Lottenberg R, Griffin R, Reinhard E: The syndrome of idiopathic myelofibrosis: Clinicopathologic review with emphasis on the prognostic variables predicting survival. Medicine (Baltimore) 1983:62:353.
Published
2018-08-27
Issue
Section
Original Article
Authors who publish with this journal agree to the following terms:
- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access at http://opcit.eprints.org/oacitation-biblio.html).
