İDİOPATİK TROMBOSİTOPENİK PURPURA VE ENFEKTİF PERİKARDİT TANISI SONRASI HODGKİN LENFOMA GELİŞMESİ

Öz

Hodgkin Lenfoma HL batı memleketlerinde genç yaşlarda en sık görülen malign lenfomadır. Çoğu hastada modern tedavi stratejileri ile kür sağlanırken, yaklaşık %20’si relaps veya progressif hastalık nedeniyle ölmektedir. Hodgkin Lenfomanın patogenezinde şüphelenilen birçok factor olmasına karşın, infeksiyöz ajanların daha belirgin rol oynadığına inanılmaktadır. Biz şimdi, daha önce Idiopatik Trombositopenik Purpura tanısı alıp kortikosteroid tedavisi verildikten sonra infektif endokardit gelişen hastada Hodgkin Lenfoma gelişmesini içeren olguyu sunacağız

Anahtar Kelimeler

• Hodgkin Lenfoma,İdiopatik Trombositopenik Purpura,infektif endokardit

HODGKIN LYMPHOMA DEVELOPMENT AFTER THE DIAGNOSIS OF IDIOPATHIC THROMBOCYTOPENIC PURPURA ITP AND INFECTIVE ENDOCARDITIS

Abstract

Hodgkin’s lymphoma HL represents the most common subtype of malignant lymphoma in young people in the western World. Most patients can be cured with modern treatment strategies, although approximately 20% will die after relapse or progressive disease. Although there are many factors, which are suspected in the pathogenesis of Hodgkin’s lymphoma, infectious agents are believed to play more marked roles. We will present in our case report development of Hodgkin’s lymphoma after the diagnosis of infective endocarditis, which has been ensued following the corticosteroid treatment given for the previous Idiopathic Thrombocytopenic Purpura diagnosis

Keywords

• Hodgkin’s Lymphoma,Idiopathic Thrombocytopenic Purpura,Infective Endocarditis

Kaynakça

1. ) Swerdlow SH, Campho E, Harris NL, et al. WHO Classification of Tumours of Haemotopoietic and Lymphoid Tissues.4 ed., Lyon:IARC, 2008;439.
2. ) Gerber HP. Emerging immunotherapies targeting CD30 in Hodgkin’s lymphoma. Biochem Pharmacol.2010;79(11): 52.
3. ) Marafioti T, Hummel M, Anagnostopoulos I, et al. Origin of nodular lymphocyte-predominant Hodgkin’s disease from a clonal expansion of highly mutated germinal-center B cells. N Eng J Med, 1997;337: 453-8.
4. ) Brune V, Tiacci E, Pfeil I, et al. Origin and pathogenesis of nodular lymphocyte-predominant Hodgkin lymphoma as revealed by global gene expression analysis. J Exp Med ;205(10):2251-68.
5. ) J. D. Fingeroth, J. J. Weis, T. F. Tedder, J. L. Strominger, P.A. Biro, and D. T. Fearon. Epstein-Barr virus receptor of human B lymphocytes is the C3d receptor CR2. Proceedings of the National Academy of Sciences of the United States of America, 1984;81(14): 4510–4.
6. ) Q. Li, M. K. Spriggs, S. Kovats et al., Epstein-Barr virus uses HLA class II as a cofactor for infection of B lymphocytes, Journal of Virology. 1997; 71(6): 4657–62.
7. ) G. J. Babcock, L. L. Decker, R. B. Freeman, and D. A. Thorley-Lawson, Epstein-Barr virus-infected resting memory B cells, not proliferating lymphoblasts, accumulate in the peripheral blood of immunosuppressed patients. Journal of Experimental Medicine. 1999;190 (4): –76.
8. ) G. J. Babcock, L. L. Decker, M. Volk, and D. A. Thorley- Lawson, EBV persistence in memory B cells in vivo. Immunity.1998; 9(3): 395–404.

9. ) E. Kieff, Epstein-Barr virus and its replication, in Virology, B. N. Fields, D.M. Knipe, P. M. Howley et al. Eds., Lippincott-Raven, Philadelphia, Pa, USA, 1996; 2343–96.
10. ) A. L. N. Chapman and A. B. Rickinson, Epstein-Barr virus in Hodgkin’s disease, Annals of Oncology, 1998; (5):S5–S16.
11. ) I. Miyazaki, R. K. Cheung, and H. M. Dosch, interleukin 10 is critical for the induction of B cell growth transformation by Epstein-Barr virus, Journal of Experimental Medicine, 1993; 178(2): 439–47.
12. ) Gaulard P, Swerdlow SH, Harris SH, et al. Other iatrogenic immunodeficiency associated lymphoprolife rative disorders. In: Swerdlow SH, Campo E, Harris NL, et al., editors. World Health Organization Classification of Tumours, Pathology and Genetics of Tumours of Haematopoietic and Lymphoid Tissues. Lyon: IARC Press; ; 350–1. ) Younes A: Novel treatment strategies for patients with relapsed classical Hodgkin lymphoma. Hematology Am Soc Hematol Educ Program 2009;507-19.
13. ) Oki Y, Younes A: Current role of gemcitabine in the treatment of Hodgkin lymphoma. Leuk Lymphoma ;49(5): 883-9. ) Correale P, Del Vecchio MT, La Placa M, et al: Chemotherapeutic drugs may be used to enhance the killing efficacy of human tumor antigen peptide-specific CTLs. J Immunother 2008;31(2):132-47.
14. ) Rassidakis GZ, Medeiros LJ, Viviani S, et al: CD20 expression in Hodgkin and Reed-Sternberg cells of classical Hodgkin’s disease: Associations with presenting features and clinical outcome. J Clin Oncol 2002;20:1278
15. ) Jones RJ, Gocke CD, Kasamon YL, et al: Circulating clonotypic B cells in classic Hodgkin lymphoma. Blood ;113(23): 5920-6.
16. ) Leonard JP, Friedberg JW, Younes A, et al: A phase I/II study of galiximab (an anti-CD80 monoclonal antibody) in combination with rituximab for relapsed or refractory, follicular lymphoma. Ann Oncol ;18(7):1216-23.
17. ) Rodig SJ, Abramson JS, Pinkus GS, et al: Heterogeneous CD52 expression among hematologic neoplasms: Implications for the use of alemtuzumab (CAMPATH-1H). Clin Cancer Res 2006;12(23):7174-9.
18. ) Bollard CM, Aguilar L, Straathof KC, et al: Cytotoxic T lymphocyte therapy for Epstein-Barr virus- Hodgkin’s disease J Exp Med . 2004;200(12):1623-33.
19. ) Bollard CM, Gottschalk S, Leen AM, et al: Complete responses of relapsed lymphoma following genetic modification of tumor-antigen presenting cells and T- lymphocyte transfer. Blood 2007;110(8): 2838-45.
20. ) Bartlett NL, Younes A, Carabasi MH, et al: A phase 1 multidose study of SGN-30 immunotherapy in patients with refractory or recurrent CD30 + hematologic malignancies. Blood 2008;111(4):1848-54.
21. ) Johnston PB, Ansell SM, Colgan JP, et al: MTOR inhibition for relapsed or refractory Hodgkin lymphoma: Promising single agent activity with everolimus (RAD001). Presented at the Annual Meeting of the American Society of Hematology, Atlanta, GA, 2007, December 8-11, (abstr ).
22. ) Zheng B, Georgakis GV, Li Y, et al: Induction of cell cycle arrest and apoptosis by the proteasome inhibitor PS- in Hodgkin disease cell lines is independent of inhibitor of nuclear factor-kappaB mutations or activation of the CD30, CD40, and RANK receptors. Clin Cancer Res ;10(9):3207-15.
23. ) Blum KA, Johnson JL, Niedzwiecki D, et al: Single agent bortezomib in the treatment of relapsed and refractory Hodgkin lymphoma: Cancer and leukemia Group B protocol 50206. Leuk Lymphoma 2007;48(7):1313-9.