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Type d’époétine

III.6. EVOLUTION ET PRONOSTIC

L’évolution de la maladie de Blackfan-Diamond peut être favorable et l’anémie peut disparaître spontanément dans 30 % des cas. Cependant, il existe un risque de survenue de leucémie aiguë chez les patients en rémission (23 % des cas chez les patients de moins de 40 ans), ce qui justifie un suivi médical prolongé chez ces sujets et explique la limitation des approches thérapeutiques utilisant les facteurs de croissance [19]. Le pronostic de la maladie est surtout fonction de la surcharge martiale induite par les transfusions globulaires itératives.

Dans le cas des érythroblastopénies secondaires, le pronostic dépend de l’affection causale sous-jacente. Globalement, la survie médiane est de 20 ans environ. 10 % de résolutions spontanées sont observées, 70 % répondent après de multiples lignes de traitement mais 80 % des cas rechutent dans les deux années qui suivent le diagnostic. À noter que des transformations en leucémie myéloïde aigüe sont décrites dans 3 à 5 % des formes réfractaires [127].

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L’érythroblastopénie est une affection rare dont le diagnostic ne doit pas être méconnu devant une anémie arégénérative. Les études concernant cette pathologie ont bien évoluées ces dernières années et la liste des étiologies ne cesse de s’élargir pour inclure d’autres entités comme par exemple l’érythroblastopénie en rapport avec les syndromes myélodysplasiques. Le traitement repose d’abord et essentiellement sur la transfusion de culôts globulaires et puis sur le traitement spécifique en rapport avec la pathologie causale.

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RESUME

Titre : Les érythroblastopénies : A propos de 03 cas et revue de littérature.

Auteur : ER-RAHALI NADIA

Mots clés : érythroblastopénie ; anémie ; parvovirus B19 ; Syndrome myélodysplasique

L'érythroblastopénie est définie par une anémie strictement arégénérative, associée à la disparition totale ou subtotale des précurseurs érythrocytaires médullaires. Les lignées granuleuses et mégacaryocytaires sont strictement normales. Le diagnostic en est habituellement facile. On peut distinguer les formes congénitales ou les formes acquises qui constituent un groupe physiopathologique hétérogène. Elles peuvent être associées à de multiples causes : infection virale, agression toxique, phénomène auto-immun, association à un thymome, une leucémie lymphoïde chronique (B ou T), une prolifération à grands lymphocytes à grains. Une érythroblastopénie peut être aussi le premier signe d'une hémopathie en particulier d'une myélodysplasie.

La distinction entre une érythroblastopénie dont l'origine est une anomalie intrinsèque de la cellule souche et les autres étiologies est très importante du point de vue thérapeutique et pronostique. C'est là que l'étude de la croissance in vitro des progéniteurs apporte une aide certaine au diagnostic. En effet, il existe une corrélation étroite entre la croissance in vitro des progéniteurs érythroblastiques et la réponse au traitement immunosuppresseur.

Au total l'érythroblastopénie est une pathologie hématologique peu fréquente, mais il est important d'en faire le diagnostic étiologique car c'est une affection curable dans un grand nombre de cas.

A travers trois cas cliniques diagnostiqués au laboratoire d’hématologie de l’hôpital militaire d’instruction Mohammed V Rabat, nous allons faire le point sur les caractéristiques cliniques, physiopathologiques, biologiques et thérapeutiques de cette pathologie.

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SUMMARY

Title: Pure red cell aplasia: About 03 cases and review of literature.

Author : ER-RAHALI NADIA

Keywords :pure red cell aplasia; anemia ; human parvovirus B19; myelodysplastic syndrome

Pure red cell aplasia is defined by aregenative anemia,linked to total or subtotal disappearance of medullar erythrocytary precursors. Granulous and megacaryocytary lines are quite normal. Diagnosis is usually easy. We can distinguish congenital forms and acquired forms wich constitute an heterogenous physiopathological group. They can be associated to a multiple cause phs : viral infection, toxic aggression, auto-immune phenomenon, an association to a thymoma, a chronic lymphoid leukemia ( B ou T), a proliferation of large granular lymphocyte. Pure red cell aplasia can also be the first sign of hemopathy.

The distinction between an pure red cell aplasia whose origin is an intrinsic abnormality of the cell and the other etiologies is very important from and prognostic point of view. It is here where the study of the in vitro growth of progenitors brings a certain help to diagnosis. In fact, there is a close correlation between the in vitro growth of erythroblastic progenitors abd the reponse to immunosupressor treatment.

In total, pure red cell aplasia is an infrequent hematological pathology, but it is important to make the etiological diagnosis because it is a curable disease in a great number of cases.

Through three clinical cases diagnosed in the laboratory of hematology , of Mohamed V military hospital in Rabat, we will review the clinical, physiopathological , biological and therapeutical features of this pathology.

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Références

Les érythroblastopénies : A propos de 03 cas et revue de littérature

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[1] Beaumont C, Beris P, Beuzard Y, Brugnara C (European school of

Hematology). Regulation of erythropoiesis. In : Disorders of iron hemostasis, erythrocytes, erythropoiesis, Chapter 2 : 38-71.

[2] Crabol Y, Berezné A, Mouthon L. Erythroblastopénies, EMC (Elsevier Masson SAS, Paris). Hématologie 2007 ; (13-006-E-10).

[3] Gazda H, Lipton JM, Willig TN, Ball S, Niemeyer CM, Tchernia G, et al. Evidence for linkage of familial Diamond-Blackfan anemia to

chromosome 8p23.3-p22 and for non-19q non-8p disease. Blood 2001; 97:2145-50.

[4] Hamaguchi I, Ooka A, Brun A, Richter J, Dahl N, Karlsson S. Gene

transfer improves erythroid development in ribosomal protein S19- deficient Diamond-Blackfan anemia. Blood 2002; 100:2724-31.

[5] Hamaguchi I, Ooka A, Brun A, Richter J, Dahl N, Karlsson S. Gene

transfer improves erythroid development in ribosomal protein S19- deficient Diamond-Blackfan anemia. Blood 2002; 100:2724-31.

[6] Dessypris EN, Redline S, Harris JW, Krantz SB.

Diphenylhydantoininduced pure red cell aplasia. Blood 1985; 65: 789-94.

[7] Dessypris EN, Redline S, Harris JW, Krantz SB.

Diphenylhydantoininduced pure red cell aplasia. Blood 1985; 65: 789-94.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 83 ~

[8] Tzioufas AG, Kokori SI, Petrovas CI, Moutsopoulos HM.

Autoantibodies to human recombinant erythropoietin in patients with systemic lupus erythematosus: correlation with anemia. Arthritis Rheum 1997; 40:2212-6.

[9] Casadevall N, Nataf J,Viron B, KoltaA, Kiladjian JJ, Martin-Dupont P, et al. Pure red-cell aplasia and antierythropoietin antibodies

in patients treated with recombinant erythropoietin. N Engl J Med 2002; 346: 469-75.

[10] Chikkappa G, Zarrabi MH, Tsan MF. Pure red-cell aplasia in

patients with chronic lymphocytic leukemia. Medicine 1986; 65:339-51.

[11] Charles RJ, Sabo KM, Kidd PG, Abkowitz JL. The pathophysiology of pure red cell aplasia: implications for therapy. Blood 1996; 87:4831.

[12] Casadevall N. Les érythroblastopénies. Les cytopénies immunologiques. Congrès, Paris, France (11/10/2007) 2008, vol. 29, HS1 (95 p.)

[13] Vlachos A, Ball S, Dahl N, et al. Diagnosing and treating

Diamond-Blackfan anaemia: results of an international clinical consensus conference. Br J Haematol 2008; 142: 859-76.

[14] Willig TN, Pérignon JL, Gustavsson P, et al. High adenosine

deaminase level among healthy probands of Diamond-Blackfan anemia (DBA) cosegregates with the DBA gene region on chromosome 19q13. Blood 1998 ; 92 : 4422-7.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 84 ~

[15] Willig TN, Pérignon JL, Gustavsson P, et al. High adenosine

deaminase level among healthy probands of Diamond-Blackfan anemia (DBA) cosegregates with the DBA gene region on chromosome 19q13. Blood 1998 ; 92 : 4422-7.

[16] Draptchinskaia N, Gustavsson P, Andersson B, et al. The gene

encoding ribosomal protein S19 is mutated in Diamond-Blackfan anaemia. Nat Genet 1999; 21 : 169-75.

[17] P, Guillet B, Tchernia G. L’erythrovirus B19 en hematologie.

Hematologie 2003 ; 9 : 389-401.

[18] Gustavsson P, Klar J, Matsson H, et al. Familial transient erythroblastopenia of childhood is associated with the chromosome 19q13.2 region but not caused by mutations in coding sequences of the ribosomal protein S19 (RPS19) gene. Br J Haematol 2002; 119 : 261-4.

[19] Ohene-Abuakwa Y, Orfali KA, Marius C, Ball SE. Twophase

culture in Diamond-Blackfan anemia : localization of erythroid defect.

Blood 2005 ; 105 : 838-46.

[20] Aase JM, Smith DW. Congenital anemia and triphalangeal thumbs: a

new syndrome. J Pediatr 1969 ; 74 : 471-4.

[21] Van Hook JW, Gill P, Cyr D, Kapur RR Diamond-Blackfan anemia

as an unusual cause of nonimmune hydrops fetalis : a case report. J Reprod Med 1995; 40 : 850-4.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 85 ~

[22] Vlachos A, Ball S, Dahl N, et al. Diagnosing and treating

Diamond-Blackfan anaemia: results of an international clinical consensus conference. Br J Haematol 2008; 142: 859-76.

[23] Willig TN, Niemeyer C, Leblanc T, et al. Diamond-Blackfan anemia:

clinical and epidemiological studies with identification of new long-term prognosis factors from the analysis of a registry of 234 patients. Pediatr Res 1999 ; 46 : 553-61.

[24] Hematol Oncol Clin North Am. 2009 April ; 23(2): 261–282.

doi:10.1016/j.hoc.2009.01.004.

[25] Tournioire B, Bertrand Y, Manuel AM, Philippe N.Transient

erythroblostopenia in early childhood. ArchPecliatr 1995 ; 2 : 124-9.

[26] Ware RE, Kinney TR. Transient erythroblasIopenia in the tint year of

life. Am J Hemurof 1991;37:156-8.

[27] Coulombel L. éyrhroblastopénies de I’enfant. Rev Prof (Paris)

1989;39:2138-42.

[28] Genirs GP. van Oostrom CG, de Vaan GA, Bakkeren IA. Transient

eryrhroblastopenia of childhood. A review of 22 cases. EurJ Pediolr 1984;142:266-70.

[29] Hays T. lane PA. Shafer F. Transient erytbmblastopenia of childhood.

A review of 26 cases and reassessment of indications for bone marrow aspiration. Am J Dis Child 1989:143:605-7.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 86 ~

[30] DESSYPRIS EN, KRANTZ SB, ROLOFF JS, LUKENS JN. Mode

of action of the IgG inhibitor of erythropoiesis in transient erythroblastopenia of childhood. Blood 1982 ; 59 : 114-123.

[31] Wang, W. C., and Mentzer, W. C. (1976). Differentiation of transient

erythroblastopenia of childhood from congenital hypoplastic anemia. Journal of Pediatrics, 88, 784-789.

[32] Cossart YE, Field AM, Cant B,Widdows D. Parvovirus-like particles

in human sera. Lancet 1975;i:72–3.

[33] Zhi N, Zadori Z, Brown KE, Tijssen P. Construction and sequencing

of an infectious clone of the human parvovirus B19. Virology 2004;318:142–52.

[34] Kaufmann B, Chipman PR, Kostyuchenko VA, Modrow S, Rossmann MG. Visualization of the externalized VP2 N termini of

infectious human parvovirus B19. J Virol 2008;82:7306–12.

[35] Von Landenberg P, Lehmann HW, Modrow S. Human parvovirus

B19 infection and antiphospholipid antibodies. Autoimmun Rev 2007;6:278–85.

[36] Agbandje-McKenna M, Rossmann MG. The structure of human

Parvovirus B19. In: Anderson LJ, Young NS, editors. Human Parvovirus B19 20,. First ed., New York: Karger; 1997. p. 3–15.

[37] Cooling LL, Koerner TA, Naides SJ. Multiple glycosphingolipids

determine the tissue tropism of parvovirus B19. J Infect Dis 1995;172:1198–1205.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 87 ~

[38] Brodin-Sartorius A, Mekki Y, Bloquel B, Rabant M, Legendre C.

Infection par le Parvovirus B19 après transplantation rénale. EMC (Elsevier Masson SAS, Paris). Néphrologie et Thérapeutique. 2012 ; 5–12.

[39] Pankuweit S, Lamparter S, Schoppet M, Maisch B. Parvovirus B19

genome in endomyocardial biopsy specimen. Circulation 2004;109: e179.

[40] Miller E, Fairley CK, Cohen BJ, Seng C. Immediate and long term

outcome of human parvovirus B19 infection in pregnancy. Br J Obstet Gynaecol 1998;105:174-8.

[41] Karmochkine M. Infection humaine par le parvovirus B19. Mise au

point. Rev Méd Interne 1995 ; 16 : 905-12.

[42] Brown KE. Haematological consequences of parvovirus B19 infection.

Clin Haematol 2000 ; 13 : 245-59.

[43] Knutsen AP, Wall D, Mueller KR, Bouhasin JD. Abnormal in vitro

thymocyte differentiation in a patient with severe combined immunodeficiency-Nezelof’s syndrome. J Clin Immunol 1996;16: 151-8.

[44] Abkowitz JL, Brown KE, Wood RW, Kovach NL, Green SW, Young NS. Clinical relevance of parvovirus B19 as a cause of anemia

in patients with human immunodeficiency virus infection. J Infect Dis 1997;176:269-73.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 88 ~

[45] Vales-Albertos LJ, Garcia-Cardenas M, Chavez-Becerra S, Gomez-Navarro B, Monteon-Ramos F, Cueto-Manzano AM. Pure

red cell aplasia associated with parvovirus B19 infection in renal transplantation: the first case report in Mexico. Transplantation 2005; 79:739.

[46] Gallinella G, Manaresi E, Venturoli S, Grazi GL, Musiani M, Zerbini M. Occurrence and clinical role of active parvovirus B19

infection in transplant recipients. Eur J Clin Microbiol Infect Dis 1999;18: 811-3.

[47] Crowley B, Woodcock B. Red cell aplasia due to parvovirus b19 in a

patient treated with alemtuzumab. Br J Haematol 2002;119: 279-80.

[48] Parekh S, Perez A, Yang XY, Billett H. Chronic parvovirus infection

and G6PD deficiency masquerading as Diamond-Blackfan anemia.Am J Hematol 2005;79:54-7.

[49] Lugassy G. Chronic pure red cell aplasia associated with parvovirus

B19 infection in an immunocompetent patient. Am J Hematol 2002;71: 238-9.

[50] Young N, Harrison M, Moore J, Mortimer P, Humphries RK.

Direct demonstration of the human parvovirus in erythroid progenitor cells infected in vitro. J Clin Invest 1984;74:2024-32.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 89 ~

[51] americain society of hematology image bank. Pure Red Cell Aplasia

(PRCA) – parvovirus infection. 12 mai 2001.

http://imagebank.hematology.org/AssetDetail.aspx?AssetID=1550&As setType=Asset

[52] Dessypris EN, Lipton JM. Red cell aplasia. In: Wintrobe’s Clinical

Hematology, Chapter 45 : 1421- 1434, Lippincott Williams & Wilkins, 11th edition, Philadelphie, 2004.

[53] société francaise d’hématologie. Commission Pédagogique. Item

163 : leucémie lymphoïde chronique. Mise à jour 2007

[54] Batlle M, Ribera JM, Oriol A, Plensa E, Milla F, Feliu E. Successful

response to rituximab in a patient with pure red cell aplasia complicating chronic lymphocytic leukaemia. Br J Haematol 2002; 118:1192-3.

[55] Kedar V. Inamdar, Carlos E. Bueso-Ramos.Pathology of chronic

lymphocytic leukemia: an update Annals of Diagnostic Pathology, Volume 11, Issue 5, October 2007, Pages 363–389

[56] Hamblin TJ. Autoimmune complications of chronic lymphocytic

leukemia. Semin Oncol 2006;33:230-9.

[57] Castelli R, Vismara A, Pavia G, Dagani R, Porro T. Relapsing pure

red cell aplasia associated with B-cell chronic lymphocytic leukemia successfully treated by intravenous immunoglobulin concentrate. Ann Ital Med Int 2002;17:47-50.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 90 ~

[58] Lamy T, Loughran Jr .TP. Current concepts: large granular

lymphocyte leukemia. Blood Rev 1999;13:230-40.

[59] Go RS, Li CY, Tefferi A, Phyliky RL. Acquired pure red cell aplasia

associated with lymphoproliferative disease of granular T lymphocytes.

Blood 2001;98:483-5.

[60] Lamy T,Thomas P, Loughran Jr. How I treat LGL leukemia. Blood.

2011 March 10; 117(10): 2764–2774

[61] Masuda M, Teramura M, Matsuda A, Bessho M, Shimamoto T, Ohyashiki K, et al. ClonalTcells of pure red-cell aplasia.AmJ Hematol

2005;79:332-3.

[62] E. Vlachaki, K. Tselios, S. Charalambidou, E. Ioannidou, and I. Klonizakis, “Pure red cell aplasia complicating B cell small

lymphocytic lymphoma: a case report,” International Journal of Hematology, vol. 88, no. 3, pp. 341–342, 2008.

[63] A. Anastasiadis, D. Margaritis, I. Kotsianidis et al., “Pure red cell

aplasia as first manifestation of splenic marginal zone lymphoma-successful treatment with rituximab: a case report,” Cases Journal, vol. 2, no. 8, article 6913, 2009.

[64] M. Hirokawa, K. I. Sawada, N. Fujishima et al., “Acquired pure red

cell aplasia associated with malignant lymphomas: a nationwide cohort study in Japan for the PRCA Collaborative Study Group,” American Journal of Hematology, vol. 84, no. 3, pp. 144–148, 2009.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 91 ~

[65] K. Narra, H. Borghaei, T. Al-Saleem, M. H¨oglund, and M. R. Smith, “Pure red cell aplasia in B-cell lymphoproliferative disorder

treated with rituximab: report of two cases and review of the literature,” Leukemia Research, vol. 30, no. 1, pp. 109–114, 2006.

[66] J. H. Choi, Y. H. Oh, and I. K. Park, “A case of pure red cell aplasia

associated with angioimmunoblastic T-cell lymphoma,” Cancer Research and Treatment, vol. 42, pp. 115– 117, 2010.

[67] Navarro I, Ruiz MA, Cabello A, Collado R, Ferrer R, Hueso J, et al. Classification and scoring systems inmyelodysplastic syndromes: a

retrospective analysis of 311 patients. Leuk Res 2006;30:971–7.

[68] Merlat A, Picard F, Dreyfus F. Syndromes myélodysplasiques et

leucémies secondaires. Encycl Méd Chir (Éditions Scientifiques et Médicales Elsevier SAS, Paris), Hématologie, 13-012-A-10, 2000, 14 p.

[69] Barrett AJ, Sloand E. Autoimmune mechanisms in the pathophysiology of myelodysplastic syndromes and their clinical relevance. Haematologica 2009;94:449–51.

[70] Charles RJ, Sabo KM, Kidd PG, Abkowitz JL. The pathophysiology

of pure red cell aplasia: implications for therapy. Blood 1996;87: 4831–8.

[71] Lacombe C, Casadevall N, Muller O, Varet B. Erythroid progenitors

in adult chronic pure red cell aplasia: relationship of in vitro erythroid colonies to therapeutic response. Blood 1984;64:71–7.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 92 ~

[72] Blagosklonny MV. The dilemma of apoptosis in myelodysplasia and

leukemia: a new promise of therapeutic intervention? Leukemia 2000;14:2017–8.

[73] Ghezzi P, Brines M. Erythropoietin as an antiapoptotic,

tissue-protective cytokine. Cell Death Differ 2004;11(Suppl. 1):S37–44.

[74] Hirokawa M, Sawada K, Fujishima N, Kawano F, Kimura A, Watanabe T, et al. Acquired pure red cell aplasia associated with

malignant lymphomas: a nationwide cohort study in Japan for the PRCA Collaborative Study Group. Am J Hematol 2009;84:144–8.

[75] Hofmann WK, Koeffler HP. Myelodysplastic syndrome. Annu Rev

Med 2005;56:1–16.

[76] C. Martinaud; S. Pons; G. Ménard; O. Gisserot; J.-P. de Jaureguiberry; P. Brisou. Syndromes myélodysplasiques érythroblastopéniques. J.revmed.2010.07.009.7

[77] Orazi A, Albitar M, Heerema NA, Haskins S, Neiman RS.

Hypoplastic myelodysplastic syndromes can be distinguished from acquired aplastic anemia by CD34 and PCNA immunostaining of bone marrow biopsy specimens. Am J Clin Pathol 1997;107:268–74.

[78] Charles RJ, Sabo KM, Kidd PG,Abkowitz JL. The pathophysiology of pure red cell aplasia: implications for therapy. Blood 1996;87:4831-8.

[79] Suzuki S, Nogawa S,Tanaka K, KotoA, FukuuchiY, Kuwana M.

Initial predictors of development of pure red cell aplasia in myasthenia gravis after thymectomy. Clin Neurol Neurosurg 2003;106:16-8.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 93 ~

[80] Habib GS, Saliba WR, Froom P. Pure red cell aplasia and lupus.

Semin Arthritis Rheum 2002;31:279-83.

[81] Bunn HF. Drug-Induced Autoimmune Red-Cell Aplasia. N Engl J

Med 2002;346:522-23.

[82] Ortho Biotech, division of Janssen-Ortho Inc. EPREX (epoetin alfa)

– Pure Red Cell Aplasia (PRCA, Erythroblastopenia). 25 juin 2002.

[83] Johnson & Johnson. STATEMENT - Report on Suspected Pure Red

Cell Aplasia Following Treatment with Erythropoietin Products. 30 septembre 2002.

[84] Association des pharmaciens du Canada. Compendium des produits

et spécialités pharmaceutiques. 38e édition. Ottawa, Association des pharmaciens du Canada, 2003.

[85] Casadevall N, Nataf J, Viron B et coll. Pure Red-Cell Aplasia and

Antierythropoietin Antibodies in Patients Treated with Recombinant Erythropoietin. N Engl J Med 2002;346:469-75.

[86] Thompson DF, Gales MA. Drug-induced pure red cell aplasia.

Pharmacotherap 1996;16:1002-8.

[87] Casadevall N, Cournoyer D, Marsh J, et al. Recommendations on haematological criteria for the diagnosis of epoetin-induced pure red

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 94 ~

[88] Ball SE, McGuckin CP, Jenkins G, Gordon-Smith EC. Diamond-

Blackfan anaemia in the U.K.: analysis of 80 cases from a 20-year birth cohort. Br J Haematol 1996;94:645-53.

[89] Mamiya S, Itoh T, Miura AB. Acquired pure red cell aplasia in Japan.

Eur J Haematol 1997;59:199–205.

[90] Ball SE, McGuckin CP, Jenkins G, Gordon-Smith EC. Diamond-

Blackfan anaemia in the U.K.: analysis of 80 cases from a 20-year birth cohort. Br J Haematol 1996;94:645-53.

[91] Ozsoylu S. High-dose intravenous corticosteroid treatment for patients

with Diamond-Blackfan syndrome resistant or refractory to conventional treatment. Am J Pediatr Hematol Oncol 1988;10:217-23.

[92] Alessandri AJ, Rogers PC, Wadsworth LD, Davis JH.

Diamondblackfan anemia and cyclosporine therapy revisited. J Pediatr Hematol Oncol 2000;22:176-9.

[93] Akiyama M, Yanagisawa T, Yuza Y, Yokoi K, Ariga M, Fujisawa K, et al. Successful treatment of Diamond-Blackfan anemia with

metoclopramide. Am J Hematol 2005;78:295-8.

[94] MarmontAM,Cerri R, Lercari G,Van LintMT, BacigalupoA, RissoM. Positive direct antiglobulin tests and heteroimmune hemolysis

in patients with severe aplastic anemia and pure red cell anemia treated with antilymphocytic globulin. Acta Haematol 1985;74:14-8.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 95 ~

[95] Siegler J, Bognar I, Kelemen K. Recovery in a case of isolated

chronic erythrocytic aplasia during treatment with 6-mercaptopurine. Kinderarztl Prax 1970;38:145-9.

[96] Abkowitz JL, Schaison G, Boulad F, Brown DL, Buchanan GR, Johnson CA, et al. Response of Diamond-Blackfan anemia to

metoclopramide: evidence for a role for prolactin in erythropoiesis. Blood 2002;100:2687-91.

[97] Ball SE, Tchernia G,Wranne L, Bastion Y, Bekassy NA, Bordigoni P, et al. Is there a role for interleukin-3 in Diamond-Blackfan anaemia?

Results of a European multicentre study. Br J Haematol 1995;91:313-8.

[98] Jabr FI, Aoun E, Azar C, Taher A. Diamond-Blackfan anemia

responding to valproic acid. Blood 2004;104:3415.

[99] KlinowskaW, Morawska Z, Jagodzinska M. Present-day views on

the mechanism of androgen activity in the treatment of congenital hypoplastic anemia of the Blackfan-Diamond type. Pediatr Pol 1976; 51:575-8.

[100] KlinowskaW, Morawska Z, Jagodzinska M. Present-day views on

the mechanism of androgen activity in the treatment of congenital hypoplastic anemia of the Blackfan-Diamond type. Pediatr Pol 1976; 51:575-8.

[101] Alter BP. Bone marrow transplant in Diamond-Blackfan anemia. Bone

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 96 ~

[102] Kurtzman G, Frickhofen N, Kimball J, Jenkins DW, Nienhuis AW, Young NS. Pure red-cell aplasia of 10 years’ duration due to persistent

parvovirus B19 infection and its cure with immunoglobulin therapy. N Engl J Med 1989;321:519-23.

[103] Koduri PR, Kumapley R, Valladares J, Teter C. Chronic pure red

cell aplasia caused by parvovirus B19 in AIDS: use of intravenous immunoglobulin--a report of eight patients. Am J Hematol 1999;61: 16-20.

[104] Ramos-Casals M, Garcia-Carrasco M, Lopez-Medrano F, Trejo O, Forns X, Lopez-Guillermo A, et al. Severe autoimmune cytopenias in

treatment-naive hepatitis C virus infection: clinical description of 35 cases. Medicine 2003;82:87-96.

[105] Ide T, Sata M, Nouno R,Yamashita F, Nakano H, Tanikawa K.

Clinical evaluation of four cases of acute viral hepatitis complicated by pure red cell aplasia. Am J Gastroenterol 1994;89:257-62.

[106] Finkel HE, Kimber RJ, Dameshek W. Corticosteroid-responsive

acquired pure red cell aplasia in adults. Am J Med 1967;43:771-6.

[107] Mamiya S, Itoh T, Miura AB. Acquired pure red cell aplasia in Japan.

Eur J Haematol 1997;59:199-205.

[108] Sato N,Takatani O, HosoiT, Shirafuji N, UrabeA,Takaku F.Treatment of pure red cell aplasia that is resistant to conventional

immunosuppressive therapy with intermittent administration of methotrexate. Acta Haematol 1989;82:98-101.

Les érythroblastopénies : A propos de 03 cas et revue de littérature

~ 97 ~

[109] Chikkappa G, Pasquale D, Phillips PG, Mangan KF, Tsan MF.

Cyclosporin-Afor the treatment of pure red cell aplasia in a patient with chronic lymphocytic leukemia. Am J Hematol 1987;26:179-89.

[110] Duarte-Salazar C, Cazarin-Barrientos J, Goycochea-Robles MV, Collazo-Jaloma J, Burgos-Vargas R. Successful treatment of pure red

cell aplasia associated with systemic lupus erythematosus with cyclosporin A. Rheumatol 2000;39:1155-7.

[111] Chng WJ, Tan LK, Liu TC. Cyclosporine treatment for patients with

CRFwho developed pure red blood cell aplasia followingEPOtherapy.

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