Original Articles
Vol. 10 (2018): Review Articles, Original Articles, Scientific Letters, Case Reports
THE SPECTRUM OF HYPEREOSINOPHILIA AND ASSOCIATED CLONAL DISORDERS – A REAL WORLD DATA FROM A TROPICAL SETTING.
Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
Received: April 2, 2018
Accepted: July 20, 2018
Accepted: July 20, 2018
2232
Views
898
Downloads
487
HTML
Hematology,
Infectious diseases
Authors
Objective: To determine the frequency, etiological spectrum and treatment outcome of hypereosinophilia (HE) and hypereosinophilic syndrome (HES) in a tropical setting.
Methods: A retrospective analysis of hospital data of five years and a comprehensive prospective evaluation of patients presenting with HE/HES over a period of 33 months was performed.
Results: HE/HES was diagnosed in total of 125 patients during study period with an estimated prevalence of 0.5-1 case per one lakh population in our hospital settings. Infections, especially helminthes were the commonest cause (34%) followed by primary/clonal HE/HES (24%) and reactive HE/HES secondary to various clonal disorders (14.3%). Lymphocytic variant of HES and FIP1L1-PDGFRA positive HES were diagnosed in 3.6% each. Imatinib responsive BCR-ABL1 negative HE/HES constitute 7.1% in our patients.
Conclusions: None of the clinical or routine laboratory features including the age of patients, duration of HE, presence or absence of organomegaly, hemoglobin levels, eosinophil %, absolute eosinophil count, total leukocyte count, platelet counts, serum IgE levels or presence of myelofibrosis can be used to predict or exclude malignancy in patients with HE/HES. The absence of blasts in peripheral blood or the absence of >5% blasts in bone marrow does not exclude primary/clonal HES. Clonal disorders (Primary HES and reactive HES secondary to clonal disorders; 38%) are diagnosed with nearly equal frequency compared to infections (34%) in tropical settings necessitating a thorough follow-up and comprehensive work-up in these patients.
Downloads
Download data is not yet available.
Citations
Chusid MJ, Dale DC, West BC, Wolff SM. The hypereosinophilic syndrome: analysis of fourteen cases with review of the literature. Medicine (Baltimore) 1977;54:1–27.
Hardy WR, Anderson RE. The hypereosinophilic syndromes. Ann Intern Med 968;68:1220–9.
Swerdlow SH CE, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, Seibert R (editors). WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues. IARC: Lyon; 2017
Valent P, Klion AD, Horny HP, Roufosse F, Gotlib J, Weller PF, Hellmann A, Metzgeroth G, Leiferman KM, Arock M, Butterfield JH, Sperr WR, Sotlar K, Vandenberghe P, Haferlach T, Simon HU, Reiter A, Gleich GJ. Contemporary consensus proposal on criteria and classification of eosinophilic disorders and related syndromes. J Allergy Clin Immunol. 2012;130:607–612.e9.
Bhatia P, Binota J, Varma N, Bansal D, Trehan A, Marwaha RK, Malhotra P, Varma S. Incidence of common chimeric fusion transcripts in B-cell acute lymphoblastic leukemia: an Indian perspective. Acta Haematol 2012;28:17–9.
Bhatia P, Binota J, Varma N, Marwaha R, Malhotra P, Varma S. Incidence of Common Fusion Transcripts in Adult and Pediatric Acute Myeloid Leukemia (AML) Cases: Experience of a Tertiary Care Research institute. Mediterr J Hematol Infect Dis. 2012;4:e2012042.
Bhatia P, Binota J, Varma N, Bansal D, Trehan A, Marwaha RK, Malhotra P, Varma S. A Study on the Expression of BCR-ABL Transcript in Mixed Phenotype Acute Leukemia (MPAL) Cases Using the Reverse Transcriptase Polymerase Reaction Assay (RT-PCR) and its Correlation with Hematological Remission Status Post Initial Induction Therapy. Mediterr J Hematol Infect Dis. 2012;4:e2012024.
Kui JS, Espinal-Witter R, Wang YL. Laboratory detection of JAK2V617F in human myeloproliferative neoplasms. Methods Mol Biol. 2013;999:41–57.
Knoll JM, Lichter P. In situ hybridization to metaphase chromosomes and interphase nuclei. In: Haines JL, editor. Current Protocols in Human Genetics. John Wiley & Sons, Inc, Hoboken, NJ, 2005;p. 4.3.1-4.3.31.
Crane MM, Chang CM, Kobayashi MG, Weller PF. Incidence of myeloproliferative hypereosinophilic syndrome in the United States and an estimate of all hypereosinophilic syndrome incidence. J Allergy Clin Immunol. 2010;126:179–81.
Song G, Liu H, Sun F, Gu L, Wang S. Acute lymphocytic leukemia with eosinophilia: a case report and review of the literature. Aging Clin Exp Res. 2012;24:555–8.
Kaneko H, Shimura K, Yoshida M, Ohkawara Y, Ohshiro M, Tsutsumi Y, Iwai T, Horiike S, Yokota S, Taniwaki M. Acute lymphoblastic leukemia with eosinophilia lacking peripheral blood leukemic cell: a rare entity. Indian J Hematol Blood Transfus. 2014;30:80–3.
Chien AJ, Argenyi ZB, Colven RM, Kirby P. Acute lymphoblastic leukemia presenting with urticarial plaques and hypereosinophilia in a child. J Am Acad Dermatol. 2004;51:S151-155.
Cogan E, Schandené L, Crusiaux A, Cochaux P, Velu T, Goldman M. Brief report: clonal proliferation of type 2 helper T cells in a man with the hypereosinophilic syndrome. N Engl J Med. 1994;330:535–8.
Ogbogu PU, Bochner BS, Butterfield JH, Gleich GJ, Huss-Marp J, Kahn JE, Leiferman KM, Nutman TB, Pfab F, Ring J, Rothenberg ME, Roufosse F, Sajous MH, Sheikh J, Simon D, Simon HU, Stein ML, Wardlaw A, Weller PF, Klion AD. Hypereosinophilic syndrome: a multicenter, retrospective analysis of clinical characteristics and response to therapy. J Allergy Clin Immunol. 2009;124:1319–1325.e3.
Roufosse F. Hypereosinophilic syndrome variants: diagnostic and therapeutic considerations. Haematologica. 2009;94:1188–93.
Helbig G, Wieczorkiewicz A, Dziaczkowska-Suszek J, Majewski M, Kyrcz-Krzemien S. T-cell abnormalities are present at high frequencies in patients with hypereosinophilic syndrome. Haematologica. 2009;94:1236–41.
Roden AC, Morice WG, Hanson CA. Immunophenotypic attributes of benign peripheral blood gammadelta T cells and conditions associated with their increase. Arch Pathol Lab Med. 2008;132:1774–80.
Morice WG. The immunophenotypic attributes of NK cells and NK-cell lineage lymphoproliferative disorders. Am J Clin Pathol. 2007;127:881–6.
Posnett DN, Sinha R, Kabak S, Russo C. Clonal populations of T cells in normal elderly humans: the T cell equivalent to “benign monoclonal gammapathy.” J Exp Med. 1994;79:609–18.
Reinhold U, Abken H. CD4+ CD7- T cells: a separate subpopulation of memory T cells? J Clin Immunol. 1997;17:265–71.
Valent P, Horny H-P, Bochner BS, Haferlach T, Reiter A. Controversies and open questions in the definitions and classification of the hypereosinophilic syndromes and eosinophilic leukemias. Semin Hematol. 2012;49:171–81.
Pardanani A, Brockman SR, Paternoster SF, Flynn HC, Ketterling RP, Lasho TL, Ho CL, Li CY, Dewald GW, Tefferi A. FIP1L1-PDGFRA fusion: prevalence and clinicopathologic correlates in 89 consecutive patients with moderate to severe eosinophilia. Blood. 2004;104:3038–45.
Schwaab J, Umbach R, Metzgeroth G, Naumann N, Jawhar M, Sotlar K, Horny HP, Gaiser T, Hofmann WK, Schnittger S, Cross NC, Fabarius A, Reiter A. KIT D816V and JAK2 V617F mutations are seen recurrently in hypereosinophilia of unknown significance. Am J Hematol. 2015;90:774–7.
Roche-Lestienne C, Lepers S, Soenen-Cornu V, Kahn JE, Laï JL, Hachulla E, Drupt F, Demarty AL, Roumier AS, Gardembas M, Dib M, Philippe N, Cambier N, Barete S, Libersa C, Bletry O, Hatron PY, Quesnel B, Rose C, Maloum K, Blanchet O, Fenaux P, Prin L, Preudhomme C. Molecular characterization of the idiopathic hypereosinophilic syndrome (HES) in 35 French patients with normal conventional cytogenetics. Leukemia. 2005;19:792–8.
S Schwaab J, Jawhar M, Naumann N, Schmitt-Graeff A, Fabarius A, Horny HP, Cross NC, Hofmann WK, Reiter A, Metzgeroth G. Diagnostic challenges in the work up of hypereosinophilia: pitfalls in bone marrow core biopsy interpretation. Ann Hematol. 2016;95:557–62.
Klion AD. How I treat hypereosinophilic syndromes. Blood. 2015;126:1069–77.
Ethics Approval
Original articlesSupporting Agencies
NilHow to Cite
“THE SPECTRUM OF HYPEREOSINOPHILIA AND ASSOCIATED CLONAL DISORDERS – A REAL WORLD DATA FROM A TROPICAL SETTING”. (2018) Mediterranean Journal of Hematology and Infectious Diseases, 10(1), p. e2018052. doi:10.4084/mjhid.2018.052.
