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Journal of Cancer Research and Therapeutics
Medknow Publications on behalf of the Association of Radiation Oncologists of India (AROI)
ISSN: 0973-1482 EISSN: 1998-4138
Vol. 4, Num. 1, 2008, pp. 50-50

Journal of Cancer Research and Therapeutics, Vol. 4, No. 1, January-March, 2008, pp. 50

Letter To Editor

Dysplastic hematopoiesis and underlying dysthyroidism

Akoum Riad, Saade Michel, Tabbara Wafic, Brihi Emile, Masri Marwan, Habib Khaled, Abadjian Gerard

Department of Oncology and Radiotherapy, Rizk Hospital, Beirut
Correspondence Address: PO Box 11-3288, Rizk Hospital, Beirut
rakoum@yahoo.com

Code Number: cr08014

Dear sir,

Thank you for your interest in our case report.

Primary myelodysplastic syndrome (MDS) is a clonal and irreversible disorder of the pluripotent hematopoietic stem cells. Cancer therapy-related MDS is a clonal secondary MDS caused by cumulative DNA damage in stem cells. [1],[2] However, clonality is not always detected and non-clonal, secondary forms may be reversible with the treatment of the underlying diseases. In patients presenting with pancytopenia and impaired hematopoiesis, the diagnostic standards of MDS are mainly morphologic . [3] In the absence of molecular or cytogenetic tests, the diagnosis of MDS requires exclusion of metabolic, autoimmune, toxic, and therapeutic causes. Anemia and pancytopenia are part of the hematological picture of both hypothyroidism and hyperthyroidism. [4],[5],[6] We described a case of MDS that resolved after treatment of hyperthyroidism. [7] The clarifications you brought are in agreement with what we postulated. Ineffective and arrested hematopoiesis may probably be due to a direct toxic effect of thyroid hormones. The results of your study on an unselected series of 138 MDS patients confirmed that an adequate treatment of hypothyroidsm revealed a progressive increase in marrow cellularity, more pronounced dysplastic abnormalities involving the three hematopoietic lineages, and a reticulin formation not previously described. You explained that the thyroid insufficiency and the consequent arrest in hematopoiesis hindered or prevented dysplastic features from manifesting. The thyroid hormone therapy corrected the hypoproliferation status and, made the dysplastic abnormalities more conspicuous and the MDS diagnosis more evident. The frequency of pancytopenia [4] and arrested hematopoiesis [4],[7] may be underestimated in hyperthyroidism and clinicians should be alert to these serious, readily manageable effects.

References

1.Yoshida Y. Physician education: Myelodysplastic syndrome. Oncologist 1996;1:284-7.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Boultwood J, Wainscoat JS. Clonality in the myelodysplastic syndromes. Int J Hematol 2001;73:411-5.  Back to cited text no. 2  [PUBMED]  
3.Schmitt-Graeff A, Mattern D, Kohler H, Hezel J, Lubbert M. Myelodysplastic syndromes (MDS): Aspects of hematopathologic diagnosis. Pathologe 2000;21: 1-15.  Back to cited text no. 3    
4.Duquenne M, Lakomsky D, Humbert JC, Hadjadj S, Weryha G, Leclere J. Pancytopenia resolved by the treatment of hyperthyroidm. Presse Med 1995;24:807-10.  Back to cited text no. 4    
5.Malgor LA, Blanc CC, Klainer E, Irizar SE, Toroles PR, Borrios l. Direct effects of thyroid hormones on bone marrow erythroid cells of rat. Blood 1975;45:671-8.  Back to cited text no. 5    
6.Dinnen RD, White SR, Elsayed S, Yeh YI, Ebisuzaki K. An endogenous signal triggering erythroid differentiation: Identification as thyroid hormone. Cell Growth Differ 1994;5:855-61.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Akoum R, Michel S, Wafic T, Emile B, Marwan M, Khaled H, et al . Myelodysplastic syndrome and pancytopenia responding to treatment of hyperthyroidism: Peripheral blood and bone marrow analysis before and after anti hormonal treatment. J Cancer Res Ther 2007;3:43-6.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]

Copyright 2008 - Journal of Cancer Research and Therapeutics

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