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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 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
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