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Prepublished online as a Blood First Edition Paper on March 6, 2003; DOI 10.1182/blood-2003-01-0128.
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Blood, 15 July 2003, Vol. 102, No. 2, pp. 514-516
HEMATOPOIESIS
Brief report
Severe telomere shortening in patients with paroxysmal nocturnal hemoglobinuria affects both GPI– and GPI+ hematopoiesis
Anastasios Karadimitris,
David J. Araten,
Lucio Luzzatto, and
Rosario Notaro
From the Memorial Sloan-Kettering Cancer Center, Department of Human Genetics and Department of Medicine, New York, NY; Imperial College School of Medicine, Hammersmith Hospital, Department of Hematology, London, United Kingdom; and Laboratory of Human Genetics, IST, Istituto Nazionale per la Ricerca sul Cancro, Laboratorio di Genetica Umana, Dipartimento di Eziologia ed Epidemiologia, Genova, Italy.
A most distinctive feature of paroxysmal nocturnal hemoglobinuria (PNH) is that in each patient glycosylphosphatidylinositol-negative (GPI–) and GPI+ hematopoietic stem cells (HSCs) coexist, and both contribute to hematopoiesis. Telomere size correlates inversely with the cell division history of HSCs. In 10 patients with hemolytic PNH the telomeres in sorted GPI– granulocytes were shorter than in sorted GPI+ granulocytes in 4 cases, comparable in 2 cases, and longer in the remaining 4 cases. Furthermore, the telomeres of both GPI– and GPI+ hematopoietic cells were markedly shortened compared with age-matched controls. The short telomeres in the GPI– cells probably reflect the large number of cell divisions required for the progeny of a single cell to contribute a large proportion of hematopoiesis. The short telomeres of the GPI+ cells indicate that the residual hematopoiesis contributed by these cells is not normal. This epigenetic change is an additional feature shared by PNH and aplastic anemia.
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