Hematological Disorders

  • Philip A. Bromberg
  • M. Patricia Rivera


The process whereby deoxygenated hemoglobin (Hb) molecules containing at least one βS chain (β6 glu→val) (α2 Aβ2 S or α2 AβSβX) form large polymers within red cells, thus causing their rigid deformation into various characteristic shapes (‘sickled’ cells), has been studied for the past half century or more and is now relatively well understood structurally and kinetically [1–7]. Understanding how this molecular defect translates into the wide spectrum of clinical manifestations that characterize the fluctuating course of sickle cell disease has challenged physicians and scientists for many years and, despite many important advances, still offers diagnostic puzzles and therapeutic dilemmas. It is clear that intravascular red cell sickling lies at the core of all the clinical features - i.e., both the chronic hemolytic anemia and the vasoocclusive manifestations. However, with improved understanding of the biology of blood vessels and especially the interactions of endothelium with the formed as well as soluble blood elements, the process of vasoocclusion in sickle cell disease now is seen to be much more complex in its pathogenesis.


Sickle Cell Hairy Cell Leukemia Invasive Pulmonary Aspergillosis Primary Pulmonary Hypertension Sickle Cell Disease Patient 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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© Springer-Verlag London Limited 1999

Authors and Affiliations

  • Philip A. Bromberg
  • M. Patricia Rivera

There are no affiliations available

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