Treatment of Sickle Crisis

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Abstract
For over 20 years, the pathogenesis of sickling and of its clinical manifestations has intrigued hematologists and molecular biologists. A series of observations has unraveled some of the mystery of the sickling phenomenon. The substitution of valine for glutamic acid in the beta chain of S hemoglobin alters the structure of the molecule in such a way that, in the reduced state, the molecules stack up in parallel or helical arrangement to form the semicrystalline structure, or tactoid, first described by Harris.1 , 2 According to Murayama, this stacking takes place because the substituted valine alters the tertiary structure by forming a . . .