Abstract

THE abnormality of granulocytic leukocytes manifested by poor segmentation and condensation of nuclear chromatin was first described by Pelger1 in 1928. Huët2 confirmed these observations and established the genetic characteristics of this disorder in 1931. Since then this benign hereditary trait has been known as the Pelger–Huët anomaly. In 1950 Nachtsheim3 , 4 discovered the heterozygous form in rabbits and, by controlled breeding, produced the homozygous type, which proved lethal. In the same year he demonstrated that the administration of colchicine to rabbits with the heterozygous trait caused the homozygous form of the anomaly.5 Recently, Darte et al.5 and Undritz6 pointed out . . .

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