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Parvovirus B19 for the hematologist

Parvovirus B19 for the hematologist Division of Hematology and Oncology, Department of Medicine, Case Western Reserve University School of Medicine and MetroHealth Medical Center, Cleveland, Ohio INTRODUCTION In 1948, the conventional wisdom and teachings concerning the pathophysiology of so-called hemolytic crises (or hyperhemolytic crises) was most abruptly and effectively turned upside down by the young Norwegian hematologist Paul A. Owren. On the basis of observations begun in 1942 that have withstood the test of time, Owren concluded that the “crises are not due to increased hemolysis, but to a sudden cessation in formation of the new red cells because of acute aplastic crisis in the blood forming tissue of the bone marrow” [l]. Sequential hematologic, biochemical, and morphologic assessments of six patients with hereditary spherocytosis firmly established the aplastic nature of the events, but Owren very perceptively went further to suggest that “they can be produced by some extraneous reason, possibly infective.” Parvovirus B19 is now known to be the causative agent responsible for the great majority of aplastic crises encountered in diverse chronic hemolytic anemias, compensated hemolytic processes, and some additional unusual immunologic or hematopoietically unstable situations. This review places major emphasis on the frequent and infrequent hematologic changes that take place http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Hematology Wiley

Parvovirus B19 for the hematologist

Harris, John W.
American Journal of Hematology , Volume 39 (2) – Feb 1, 1992
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References (218)

Publisher
Wiley
Copyright
Copyright © 1992 Wiley‐Liss, Inc., A Wiley Company
ISSN
0361-8609
eISSN
1096-8652
DOI
10.1002/ajh.2830390209
Publisher site
See Article on Publisher Site

Abstract

Division of Hematology and Oncology, Department of Medicine, Case Western Reserve University School of Medicine and MetroHealth Medical Center, Cleveland, Ohio INTRODUCTION In 1948, the conventional wisdom and teachings concerning the pathophysiology of so-called hemolytic crises (or hyperhemolytic crises) was most abruptly and effectively turned upside down by the young Norwegian hematologist Paul A. Owren. On the basis of observations begun in 1942 that have withstood the test of time, Owren concluded that the “crises are not due to increased hemolysis, but to a sudden cessation in formation of the new red cells because of acute aplastic crisis in the blood forming tissue of the bone marrow” [l]. Sequential hematologic, biochemical, and morphologic assessments of six patients with hereditary spherocytosis firmly established the aplastic nature of the events, but Owren very perceptively went further to suggest that “they can be produced by some extraneous reason, possibly infective.” Parvovirus B19 is now known to be the causative agent responsible for the great majority of aplastic crises encountered in diverse chronic hemolytic anemias, compensated hemolytic processes, and some additional unusual immunologic or hematopoietically unstable situations. This review places major emphasis on the frequent and infrequent hematologic changes that take place

Journal

American Journal of Hematology – Wiley

Published: Feb 1, 1992

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