Heinz body hemolytic animea. "Bite cells" -a clue to diagnosis

1976 ◽  
Vol 136 (2) ◽  
pp. 153-155 ◽  
Author(s):  
M. S. Greenberg
Keyword(s):  
1976 ◽  
Vol 136 (9) ◽  
pp. 1067a-1067
Author(s):  
E. P. Gabor
Keyword(s):  

PEDIATRICS ◽  
1957 ◽  
Vol 19 (6) ◽  
pp. 1001-1001

The association of Heinz-bodies within erythrocytes, extreme distortion of the size and shape of erythrocytes and hemolytic anemia in newborn infants, especially premature infants, has been sporadically reported in the medical literature since 1948. Heinz-bodies are thought to be either remnants of disintegrated membranes of erythocytes or abnormal products of hemoglobin metablism, and are demonstrable only by supravital staining techniques. The present study contributes two case reports and discusses the sequence of the clinical and hematologic manifestations. The first patient was a full-term infant who developed jaundice and symptoms attributable to anemia at 2 weeks of life. The second infant was prematurely born, did not develop jaundice but showed large numbers of Heinz-bodies (70%) as the anemia progressed. Both patients responded well to a single transfusion of packed blood cells, with complete reversal of the abnormal peripheral blood findings. None of the usual causes of hemolysis could be demonstrated by extensive laboratory tests. Agents such as phenylhydrazine, known to produce Heinz-bodies, could not be incriminated. The phenomenon of Heinz-body formation in infants may be more common than is apparent as the technique of demonstration is not commonly a part of the routine study of infants with evidence of hemolytic anemia. This technique is described and illustrations of erythrocytes containing Heinz-bodies are provided.


1964 ◽  
Vol 10 (3) ◽  
pp. 281-290 ◽  
Author(s):  
A. J. Grimes ◽  
A. Meisler ◽  
J. V. Dacie
Keyword(s):  

BMJ ◽  
1959 ◽  
Vol 1 (5127) ◽  
pp. 970-971
Author(s):  
M. Skogh
Keyword(s):  

1964 ◽  
Vol 10 (3) ◽  
pp. 388-402 ◽  
Author(s):  
J. V. Dacie ◽  
A. J. Grimes ◽  
A. Meisler ◽  
L. Steingold ◽  
E. H. Hemsted ◽  
...  
Keyword(s):  

1971 ◽  
Vol 19 (11) ◽  
pp. 259-263 ◽  
Author(s):  
D. Martinovich ◽  
D.A. Woodhouse

1983 ◽  
Vol 15 (2) ◽  
pp. 135-146 ◽  
Author(s):  
Patrick C. J. Ward ◽  
Burton S. Schwartz ◽  
James G. White

2020 ◽  
Vol 49 (2) ◽  
pp. 232-239
Author(s):  
Courtney E. Johnson ◽  
Davis M. Seelig ◽  
Frances M. Moore ◽  
Tammy J. Ruska ◽  
Daniel A. Heinrich
Keyword(s):  

Blood ◽  
1989 ◽  
Vol 73 (1) ◽  
pp. 312-317 ◽  
Author(s):  
Y Maede ◽  
M Kuwabara ◽  
A Sasaki ◽  
M Inaba ◽  
W Hiraoka

Abstract It has been shown that certain dogs have erythrocytes characterized by an inherited high concentration of reduced glutathione (GSH), five to seven times the normal level (high-GSH RBCs). We examined whether increased GSH in dog erythrocytes leads to increased protection against oxidative damage induced by acetylphenylhydrazine (APH) and/or 4- aminophenyl disulfide (4-AD). When erythrocytes were incubated with 30 mmol/L APH, the Heinz body count was appreciably higher in normal RBCs than in high-GSH RBCs, while there was no difference in the increase of the methemoglobin (metHb) concentration in both RBCs. In contrast, both the Heinz body count and metHb production were much higher in high-GSH RBCs than in normal RBCs when erythrocytes were incubated with 4-AD. Furthermore, the generation of the superoxide in erythrocytes treated with 4-AD, which was measured by spin trapping combined with electron spin resonance (ESR), was obviously higher in high-GSH RBCs than in normal RBCs. These results clearly indicate that erythrocyte GSH is an important defense against oxidative damage induced by certain compounds such as APH, but that, in contrast, elevated GSH appears to accelerate oxidative damage to erythrocytes produced by aromatic disulfides, such as 4-AD, which generated a superoxide in erythrocytes via its redox reaction with GSH.


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