scholarly journals The Morphology of Glucose 6 Phosphate Dehydrogenase Deficient Erythrocytes: Electron-microscopic Studies

Blood ◽  
1961 ◽  
Vol 17 (2) ◽  
pp. 229-234 ◽  
Author(s):  
D. DANON ◽  
CH. SHEBA ◽  
B. RAMOT

Abstract The conclusion that may be drawn is that though under normal conditions the survival time of enzyme deficient red blood cells is not too far from normal, the ageing of these cells from a morphological point of view occurs at a much faster rate; in other words, one could speak of "progeria" of the enzyme deficient red blood cells.

Author(s):  
Kosuke Ueda ◽  
Hiroto Washida ◽  
Nakazo Watari

IntroductionHemoglobin crystals in the red blood cells were electronmicroscopically reported by Fawcett in the cat myocardium. In the human, Lessin revealed crystal-containing cells in the periphral blood of hemoglobin C disease patients. We found the hemoglobin crystals and its agglutination in the erythrocytes in the renal cortex of the human renal lithiasis, and these patients had no hematological abnormalities or other diseases out of the renal lithiasis. Hemoglobin crystals in the human erythrocytes were confirmed to be the first case in the kidney.Material and MethodsTen cases of the human renal biopsies were performed on the operations of the seven pyelolithotomies and three ureterolithotomies. The each specimens were primarily fixed in cacodylate buffered 3. 0% glutaraldehyde and post fixed in osmic acid, dehydrated in graded concentrations of ethanol, and then embedded in Epon 812. Ultrathin sections, cut on LKB microtome, were doubly stained with uranyl acetate and lead citrate.


Blood ◽  
1965 ◽  
Vol 25 (1) ◽  
pp. 92-95 ◽  
Author(s):  
IVO PANNACCIULLI ◽  
ALBERTO TIZIANELLO ◽  
FRANCO AJMAR ◽  
EMANUELE SALVIDIO

Abstract Two severe hemolytic crises, in a month’s period, were induced by primaquine in a glucose-6-phosphate dehydrogenase deficient Sardinian male. Young red blood cells tagged with Fe59 10 to 16 days earlier were destroyed in the second hemolytic episode. The implications of these experiments on the nature of drug-induced hemolysis in Caucasians are briefly discussed.


1989 ◽  
Vol 565 (1 Sickle Cell D) ◽  
pp. 409-412
Author(s):  
A. ANNE KAPERONIS ◽  
ROBERT G. KING ◽  
JEANNE A. SMITH ◽  
SHU CHIEN

2021 ◽  
pp. 49-56
Author(s):  
O. D. Ostroumova ◽  
S. A. Bliznyuk ◽  
A. I. Kochetkov ◽  
A. G. Komarova

One of the reasons for the development of hemolytic anemia (HA) can be drugs, including some antibacterial, non-steroidal anti-inflammatory, antitumor and antihypertensive drugs. It was found that the most common drug-induced hemolytic anemia (DIHA) develops against the background of taking antibacterial drugs. The true prevalence of DIHA is not known and is approximately one case per 1.0–1.2 million patients. The mechanisms of the occurrence of DIHA are divided into immune and metabolic (non-immune). The first mechanism is associated with the formation of haptens, the second option – with the formation of immune complexes, the third option is mediated by the formation of true autoantibodies to red blood cells, the fourth option of the immune mechanism of the occurrence of DIHA is non-immunological protein absorption on the membranes of red blood cells. The risk factors for the development of DIHA are not fully established. The most common hereditary risk factor for DIHA is glucose-6-phosphate dehydrogenase deficiency. The main method of diagnosing DIHA is a direct antiglobulin test (direct Coombs’ test). The temporal relationship between the use of the inducer drug and the development of HA symptoms is important. The treatment strategy of DIHA is determined by the severity of the disease. In all cases, treatment should be initiated with the identification and withdrawal of the drug that initiated the occurrence of HA. With the development of severe HA, hemodialysis may be required. Prevention of DIHA involves avoiding the use of drugs associated with a high risk of its development.


Biorheology ◽  
1995 ◽  
Vol 32 (2-3) ◽  
pp. 388-388
Author(s):  
C BUCHERER ◽  
C ZEITOUN ◽  
C LACOMBE ◽  
J LELIEVRE ◽  
M FONFREDE ◽  
...  

Author(s):  
Shaun R. McCann

Red blood cells, erythrocytes, are unique in that they do not contain a nucleus. This fact facilitates the study of their metabolism. Erythrocytes contain the protein pigment haemoglobin, which is in solution in the cells and consists of globin chains and iron. In this chapter, the development of the understanding of erythrocytes is linked to the blood conditions haemolytic anaemia and paroxysmal nocturnal haemoglobinuria. Premature destruction of erythrocytes, in the absence of blood loss, is termed haemolysis. If the bone marrow is unable to compensate adequately, then anaemia ensues and the condition is called haemolytic anaemia. The underlying defect is a deficiency in the activity of the enzyme glucose-6-phosphate dehydrogenase, termed G6PD deficiency.


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