scholarly journals Sulfhemoglobinemia and Acute Hemolytic Anemia with Heinz Bodies Following Contact with a Fungicide— Zinc Ethylene Bisdithiocarbamate—in a Subject with Glucose-6-Phosphate Dehydrogenase Deficiency and Hypocatalasemia

Blood ◽  
1963 ◽  
Vol 21 (4) ◽  
pp. 484-494 ◽  
Author(s):  
JACK PINKHAS ◽  
MEIR DJALDETTI ◽  
HENRY JOSHUA ◽  
CHAIM RESNICK ◽  
ANDRÉ DE VRIES

Abstract Sulfhemoglobinemia associated with Heinz body formation and acute hemolytic anemia following contact with a fungicide, zinc ethylene bisdithiocarbamate, is described in a Persian Jew whose red blood cells had low glucose-6-phosphate dehydrogenase activity with low and unstable reduced glutathione and low catalase activity. The fungicide, similarly to acetylphenylhydrazine, was capable of decreasing in vitro the reduced glutathione of the patient’s red blood cells, as well as of those of other subjects with the same enzymatic defect. The sulfhemoglobinemia and the hemolytic anemia are considered to have been produced independently by the fungicide, the glucose-6-phosphate dehydrogenase deficiency having played a role only in the latter. The possibility that the hypocatalasemia was a factor in rendering the patient’s red blood cells sensitive to the hemolysis- and sulfhemoglobin-producing action of the fungicide is discussed. The importance of zinc ethylene bisdithiocarbamate as a sulfhemoglobin-producing and hemolytic agent is stressed, in view of the widespread use of this fungicide.

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.


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.


2016 ◽  
Vol 8 (38) ◽  
pp. 6856-6864 ◽  
Author(s):  
Ruipeng Mu ◽  
Chengpeng Chen ◽  
Yimeng Wang ◽  
Dana M. Spence

A combination of 3D printed tools and classic cellular analyses reveals the benefits of reducing the glucose content of currently approved solutions used to process and store red blood cells for transfusion medicine.


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