scholarly journals The Course of Experimentally Induced Hemolytic Anemia in a Primaquine-Sensitive Caucasian

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.


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.


Transfusion ◽  
2004 ◽  
Vol 44 (7) ◽  
pp. 1033-1040 ◽  
Author(s):  
Beatrice Großjohann ◽  
Petra Eichler ◽  
Andreas Greinacher ◽  
Sentot Santoso ◽  
Hartmut Kroll

2021 ◽  
Vol 49 ◽  
Author(s):  
Alana Trayjen Martins ◽  
Gabriela Reis Ledur ◽  
Luciana Branquinho Queiroga ◽  
Carlos Afonso De Castro Beck ◽  
Anderson Luiz Carvalho ◽  
...  

Background: Immune-mediated hemolytic anemia (IMHA) is characterized by an autoimmune response with production of auto-antibodies and destruction of erythrocytes resulting in anemia. Primary IMHA is referred to a condition when the cause is unknown (idiopathic), whereas secondary IMHA involves changes in red blood cells caused by the action of drugs, neoplasms, or infectious diseases. The diagnosis can be made through changes in the blood count, usually of a regenerative character, Coombs test, and autoagglutination test. The present study aimed to report a case of drug-induced hemolytic anemia, with emphasis on the clinical signs, diagnostic methods, and treatment, in a female dog.Case: A 9-year-old mixed-breed bitch weighing 29.6 kg was referred to the Veterinary Medical Teaching Hospital (HCV-UFRGS) with a previous diagnosis of gallbladder mucocele that was unresponsive to clinical treatment. After laboratory tests, cholecystectomy was performed, and the procedure required conversion from laparoscopic to open cholecystectomy. Therapy included administration of amoxicillin, dipyrone, tramadol hydrochloride, and meloxicam. Three days after surgery, the dog presented with apathy, lethargy, hyporexia, and a pale and subicteric mucosa. The patient developed hypochromic macrocytic anemia with reticulocytosis, spherocytosis, anisocytosis, and leukocytosis with neutrophilia. The result of the autoagglutination test was positive, confirming the diagnosis. All medications were suspended, and immunosuppressive treatment with dexamethasone was included, with a subsequent switch to prednisolone. After 10 days of treatment, the patient experienced significant improvement, and therapy was discontinued.Discussion: Based on the patient's history, the cause of the IMHA was secondary to drug administration, and it is not possible to distinguish if it was due to one or a combination of drugs, as they were all started and stopped simultaneously. The patient had hypothyroidism, which may have contributed to the production of antibodies against TSH receptors, blocking the hormone's action, thereby causing tissue damage due to T cell-mediated cytotoxicity and the effect of cytokines. The pale and subicteric mucosa, apathy, weakness, lethargy, exercise intolerance, and dyspnea resulted from extravascular hemolysis and bilirubin released from erythrocyte rupture with a subsequent decrease in the number of red blood cells, leading to oxygen transport deficiency. The diagnosis is based on the blood count and results of autoagglutination supported by the response to immunosuppressive therapy. Anemia results in increased production and release of precursor cells from the bone marrow, accompanied by reticulocytosis and increased mean corpuscular volume (MCV) and mean corpuscular hemoglobin concentration (MCHC). The treatment of IMHA consists of supportive care and immunosuppressive therapy with corticosteroids to ensure suppression of the immune system, preventing response against erythrocytes. Initially, tramadol hydrochloride, dipyrone, and amoxicillin with potassium clavulanate were suspended to interrupt the cause of IMHA, and administration of dexamethasone in an immunosuppressive dose was started. Therefore, it is important to include drug-induced IMHA in the differential diagnosis of patients who present with anemia after using medications. Early diagnosis, initiation of therapy, and adequate care were important factors for the recovery of the animal.Título: Anemia hemolítica imunomediada medicamentosa em uma cadelaKeywords: dog, hypochromic macrocytic anemia, erythrocyte, hemoglobin, spherocyte.Descritores: cão, anemia macrocítica hipocrômica, eritrócito, hemoglobina, esferócito. 


Blood ◽  
2012 ◽  
Vol 120 (20) ◽  
pp. 4123-4133 ◽  
Author(s):  
Allan Pamba ◽  
Naomi D. Richardson ◽  
Nick Carter ◽  
Stephan Duparc ◽  
Zul Premji ◽  
...  

AbstractDrug-induced acute hemolytic anemia led to the discovery of G6PD deficiency. However, most clinical data are from isolated case reports. In 2 clinical trials of antimalarial preparations containing dapsone (4,4′-diaminodiphenylsulfone; 2.5 mg/kg once daily for 3 days), 95 G6PD-deficient hemizygous boys, 24 G6PD-deficient homozygous girls, and 200 girls heterozygous for G6PD deficiency received this agent. In the first 2 groups, there was a maximum decrease in hemoglobin averaging −2.64 g/dL (range −6.70 to +0.30 g/dL), which was significantly greater than for the comparator group receiving artemether-lumefantrine (adjusted difference −1.46 g/dL; 95% confidence interval −1.76, −1.15). Hemoglobin concentrations were decreased by ≥ 40% versus pretreatment in 24/119 (20.2%) of the G6PD-deficient children; 13/119 (10.9%) required blood transfusion. In the heterozygous girls, the mean maximum decrease in hemoglobin was −1.83 g/dL (range +0.90 to −5.20 g/dL); 1 in 200 (0.5%) required blood transfusion. All children eventually recovered. All the G6PD-deficient children had the G6PD A− variant, ie, mutations V68M and N126D. Drug-induced acute hemolytic anemia in G6PD A− subjects can be life-threatening, depending on the nature and dosage of the drug trigger. Therefore, contrary to current perception, in clinical terms the A− type of G6PD deficiency cannot be regarded as mild. This study is registered at http://www.clinicaltrials.gov as NCT00344006 and NCT00371735.


Blood ◽  
1953 ◽  
Vol 8 (9) ◽  
pp. 857-857
Author(s):  
Matthew C. Dodd ◽  
Claude-Starr Wright ◽  
J. Albert Baxter ◽  
Bertha A. Bouroncle ◽  
Alvinza E. Bunner ◽  
...  

Abstract The Addendum which appeared on page 647 of an article entitled "The Immunologic Specificity of Antiserum for Trypsin-Treated Red Blood Cells and Its Reactions with Normal and Hemolytic Anemia Cells" by Matthew C. Dodd, Claude-Starr Wright, J. Albert Baxter, Bertha A. Bouroncle, Alvinza E. Bunner, and Henry J. Winn (Blood 8: 640-647, 1953) belongs, instead, with the article entitled "Production of Nucleophagocytosis by Rabbit Antileukocytic Serum" by Hyman J. Zimmerman, John R. Walsh, and Paul Heller (Blood 8: 651-654, 1953).


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