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.
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
