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In drug-induced nonautoimmune hemolytic anemia, red blood cells (RBC) are destroyed from various non-immune mechanisms such as direct oxidative stress from certain drugs. [1] This is in contrast to drug-induced autoimmune hemolytic anemia where certain drugs result in the formation of antibodies against RBCs, resulting in hemolysis.
Hemolytic anemia accounts for 5% of all existing anemias. [2] It has numerous possible consequences, ranging from general symptoms to life-threatening systemic effects. [2] The general classification of hemolytic anemia is either intrinsic or extrinsic. [3] Treatment depends on the type and cause of the hemolytic anemia. [2]
Zieve's syndrome is an acute metabolic condition that can occur during withdrawal from prolonged heavy alcohol use. It is defined by hemolytic anemia (with spur cells and acanthocytes), hyperlipoproteinemia (excessive blood lipoprotein), jaundice (elevation of unconjugated bilirubin), and abdominal pain. [1]
The test was premature and was forgotten. In 1946, Boorman, Dodd, and Loutit applied the direct antiglobulin test to a variety of hemolytic anemias, and laid the foundation for the clear distinction of autoimmune from congenital hemolytic anemia. [citation needed] A hemolytic state exists whenever the red cell survival time is shortened from ...
Its overall phenotype resembles a combination of autoimmune hemolytic anemia and immune thrombocytopenic purpura. [1] [4] [5] Autoimmune hemolytic anemia is a condition in which the red blood cells that normally carry oxygen are destroyed by an autoimmune process. Immune thrombocytopenic purpura is a condition in which platelets are destroyed ...
An appropriate course of treatment for drug-induced autoimmune hemolytic anemia hasn't yet been established. Once DIIHA has been recognized, the patient must stop whatever drug caused the anemia in order to provide proper treatment. Patients should be given blood transfusions as needed.
The most common antibody isotype involved in warm antibody AIHA is IgG, though sometimes IgA is found. The IgG antibodies attach to a red blood cell, leaving their F C portion exposed with maximal reactivity at 37 °C (versus cold antibody induced hemolytic anemia whose antibodies only bind red blood cells at low body temperatures, typically 28–31 °C).
Treatment of the condition is specific to the cause of hemolysis, but intense phototherapy and exchange transfusion can be used to help the patient excrete accumulated bilirubin. [11] Complications related to hemolytic jaundice include hyperbilirubinemia and chronic bilirubin encephalopathy, which may be deadly without proper treatment. [12] [13]