Immune-mediated causes could include transient factors as in Mycoplasma pneumoniae infection (cold agglutinin disease) or permanent factors as in autoimmune diseases like autoimmune hemolytic anemia (itself more common in diseases such as systemic lupus erythematosus, rheumatoid arthritis, Hodgkins lymphoma, and chronic lymphocytic leukemia). Spur cell hemolytic anemia
Any of the causes of hypersplenism (increased activity of the spleen), such as portal hypertension. Acquired hemolytic anemia is also encountered in burns and as a result of certain infections (e.g. malaria). Paroxysmal nocturnal hemoglobinuria (PNH), sometimes referred to as Marchiafava-Micheli syndrome, is a rare, acquired, potentially life-threatening disease of the blood characterized by complement-induced intravascular hemolytic anemia. Lead poisoning resulting from the environment causes non-immune hemolytic anemia. Similarly, poisoning by arsine or stibine also causes hemolytic anemia. Runners can develop hemolytic anemia due to "footstrike hemolysis", owing to the destruction of red blood cells in feet at foot impact. Low-grade hemolytic anemia occurs in 70% of prosthetic heart valve recipients, and severe hemolytic anemia occurs in 3%. Mechanism
In hemolytic anemia, there are two principal mechanisms of hemolysis; intravascular and extravascular. Intravascular hemolysis
Intravascular hemolysis describes hemolysis that happens mainly inside the vasculature. As a result, the contents of the red blood cell are released into the general circulation, leading to hemoglobinemia and increasing the risk of ensuing hyperbilirubinemia.Intravascular hemolysis may occur when red blood cells are targeted by autoantibodies, leading to complement fixation, or by damage by parasites such as Babesia. Extravascular hemolysis
Extravascular hemolysis refers to hemolysis taking place in the liver, spleen, bone marrow, and lymph nodes.
A lab at the Childrens Cancer Research Institute in Vienna, in collaboration with a network of European oncologists, had developed an anti-GD2 mAb that it made in CHO cells, and by 2011, it was in Phase III clinical trials, and the institute licensed its rights to Apeiron, a local biotech company.The FDA approved United Therapeutics application in March 2015, as did the European Medicines Agency.In 2017, United Therapeutics withdrew the European marketing authorization, and said that it was having trouble making enough of the drug to sell in Europe.In October 2016, Apeiron licensed the rights to Ch14.18 to the UK biotech company, EUSA, and in May 2017, Apeiron and EUSA obtained EMA approval to market Ch14.18, by then called dinutuximab beta. References
External links
"Dinutuximab". Drug Information Portal. U.S. National Library of Medicine. "Dinutuximab beta". Drug Information Portal. U.S. National Library of Medicine.