الفهرس 
ANEMIAOnly 14 pages are availabe for public view
 |  | from | 122 |  |  |
| | | from | 122 | | |
Abstract
Autoimmune hemolytic anemia (AIHA) is one of the major causes of acquired hemolytic anemias in which the patient’s red blood cells (RBCs) are selectively attacked and destroyed (hemolyzed) by autoantibodies produced by the patient’s own immune system. These patients generally display the common symptoms of anemia: weakness, pallor, fatigue, and jaundice. Less obvious is the frequent occurrence of mild splenomegaly. AIHA is mainly divided into warm and cold autoantibody types based on the temperatures at which the antibodies maximally react with red blood cells in vivo and in vitro. Warm autoantibodies are more reactive at 37 oC than at lower temperatures, whereas cold autoantibodies react at temperatures less than 37 oC (optimally from 0 to 4 oC) and less strongly at higher temperatures. These two principal types are further subdivided into primary (idiopathic) and secondary forms which are associated with an underlying disease. Rarely patients develop a mixed-type of AIHA with both cold and worm antibodies. AIHA also may develop as a result of administration of certain drugs. Diagnosis of AIHA requires both serologic evidence of autoantibodies production and hemolysis. In most cases, immune-mediated hemolysis occurs extravascularly and is associated with IgG and less commonly IgM antibodies on the surface of red cells. Rare syndromes include IgG antibodies that cause direct intravascular hemolysis, such as paroxysmal cold hemoglobinuria. The appropriate therapy of AIHA is dependent on the correct diagnosis and classification of this family of hemolytic disorders. The therapeutic lines vary depending on the underlying cause and severity of the conditions. Corticosteroids and other drugs may be required in some cases. Blood transfusions and even surgical removal of the spleen may be carried out in severe cases.