10th World Summit on Immunology, Microbiology & Infectious Diseases
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Accepted Abstracts

Understanding Autoimmune Hemolytic Anemia: Pathophysiology and Classification

Moueden Mohamed Amine*
University of Oran, Algeria

Citation: Amine MM (2020) Understanding Autoimmune Hemolytic Anemia: Pathophysiology and Classification. SciTech Immuno-Microbiology 2020

Received: July 29, 2020         Accepted: July 31, 2020         Published: July 31, 2020

Abstract

Autoimmune hemolytic anemia (AHAI) is acquired extra corpuscular hemolysis caused by auto antibodies directed against red blood cells (RBCs). These auto antibodies are present on RBCs.  and / or in plasma. And they are often directed against high incidence antigens.
The AHAI is not rare and 2/3 of disease is seen in women.
There are 03 types of antibodies:
Warm-antibody type: The auto antibodies in warm AIHA have temperature optimum at 37°C and they are of the immunoglobulin G (IgG) class in most cases, IgA auto antibodies occur in 15–20% of the patients.
Cold-antibody type: observed in cold agglutinin disease (CAD). The auto antibodies in cold AIHA have temperature optimum of 3-4°C .More than 90% of pathogenic CA are of the IgM class.
Paroxysmal cold hemoglobinuria,
Mixed warm- and cold-antibody AIHA is very rare.
- Acute AHAIs are generally post-infectious, most often viral and chronic AHAI are often observed following autoimmune pathologies as malignant lymphoid proliferation.
Several mechanisms are involved in AIHA we can cite:
  • Similarities in structures between some antigen of the erythrocyte membrane and other antigens introduced into the body would lead to a cross-immune response like Mycoplasma pneumoniaepneumonia and antigen I.
  • Dysregulation of the immune system: deficit in regulatory lymphocytes (Alpha methyl dopa can block suppressor T cells and thus cause AHAI).
  • Activation of autoreactive cells.
  • Family forms: Some class II of major histocompatibility complex (MHC) HLA-DQB1 and HLADRB1.
The mechanism of hemolysis depends on the type of antibody, we can seen: IgG dependent erythrophagocytosis, complement dependent erythrophagocytosis and complete intravascular hemolysis , here the antibody can activate completely the classic pathway of complement .
  • A better knowledge of the pathophysiology, allows to adapt the appropriate therapeutic protocol.
Keywords:  Hemolysis , Autoantibodies, Warm ,Cold, Complement