Which statement is true regarding warm autoimmune hemolytic anemia
Which statement is true regarding warm autoimmune hemolytic anemia Warm autoimmune hemolytic anemia (WAIHA) is a unique form of hemolytic anemia characterized by the immune system mistakenly attacking the body’s own red blood cells. It is distinguished from other types of autoimmune hemolytic anemia primarily by the temperature at which the pathogenic autoantibodies are most active. In the case of WAIHA, the autoantibodies are active at body temperature, around 37°C, leading to the destruction of red blood cells predominantly within the spleen and liver.
A key feature of WAIHA is the presence of warm-reactive IgG autoantibodies. These antibodies bind to antigens on the surface of red blood cells at normal body temperature. Once bound, they mark the cells for destruction by macrophages in the spleen—a process known as extravascular hemolysis. This mechanism differs from cold agglutinin disease, where autoantibodies are active at lower temperatures and often cause agglutination of red blood cells in peripheral circulation.

Clinically, patients with WAIHA often present with symptoms typical of hemolytic anemia, such as fatigue, pallor, jaundice, dark urine, and splenomegaly. The rapid destruction of red blood cells can lead to anemia, and in some cases, a transient increase in reticulocyte count as the bone marrow attempts to compensate for the loss. Laboratory findings usually reveal a positive direct antiglobulin test (DAT), also known as the Coombs test, which detects IgG or complement proteins on the surface of red blood cells.
The etiology of WAIHA can be idiopathic, where no underlying cause is identified, or secondary, linked to conditions such as autoimmune diseases (e.g., systemic lupus erythematosus), lymphoproliferative disorders, infections, or certain drugs. The treatment approach often involves corticosteroids as the first line, which suppress immune activity and reduce autoantibody production. In cases where steroids are ineffective or contraindicated, other therapies like immunosuppressants, intravenous immunoglobulin (IVIG), or splenectomy might be considered.
It is important to recognize that WAIHA is distinct from cold autoimmune hemolytic anemia, primarily due to the temperature at which the autoantibodies operate and their immunoglobulin class. The statement that is true regarding WAIHA is that it involves warm-reactive IgG autoantibodies which cause red blood cell destruction at body temperature through extravascular hemolysis. This understanding helps guide diagnosis and therapeutic strategies, ensuring appropriate management of affected individuals.
In summary, the hallmark of warm autoimmune hemolytic anemia is the presence of IgG autoantibodies that react at body temperature, leading to the destruction of red blood cells mainly in the spleen. Recognizing this feature is crucial for accurate diagnosis and effective treatment.









