<unk>  is a type of hemolytic anemia where the body's immune system attacks its own red blood cells, leading to their destruction (hemolysis).  Antibodies and associated complement system components become fixed onto the red blood cell surface. These antibodies can be detected with the Coombs test or direct Coombs test.<unk>  can also be induced by infections such as Mycoplasma pneumoniae, drugs such as methyldopa and fludarabine, or malignancies such as chronic lymphocytic leukemia or non-Hodgkin lymphoma.<unk>  is classified into 3 broad categories. These include warm-antibody type, cold-antibody type, and mixed-antibody type. Each category is characterized by a different autoantibody (IgG or IgM) and different optimal binding temperatures (37 degrees Celsius or 4-18 degrees Celsius). A variety of conditions comprise the differential diagnosis of<unk> . These include microangiopathic hemolytic anemia, paroxysmal cold hemoglobinuria, paroxysmal nocturnal hemoglobinuria, hereditary spherocytosis, pernicious anemia, and chronic lymphocytic leukemia. The risk factors for<unk>  include systemic lupus erythematosus and immunotherapeutic medications. The natural history of<unk>  begins with the hemolytic event. A diagnostic workup is typically initiated soon after the hemolytic event, and the hemolysis subsides after the start of corticosteroids. Most patients will generally achieve remission with no long-term complications. Complications of<unk>  usually include infection, thrombosis, iron overload, and end-organ damage from impaired oxygen delivery. Patients with<unk>  have a gradual onset of fatigue and can develop shortness of breath and decreased exercise tolerance. The symptoms of<unk>  depend on the severity of the disease. Laboratory findings in patients with<unk>  include anemia, positive Coombs test, positive indirect antiglobulin test, hemoglobinuria, low haptoglobin, increased spherocytes, and elevated lactate dehydrogenase (LDH). Not all patients will have all of these findings. The severity of hemolysis will determine the degree of laboratory abnormalities. The mainstay of therapy for<unk>  is immunosuppression, since the pathophysiology of<unk>  involves immunological activation which leads to the destruction of red blood cells. Suppression of the immunological activation via medications has been the cornerstone of therapy for many decades. Medications include corticosteroids, azathioprine, rituximab, mycophenolate mofetil, cyclosporine A, and cyclophosphamide. Splenectomy is the only surgical management option for patients with<unk> . The response rate is moderately high. Assessment for candidacy for splenectomy involves evaluation of the surgical risk and the risk of sepsis from encapsulated organisms. Proper vaccinations must thus be given prior to splenectomy. The primary prevention strategies for<unk>  include avoidance of exposure to precipitants.
Autoimmune hemolytic anemia
Warm autoimmune hemolytic anemia
Immune hemolytic anemia
Non immune hemolytic anemia
Microangiopathic hemolytic anemia
Drug induced hemolytic anemia
Mechanical hemolytic anemia
Drug-induced nonautoimmune hemolytic anemia