Autoimmune hemolytic anemia natural history, complications and prognosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Assosciate Editor(s)-In-Chief: Prashanth Saddala M.B.B.S
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Overview
Natural History
Complications
- Infection is a serious concern in patients on long-term immunosuppressant therapy, especially in very young children (less than two years).[1]
- Iron overload: Autoimmune hemolytic anemia is frequently complicated by iron overload due to frequent red blood cell transfusions. In patients for whom steroids do not work, red blood cell transfusions can be an important temporizing measure to maintain the hemoglobin concentration with a safe range. For example, a typical hemoglobin threshold of 7g/dl is used when considering transfusion requirements. However, a major adverse effect of frequent transfusions is iron overload, as iron can deposit in a variety of organs and result in impaired organ function. For these reasons, it is best to address the underlying cause (immune activation) of autoimmune hemolytic anemia, rather than provide transfusional support in the long-term.
- Hepatic iron overload: Iron deposition in the liver can be detected via T2 STAR magnetic resonance imaging MRI or by liver biopsy showing Prussian blue staining of hepatocytes. Iron deposition in the liver can result in symptoms of abdominal distension, bleeding, jaundice, edema, and portal hypertension. Treatment involves iron chelators such as deferoxamine, dereasirox, or deferiprone.
- End-organ damage from impaired oxygen delivery: The effects of severe anemia affect a variety of organs and tissues that rely heavily upon oxygen for energy metabolism. If hemoglobin decreases significantly, typically to values lower than 7g/dl, patients can experience impaired oxygen delivery and end-organ hypoxia. If hemoglobin decreases significantly, typically to values lower than 7g/dl, patients can experience impaired oxygen delivery and end-organ hypoxia.
- Hypoxic brain injury: This is a rare but important complication of severe anemia. Low oxygen delivery to the brain as a result of autoimmune hemolytic anemia can result in ischemic injury to neurons and supporting tissue. This is functionally similar to cerebrovascular accident, or stroke, which is due to atherosclerotic or embolic blockage of the cerebral circulation. Patients can experience severe symptoms such as numbness, weakness, paralysis, and dysarthria, or slurred speech. Patients can have significant neurological impairment (including deficits in motor, sensory, cortical, and cerebellar function). Overall, the likelihood of hypoxic brain injury due to autoimmune hemolytic anemia is very low.
- Myocardial injury: Autoimmune hemolytic anemia can result in impaired oxygen delivery to the cardiac tissue. Myocardial infarction can result from poor oxygen content in the coronary circulation, which is functionally similar to having ischemia due to blockage by an atherosclerotic plaque. Patients can experience severe symptoms such as shortness of breath, fatigue, and decreased exercise tolerance. Anemia is associated with poor outcomes.[2] Patients can have long-term complications such as congestive heart failure.
- High-output cardiac failure: Hemolytic anemia can also be associated with high-output cardiac failure, in which the ejection fraction and cardiac output are higher than normal. This is a manifestation of impaired oxygen delivery at the tissue level, for which the body compensated by increasing the circulatory output in an attempt to deliver more oxygen to tissues. High-output cardiac failure can lead to congestive heart failure.
Prognosis
References
- ↑ Zecca M, Nobili B, Ramenghi U; et al. (2003). "Rituximab for the treatment of refractory autoimmune hemolytic anemia in children". Blood. 101 (10): 3857–61. doi:10.1182/blood-2002-11-3547. PMID 12531800. Unknown parameter
|month=ignored (help) - ↑ Park S, Jung CW, Kim K, Kim SJ, Kim WS, Jang JH (2015). "Iron deficient erythropoiesis might play key role in development of anemia in cancer patients". Oncotarget. 6 (40): 42803–12. doi:10.18632/oncotarget.5658. PMC 4767472. PMID 26517509.