Drug-induced autoimmune hemolytic anemia

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Drug-induced autoimmune hemolytic anemia
Blood smear showing autoimmune hemolytic anemia
Synonyms	N/A
Pronounce	N/A
Specialty	N/A
Symptoms	Fatigue, pallor, jaundice, dark urine, tachycardia
Complications	Heart failure, kidney failure, shock
Onset	Variable, depending on drug exposure
Duration	Variable, may resolve after discontinuation of the drug
Types	N/A
Causes	Drug-induced
Risks	Use of certain medications (e.g., penicillin, cephalosporins, methyldopa)
Diagnosis	Coombs test, blood smear, complete blood count
Differential diagnosis	Hereditary spherocytosis, G6PD deficiency, cold agglutinin disease
Prevention	N/A
Treatment	Discontinuation of the offending drug, corticosteroids, immunosuppressive therapy
Medication	N/A
Prognosis	Generally good if the drug is discontinued
Frequency	Rare
Deaths	N/A

Drug-induced autoimmune hemolytic anemia (DIAHA) is a form of hemolytic anemia, a condition in which red blood cells are destroyed more quickly than they can be produced. In DIAHA, the destruction of red blood cells is triggered by the body's immune response to certain medications. This condition is a type of autoimmune disorder, where the body's immune system mistakenly attacks its own cells, in this case, red blood cells, leading to their premature destruction—a process known as hemolysis.

Causes

DIAHA can be caused by various medications that induce the body's immune system to produce antibodies against red blood cells. These drugs can be classified into three main categories based on their mechanism of action:

• 1. Hapten Mechanism: In this mechanism, the drug acts as a hapten by binding to the red blood cell membrane, forming a complex that is recognized as foreign by the immune system. This recognition leads to the production of antibodies against the drug-cell complex, resulting in cell destruction. Drugs commonly associated with this mechanism include penicillin and other beta-lactam antibiotics.
• 2. Immune Complex Mechanism: Here, the drug binds to plasma proteins, forming a complex that subsequently binds to the red blood cell surface. The immune system then targets these complexes, causing cell lysis. Examples of drugs that can cause DIAHA through this mechanism include quinidine and cephalosporins.
• 3. Autoantibody Mechanism: Some drugs can induce the immune system to produce autoantibodies that react with red blood cells in the absence of the drug. This is less common but can be induced by drugs such as levodopa and methyldopa.

Symptoms

Symptoms of DIAHA may vary from mild to severe and can include:

• Fatigue
• Pallor
• Jaundice (yellowing of the skin and eyes)
• Dark urine
• Shortness of breath
• An increased heart rate

Diagnosis

Diagnosis of DIAHA involves a combination of clinical history, physical examination, and laboratory tests. Key diagnostic tests include:

• Complete blood count (CBC), which may show anemia and an increased number of reticulocytes (immature red blood cells).
• Direct Coombs test, also known as the direct antiglobulin test (DAT), which detects antibodies or complement proteins attached to the surface of red blood cells.
• Indirect Coombs test, which detects free antibodies in the patient's serum that could bind to red blood cells.

Treatment

The primary treatment for DIAHA involves discontinuing the offending drug. In cases where anemia is severe, treatment may also include:

• Corticosteroids to reduce the immune response.
• Immunosuppressive drugs in severe cases or when steroids are ineffective.
• Blood transfusions, if necessary, to manage severe anemia.

Prevention

Preventing DIAHA involves careful selection of medications, especially in individuals with a history of drug-induced reactions. Healthcare providers should be vigilant about the potential for drugs to cause hemolytic anemia and monitor patients accordingly.

See Also

• Hemolytic anemia
• Autoimmune disease
• Pharmacology
• Immunology

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