Hemolytic anemia can be inherited or acquired. Some of the most common types include sickle cell anemia, thalassemia, and autoimmune hemolytic anemia.

Your body naturally gets rid of aging or damaged red blood cells (RBCs) in a process called hemolysis. If you have hemolytic anemia, you have too much hemolytic activity and your body can’t replace the destroyed cells with healthy RBCs quickly enough. The result is fewer RBCs to carry oxygen throughout your body.

Several different types and underlying causes of hemolytic anemia exist. In some types, RBCs are weak or structurally damaged, so they don’t last as long as they should. In other types, your body mistakenly attacks healthy RBCs.

Here’s a rundown of some of the main types of hemolytic anemia.

Hemolytic anemia can be due to a genetic (inherited) condition or acquired later in life.

While you can’t change your genes, you might be able to manage inherited hemolytic anemia with diagnosis and treatment.

Acquired hemolytic anemia can occur from medical events, infections, or chronic diseases, among many other factors.

Other ways of classifying hemolytic anemia

Doctors also classify types of hemolytic anemia in other ways:

  • Intrinsic versus extrinsic: Hemolytic anemia can result from an irregularity inside the RBCs (intrinsic) or from an outside cause (extrinsic). Another way of saying this is intracorpuscular versus extracorpuscular.
  • Immune versus non-immune: With immune forms of hemolytic anemia, antibodies mediate the condition.
  • Intravascular versus extravascular: RBC destruction can happen inside (intravascular) or outside (extravascular) the blood vessels.

Some inherited conditions can lead to hemolytic anemia. Doctors may discover some of these conditions during a newborn screening. In other conditions, symptoms may become apparent during childhood or adolescence.

In most cases, doctors can confirm the presence of genetic mutations that cause these conditions with genetic testing.

Sickle cell disease

Sickle cell disease is a group of conditions where some RBCs become misshapen, or sickled. They cannot move oxygen throughout the body as effectively. Sickle-shaped RBCs only live about 10 to 20 days, while other RBCs live for 90 to 120 days.

Although people often use the terms “sickle cell anemia” and “sickle cell disease” interchangeably, the former refers to a specific type of sickle cell disease, which is usually the most severe. All types of sickle cell disease can cause hemolytic anemia, though to varying degrees.

Thalassemia

Thalassemia is a condition in which your body doesn’t make enough hemoglobin, a protein in RBCs. Without enough hemoglobin, RBCs don’t live as long as they should.

You can have alpha- or beta-thalassemia, depending on the specific part of the hemoglobin protein affected.

Red cell membrane disorders

Red cell membrane disorders, such as hereditary spherocytosis, cause lower deformability of RBCs. Deformability is the ability of RBCs to change shape for optimal flow through vessels. With lower deformability, RBCs don’t live as long and there are fewer in circulation.

Pyruvate kinase deficiency

RBCs rely on the pyruvate kinase enzyme to convert sugar into energy. Pyruvate kinase deficiency is a change in the PKLR gene that leads to low levels of this enzyme.

Low pyruvate kinase enzyme levels result in reduced conversion of sugar into energy. Low energy levels lead to early death of RBCs, which last only a few days or weeks.

G6PD deficiency

Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme that prevents cell damage from reactive oxygen species (ROS). ROS are free radicals that can react with other cell molecules and cause cell death.

Because RBCs carry oxygen, they are particularly vulnerable to ROS. When ROS production is high, G6PD deficiency can lead to hemolytic anemia.

Acquired forms of hemolytic anemia are not due to genetics or inherited traits. They’re more likely to develop later in life, though some can affect children.

Autoimmune hemolytic anemia (AIHA)

Autoimmune disorders occur when your body’s immune system attacks healthy cells. In AIHA, your immune system attacks RBCs by “tagging” them with antibodies.

Warm vs. cold hemolytic anemia

Doctors classify AIHA as warm or cold.

In warm AIHA — the more common form — antibodies are active at body temperature (37ºC or 98.6º F).

In cold AIHA, also called cold agglutinin disease, antibodies are active at very cold temperatures (0º to 4°C or 32º to 39ºF).

Alloimmune hemolytic anemia

Alloimmune hemolytic anemia occurs when your body makes antibodies against RBCs, usually after a blood transfusion.

It can also occur in newborns when their blood has an Rh factor different from their birthing parent’s. This is called Rh incompatibility. The birthing parent passes on their anti-Rh antibodies to their child’s blood.

Drug-induced hemolytic anemia

Drug-induced hemolytic anemia results when certain medications trigger immune hemolysis. Experts suspect at least 130 drugs of causing immune hemolytic anemia. Like with AIHA, your immune system mistakenly tags RBCs with antibodies and destroys them.

Mechanical hemolytic anemia

Hemolytic anemia can also result from physical damage to the RBCs. This is called mechanical hemolytic anemia (MHA). Causes of MHA include:

Paroxysmal nocturnal hemoglobinuria

Paroxysmal nocturnal hemoglobinuria (PNH) occurs when stem cells in the bone marrow acquire a mutation. The affected stem cells grow into RBCs that are vulnerable to destruction by the immune system. People with PNH can release hemoglobin into the urine (hemoglobinuria), which might be most noticeable in the morning.

PNH might cause blood clots. The bone marrow dysfunction can lead to low levels of platelets and red and white blood cells.

Infectious anemias

Some infectious diseases can also result in hemolytic anemia. Examples include malaria, which is spread by mosquitoes, and babesiosis, which is spread through ticks.

Doctors suspect hemolytic anemia in cases of anemia where the reticulocyte count is high. Reticulocytes are immature RBCs.

RBC morphology, where doctors examine the structure of RBCs on a peripheral blood smear, often indicates anemia. The smear can often reveal fragments of RBCs.

Other blood tests may also show affected bilirubin, LDH, or haptoglobin levels that suggest hemolytic anemia.

Doctors perform further testing to determine the type of hemolytic anemia. Multiple blood tests are available to determine the cause of hemolysis, including:

  • Coombs test
  • quantitative hemoglobin electrophoresis and high performance liquid chromatography
  • RBC enzyme assay
  • flow cytometry
  • cold agglutinin testing
  • osmotic fragility testing
  • genetic testing

Treatment for hemolytic anemia will depend on the underlying cause and the severity of your symptoms. Typical treatments include:

Doctors may also consider other factors, such as your age and overall health.

For example, some children may be candidates for a stem cell transplant to treat sickle cell anemia while Food and Drug Administration (FDA)-approved gene therapies are better options for adults and children ages 12 years and older.

Hemolytic anemia is a group of conditions in which your body gets rid of RBCs more quickly than it replaces them. RBCs might be damaged or weak because of inherited genetic differences or an acquired condition. Symptoms range in severity, with some people not experiencing any symptoms.

Doctors diagnose hemolytic anemia after a series of tests that examine RBC levels and structure. If you have anemia symptoms or recurrent anemia with no known cause, consider talking with a doctor.