Acquired Hemolytic Anemias

Acquired hemolytic anemias (AHA) are a group of disorders in which red blood cells (erythrocytes) are destroyed by immune or non-immune mechanisms without a hereditary basis. These conditions often develop secondary to other diseases, drug exposure, infections, or autoimmune processes.

1. Immune Hemolytic Anemias (IHA)

Immune hemolytic anemias occur when the body produces antibodies against its own erythrocytes.

Types:

Warm antibody IHA – the most common form; antibodies are active at normal body temperature (36.6–37°C).

Cold agglutinin disease – antibodies are activated at low temperatures, often associated with peripheral cyanosis after cold exposure.

Paroxysmal cold hemoglobinuria (PCH) – a rare but severe form, often developing after infections.

Drug- or infection-related nonspecific immune hemolysis – may occur following viral or mycoplasma infections, or after certain medications.

Clinical manifestations: Jaundice, weakness, fatigue, palpitations, dark-colored urine (hemoglobinuria), splenomegaly (mainly in warm antibody IHA).

Diagnostic methods: Direct and indirect Coombs (antiglobulin) tests, peripheral blood smear, laboratory indicators of hemolysis (elevated LDH, increased indirect bilirubin, decreased haptoglobin, etc.).

2. Non-Immune Hemolytic Anemias

These forms develop due to physical or chemical injury to erythrocytes, without antibody involvement.

Causes:

Mechanical hemolysis – in patients with cardiac prostheses or artificial valves.

Microangiopathic hemolysis – in thrombotic hemolytic syndromes (TTP, HUS).

Toxins – snake venom, arsenic, copper.

Infections – malaria, babesiosis.

Acquired somatic mutation – Paroxysmal nocturnal hemoglobinuria (PNH).

Diagnostic methods: Detection of schistocytes in peripheral blood, urinalysis for hemoglobinuria, direct Coombs test, and specific tests according to the underlying cause.