Hemolíticas

Hemolíticas refers to processes, agents, or conditions that cause hemolysis, the destruction or rupture of red blood cells (RBCs). Hemolysis can be intravascular, occurring within the blood vessels, or extravascular, primarily in the spleen and liver. The result is the release of hemoglobin into the plasma and, in some cases, into the urine, along with signs of anemia and increased bilirubin.

Causes and mechanisms are diverse. Immune-mediated hemolysis includes autoimmune hemolytic anemia, where antibodies target RBCs (warm or cold agglutinin types) and a direct antiglobulin test (Coombs test) helps establish the diagnosis. Mechanical or traumatic causes include prosthetic heart valves and severe microangiopathy, leading to schistocyte formation and intravascular hemolysis. Infections such as malaria and babesiosis can damage RBCs. Hereditary defects affecting the RBC membrane (hereditary spherocytosis, elliptocytosis), enzymes (G6PD deficiency, pyruvate kinase deficiency), or hemoglobin structure (sickle cell disease, thalassemias) predispose to hemolysis. Drug- or toxin-induced hemolysis can occur with oxidative drugs (e.g., certain antibiotics or fava beans in G6PD deficiency) or other agents that injure RBCs.

Clinical features commonly include fatigue, pallor, and jaundice, with reticulocytosis reflecting a compensatory marrow response. Laboratory findings often show anemia with elevated lactate dehydrogenase (LDH), decreased haptoglobin, and increased unconjugated bilirubin; a peripheral smear may reveal schistocytes or spherocytes. In intravascular cases, hemoglobinemia and hemoglobinuria may be present.

Management targets the underlying cause and may involve stopping offending drugs, treating infections or autoimmune processes, corticosteroids for autoimmune hemolysis, transfusions in severe anemia, and, in some neonatal or specific conditions, exchange transfusion or specialized therapies. The prognosis depends on the etiology and response to treatment.