Hemolytic Anemia Broad category of anemias where red blood cells are destroyed faster than they can be replaced, prompting the bone marrow to increase red blood cell production and the release of immature red blood cells into the bloodstream. Reticulocytosis provides strong suspicion of hemolysis when present along with many other markers like elevations in lactate dehydrogenase and unconjugated bilirubin or a decrease in haptoglobin. •
Hereditary spherocytosis: a genetic disorder where defects in red blood cell membrane proteins cause them to lose their normal shape, becoming spherical (spherocytes) which are prone to getting stuck and rupturing in the spleen. This hemolysis creates a chronic shortage of red blood cells, stimulating the bone marrow to increase production and release reticulocytes into circulation. •
Glucose-6-phosphate dehydrogenase (G6PD) deficiency: a genetic disorder that makes red blood cells vulnerable to
oxidative stress. When individuals with this deficiency consume fava beans, experience stress or are exposed to certain medications, oxidative damage leads to red blood cell destruction (hemolysis). In response to this rapid hemolysis, the bone marrow increases RBC production, resulting in reticulocytosis as it attempts to replace the destroyed cells. •
Autoimmune hemolytic anemia: caused by the host immune system attacking and destroying its own red blood cells. In response to this, the bone marrow will begin to produce more red blood cells to compensate for this destruction.
Blood Loss In response to significant blood loss, either acute (e.g., trauma or surgery) or chronic (e.g., gastrointestinal bleeding), the bone marrow increases production to replace lost red blood cells. This results in an increased reticulocyte count, as new immature cells are released and make up a larger proportion of the blood volume. == Diagnosis ==