Epidemiology


Etiology


Pathophysiology

  • Autosomal Dominant inheritance (most common).
  • Defect in RBC membrane scaffolding proteins: ankyrinband 3, or spectrin.
  • This defect uncouples the cytoskeleton from the lipid bilayer, leading to loss of membrane blebs.
  • Results in ↓ surface-area-to-volume ratio, causing RBCs to assume a spherical shape (spherocytes).
  • Spherocytes are less deformable and are trapped and destroyed by macrophages in the splenic cords of Billroth.
  • This leads to extravascular hemolysis.

Clinical features

  • Anemia and pallor
  • Jaundice (due to ↑ unconjugated bilirubin)
  • Splenomegaly with left upper quadrant pain
  • Black pigment gallstones (made of calcium bilirubinate), may lead to cholecystitis

Diagnostics

  • Peripheral Smear: Presence of spherocytes (small, round RBCs lacking central pallor). Howell-Jolly bodies may be present if post-splenectomy.
  • Labs:
    • Normocytic anemia (↓ Hgb, ↓ Hct).
    • ↑ Mean Corpuscular Hemoglobin Concentration (MCHC) is a classic finding due to cellular dehydration and membrane loss.
    • ↑ Reticulocyte count.
    • ↑ Unconjugated bilirubin.
    • ↑ LDH.
    • ↓ Haptoglobin.
  • Confirmatory Tests:
    • Osmotic fragility test: Positive. Spherocytes are more fragile and lyse more readily in hypotonic solution.
    • Eosin-5-maleimide (EMA) binding test: More specific test, shows decreased binding.
  • Coombs testNegative. Differentiates from autoimmune hemolytic anemia, which also presents with spherocytes.

Treatment