Case Goals
  • Take a thorough history from the patient
  • Generate a broad differential diagnosis based on the history
  • Perform targeted physical examination and order appropriate labs
  • Identify the correct diagnosis
  • Goals

  • Take a thorough history from the patient
  • Generate a broad differential diagnosis based on the history
  • Perform targeted physical examination and order appropriate labs
  • Identify the correct diagnosis
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    Welcome, young medical students, as I guide you from start to finish on a journey of intrigue. This case was handcrafted for medical students, by medical students. So, if you are a resident or attending, have fun reaching back into the depths of your brain for knowledge so long forgotten that you might not be able to solve this one without reaching for your textbooks! We welcome Marcus Jones, a 22-year-old who has come to your clinic. Why don't you ask him what brought him in?

    Case Complete!

    High Yield points about this case:

    • A practical anemia framework is mechanism-based: decreased production, blood loss, or increased destruction (hemolysis). Key hemolysis labs include elevated LDH, elevated indirect bilirubin, low haptoglobin, and reticulocytosis.
    • Mature red blood cells have no mitochondria or nucleus — the pentose phosphate pathway is their ONLY source of NADPH, making them uniquely vulnerable to G6PD deficiency.
    • Bite cells form when splenic macrophages recognize and remove Heinz body inclusions (denatured, precipitated hemoglobin) from damaged RBCs, physically 'biting out' part of the membrane. Heinz bodies require supravital staining (crystal violet) and are not visible on routine Wright-Giemsa stain.
    • G6PD deficiency is the most common enzyme deficiency worldwide (>400 million affected), inherited in an X-linked recessive pattern. It confers evolutionary protection against Plasmodium falciparum malaria, similar to sickle cell trait. Highest prevalence in African, Mediterranean, Middle Eastern, and Southeast Asian populations.
    • Common triggers for G6PD hemolytic crises include sulfonamides (TMP-SMX), antimalarials (primaquine), dapsone, nitrofurantoin, rasburicase, fava beans, infections (the most common trigger overall), and mothballs (naphthalene).
    • G6PD levels should NOT be tested during acute hemolysis — the most deficient cells are already destroyed and reticulocytes have higher enzyme levels, potentially giving a false-negative result. Confirmatory testing should be performed 2-3 months after the episode resolves.
    • Urine dipstick heme-positive with no RBCs on microscopy suggests hemoglobinuria (or myoglobinuria), not true hematuria. A negative DAT (direct Coombs) distinguishes non-immune from immune-mediated hemolysis, ruling out autoimmune hemolytic anemia.