↓ marrow iron & depleted body iron stores → ↓ heme synthesis → microcytosis → anemia
↓ iron stores and ↓ ferritin → ↓ transferrin saturation, ↑ zinc protoporphyrin → anemia, microcytosis
(pre–latent phase) depleted iron stores and ↓ ferritin levels → (latent iron deficiency) ↓ transferrin saturation → ↓ heme formation (↓ incorporation Fe into the porphyrin ring) → ratio of zinc protoporphyrin:heme → iron-deficiency anemia (diminution in RBC volume and quantity)
Special clinical manifestations: angular cheilosis, atrophic glossitis, pica (consumption of nonnutritive substances such as ice, clay), koilonychia (nail spooning)
Plummer-Vinson syndrome (iron deficiency anemia, esophageal web & atrophic glossitis)
Etiologies: chronic bleeding (GI - including cancer, menstrual, etc.), ↓ supply(malnutrition; ↓ absorp. due to celiac sprue, Crohn’s, ↑ gastric pH, subtotal gastrectomy), ↑ demand (preg., epo). Rare Fe-refractory genetic disorder due to hepcidin dysregulation
Diagnosis ↓ Fe, ↑ TIBC, ↓ ferritin(espec. <15), ↓ transferrin sat (Fe/TIBC; espec. <15%), ↑ soluble transferrin receptor; ↑ plt; unless hx c/w different etiology, initiate workup for GIB; incl. H. pylori serology, ? celiac sprue labs (anti-TTG, antigliadin, antiendomysial Ab)
Treatment (Fe supplementation): oral Fe tid (~6 wk to correct anemia; ~6 mo to replete Fe stores); in cases of excessive/persistent GI losses or for dialysis or cancer Pts prior to EPO Rx, IV iron (Fe-sucrose, -gluconate, -dextrose) should be considered