Iron-Deficiency Anemia

Iron-deficiency anemia (IDA) is a common anemia caused by body iron deficiency affecting hemoglobin synthesis. Before erythropoiesis becomes limited, body iron stores are already exhausted - this state is called iron deficiency. This anemia is characterized by lack of stainable iron in marrow, liver, spleen and other tissues, with low serum iron and low serum transferrin saturation; typical cases are microcytic hypochromic. It is a common type of anemia worldwide. Causes: (1) increased iron requirement with insufficient intake; (2) poor iron absorption; (3) excessive blood loss - all affect hemoglobin and RBC survival and cause anemia.

Common Symptoms

Syncope; heart failure; koilonychia of index finger; dysphagia; tinnitus; upcurved nails; hookworm larva dermatitis; nausea

Causes and Pathogenesis

Iron needs increase during child growth and lactation, especially in premature/twins or infants of anemic mothers; low initial iron stores plus low-iron breastfeeding without timely iron-rich complementary foods (eggs, greens, meat, liver) cause IDA. Pregnancy/lactation raises needs, plus GI dysregulation and achlorhydria impair absorption, especially after multiple pregnancies. Adolescents (especially young women) have high needs; menstrual blood loss plus low-iron diet causes deficiency. Most common cause is insufficient dietary iron, food faddism or malabsorption. Heme iron is easily absorbed and unaffected by food/gastric acid; non-heme iron must first be reduced to Fe2+. Vegetable/cereal/tea phosphate, phytic acid and tannin inhibit absorption. Adult daily need ~1-2 mg; males 1 mg/d enough; women of childbearing age/growing adolescents 1.5-2 mg/d. Drugs/metals (gallium, magnesium), antacid calcium carbonate/magnesium sulfate, H2 blockers for ulcers inhibit absorption; atrophic gastritis and post-gastrectomy achlorhydria impair absorption. Pregnancy loses ~1300 ml blood (~680 mg iron), requiring 2.5 mg/d supplementation; last 6 months need 3-7 mg/d; lactation adds 0.5-1 mg/d; multiple pregnancies increase needs. Blood donation of 400 ml loses ~200 mg iron; ~8% male and 23% female donors have low ferritin, worsened by frequent donation. Since 2/3 of body iron is in RBCs, repeated heavy blood loss depletes stores: hookworm chronic intestinal bleeding, recurrent upper-GI ulcer bleeding, years of anorectal bleeding, menorrhagia; also paroxysmal nocturnal hemoglobinuria, mechanical hemolysis from prosthetic valves, idiopathic pulmonary hemosiderosis cause chronic urinary iron loss. Normal daily iron loss via GI/urinary/skin epithelium is ~1 mg; women lose more during menses/delivery/lactation; male iron loss is usually GI bleeding, female usually menorrhagia. Iron deficiency reduces heme synthesis and lowers iron-containing enzymes (cytochrome oxidase), impairing electron transport and lipid/protein/carbohydrate metabolism, causing RBC abnormalities and splenic destruction with shortened life. Iron circulates in a closed loop; normal absorption/excretion balance prevents deficiency; only increased need, low intake or chronic blood loss causing long-term negative balance leads to deficiency. Mechanism: iron is an essential trace element in all living cells; besides hemoglobin, it participates in mitochondrial electron transport, catecholamine metabolism and DNA synthesis; many enzymes need iron (peroxidase, cytochrome-c reductase, succinate dehydrogenase, ribonucleotide reductase, xanthine oxidase). Iron deficiency impairs cellular redox function. Lower iron-containing enzyme activity impairs mitochondrial oxidative glycolysis, causing epithelial keratinization, digestive-mucosa atrophy and reduced gastric acid. In skeletal muscle, alpha-glycerophosphate dehydrogenase decreases, causing post-exercise lactate accumulation and reduced muscle function. Monoamine oxidase (iron-containing) is important for neurotransmitter synthesis/breakdown (dopamine, norepinephrine, serotonin); deficiency affects neural development and intelligence. Developing RBCs need iron, protoporphyrin and globin; insufficient hemoglobin causes hypochromic anemia. On iron deficiency and infection: iron deficiency impairs macrophage function and splenic NK activity, lowers neutrophil myeloperoxidase/oxidative burst, blocks lymphocyte transformation/MIF production and reduces cellular immunity. But others stress iron is needed by bacteria, arguing iron deficiency offers some protection; infection is more common with iron sufficiency.

Treatment

Drug therapy, supportive therapy

Preventive Measures

IDA is mostly preventable. 1. Feeding guidance: promote breastfeeding; timely add iron-rich/high-absorption complementary foods (liver, lean meat, fish); balanced diet; iron for pregnant/lactating women. 2. Fortify infant foods with iron. 3. Give iron prophylaxis early to premature/low-birth-weight infants. 4. Large-scale hookworm control in endemic areas. 5. Promptly cure chronic GI bleeding diseases.

Department to Visit

It is recommended to visit the Hematology department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.