Anemia, often manifested as pallor, dizziness, weakness, tinnitus, etc. The severity of symptoms is not only related to the degree of anemia, but also to the speed of its onset. If a person has the above symptoms and goes to the hospital for a routine blood test and is found to have severe anemia (hematocrit below 60 g/L), this often suggests a chronic development of anemia rather than a recent occurrence.
Iron is one of the main components of hemoglobin, and when there is an imbalance between the body’s demand and supply of iron, it leads to depletion of stored iron in the body (ID), followed by intraerythrocytic iron deficiency (IDE), which eventually causes iron deficiency anemia (IDA).
Etiology: It is important to find the cause and treating the cause is the key to treating iron deficiency anemia.
Insufficient intake: iron deficiency in food.
Oversupply: pregnant women or growing children.
malabsorption: gastrointestinal disorders
impaired transfer: anoferritinemia, liver disease, chronic inflammation
excessive loss: various types of blood loss.
Utilization disorders: iron granulocytic anemia, lead poisoning, chronic diseases
Iron metabolism.
Functional state iron: hemoglobin iron (67%), myoglobin iron (15%), transferrin iron, lactoferrin, enzyme and cofactor iron.
Storage iron: ferritin and iron-containing hemoglobin.
Normal human blood production requires 20 – 25mg of iron per day, the vast majority from their own aging red blood cells and only 1 – 1.5mg from food intake, pregnant and lactating women need 2 – -4mg/day.
Iron absorption is mainly in the upper duodenum and jejunum.
Pathogenesis.
1. iron metabolism: storage iron deficiency: reduced ferritin and iron-containing hemoglobin.
Diminished serum iron and transferrin saturation.
Elevated total iron binding and unbound iron loading ferritin.
Iron deficiency in tissues and red blood cells
Serum soluble transferrin receptor (sTfR) is by far the best indicator of iron deficiency erythropoiesis.
2.Impact on hematopoiesis: due to iron deficiency, heme synthesis is impaired and a large amount of free protoporphyrin (FEP) is formed, or combined with zinc atoms to form zinc protoporphyrin (ZEP).
3. Effect on tissue metabolism: It affects the activity of iron-containing enzymes and iron-dependent enzymes, which in turn affects mental, behavioral, physical and immune functions, etc., causing mucosal tissue lesions and nutritional disorders in ectodermal tissues.
Laboratory tests: (this part can be skipped)
Hematology: small cell hypochromic anemia with mean red blood cell volume (MCV) less than 80fl, mean red blood cell hemoglobin volume (MCH) less than 27pg, and mean red blood cell hemoglobin concentration (MCHC) less than 32%. Reticulocytes were normal or mildly elevated. Leukocytes and platelets were basically normal.
Bone marrow routine: active hyperplasia, mainly red lineage hyperplasia, red lineage hyperplasia suggests poor hemoglobin formation, showing “old nucleus and young pulp”.
Iron metabolism: serum iron was lower than 8.95 umol/L; total iron binding capacity was elevated, greater than 64.44 umol/L; transferrin saturation was reduced, lower than 15%; sTfR is by far the best indicator of iron deficiency erythropoiesis, exceeding 8 mg/L, and generally its concentration is greater than 26.5 umol/L (2.25ug/ml), iron deficiency can be diagnosed; serum ferritin below 12ug/L; negative bone marrow potassium ferricyanide (Prussian blue reaction) staining; reduced or absent iron in young erythrocytes.
Intraerythrocytic porphyrin metabolism: FEP less than 0.9 umol/L (whole blood), ZPP greater than 0.96 umol/L (whole blood), FEP/Hb greater than 4.5ug/gHb.
Diagnosis.
Storage iron deficiency.
1) Serum ferritin <12ug/L.
2) Extramedullary iron deficiency with <15% iron granulocytes; normal hemoglobin and serum iron.
Iron deficiency erythropoiesis.
1) storage iron deficiency.
2) transferrin saturation <15%.
3) FEP/Hb greater than 4.5ug/gHb.
4) Normal hemoglobin.
Iron deficiency anemia.
1) iron deficiency erythropoiesis.
2) Small cell hypochromic anemia: Hb < 120g/L in men, Hb < 110g/L in women, Hb < 100g/L in pregnant women, MCV < 80fl; MCH < 27pg.
Etiological diagnosis: In particular, chronic blood loss due to gastrointestinal tumors needs to be alerted and needs to be diagnosed and treated early.
Treatment.
Principle: Eradicate the cause and replenish stored iron.
1. Oral iron supplementation: Eating cereals, dairy and tea will inhibit iron absorption, while fish, meat and vitamin C can enhance iron absorption.
Effective generally manifested as a rise in peripheral reticulocytes, the peak appears 5 – 10 days after taking the drug, 2 weeks after the rise in hemoglobin, generally 2 months after the return to normal. And iron treatment should be continued for at least 4–6 months after the hemoglobin returns to normal, and stop the drug after the ferritin returns to normal.
2. Intramuscular injection: Iron dextran: (Hb to be achieved – patient Hb) x 0.33 x patient weight. Need to test first, no allergy before use.
3. Most important is the etiological treatment: excessive menstruation (the most common cause in women of childbearing age): ask for a gynecological consultation.
Purely nutritional (e.g. severe partiality): change the diet.
absorption problems (gastrointestinal disorders): consult a gastroenterologist
Chronic blood loss (gastrointestinal, respiratory, urinary tract): search for and treat the cause of blood loss, especially for malignant tumors of the gastrointestinal tract, which require early diagnosis and treatment.