Megaloblastic anemia

Introduction to megaloblastic anemia Megaloblastic anemia is a group of anemia caused by deoxyribonucleic acid (DNA) synthesis disorders, mainly caused by the lack of vitamin B12 or folic acid in the body, or due to acquired DNA synthesis disorders such as heredity or drugs. . The disease is characterized by macrocytic anemia, a series of giant red blood cells in the bone marrow, and giant changes in cell morphology are also found in granulocytes, megakaryocyte series, and even some proliferating somatic cells. The megaloblasts are easily destroyed in the bone marrow, and ineffective erythropoiesis occurs. About 95% of the cases are caused by folate or (and) vitamin B12 deficiency, and in the early stage, they are simply folate or vitamin B12 deficiency. It is not uncommon in clinical practice. Nutritional megaloblastic cell anemia is regional. China is more common in northwestern regions such as Shanxi and Shaanxi provinces, with a prevalence rate of 5.3%; malignant anemia is rare in China. basic knowledge The proportion of illness: 0.02% Susceptible people: no specific population Mode of infection: non-infectious Complications: heart failure, gout, anemia

The cause of megaloblastic anemia

Vitamin B12 deficiency (30%):

Due to insufficient intake, the need for an increase in the amount, the body's absorption disorder, the use of the body's utilization of vitamin B12 deficiency caused by megaloblastic anemia, the lack of simple intake is rare, only long-term vegan. Increased demand is seen in pregnancy, infants, hemolytic anemia, infection, hyperthyroidism and malignant tumors.

Folate deficiency (25%):

Due to insufficient intake of folic acid in the body, the increased dose is seen in babies, children and women during pregnancy. Malnutrition is mainly due to insufficient intake of fresh vegetables and animal protein. The increase in demand is still seen in chronic hemolysis, myeloproliferative disorders, malignant tumors, hyperthyroidism, and exfoliative dermatitis. Chronic alcoholic cirrhosis, folic acid intake and storage are reduced, and alcohol consumption reduces folic acid intake. Giant folate anemia can also be caused by folate deficiency, intestinal malabsorption, folic acid utilization, and excessive loss of hemodialysis.

DNA synthesis disorders (30%) that are ineffective in vitamin B12 or folic acid therapy:

Includes many anti-metabolites such as 6-, fluorouracil, hydroxyurea, and cytarabine; some hereditary diseases such as orotic aciduria, Lesch-Nyhan syndrome, iminomethyltransferase or N5 - Deficiency of methyltetrahydrofolate transferase; vitamin B6 reactive megaloblastic anemia and vitamin B1 reactive megaloblastic anemia.

Megaloblastic anemia prevention

Strengthen nutrition knowledge education, correct partial eclipse habits and incorrect cooking habits, infants should promote breastfeeding, reasonable feeding, timely addition of complementary foods, pregnant women should eat more fresh vegetables and animal protein, can be supplemented with folic acid in the late pregnancy, in the nutritional giant Cellular anemia-prone areas should actively promote improved diets. For patients with chronic hemolytic anemia or long-term anti-epileptic drugs, folic acid should be given prophylactic treatment. For patients with total gastrectomy, monthly preventive intramuscular injection of vitamin B12 should be given.

Megaloblastic anemia complications Complications, heart failure, gout anemia

Common complications:

1. Heart failure: Severe anemia can cause myocardial hypoxia and heart failure.

2. Bleeding: thrombocytopenia and the lack of other clotting factors, bleeding is not uncommon.

3. Gout: Severe megaloblastic anemia can be seen in the blood cells caused by ineffective hematopoiesis in the bone marrow, resulting in increased serum uric acid, causing the onset of gout, but extremely rare.

4. Psychiatric abnormalities: severe megaloblastic anemia can not only occur in peripheral neuritis, but also in people with mental disorders, which may be related to vitamin B12 deficiency.

5. Hemolysis: Some patients may have hemolysis during the onset of the disease (may be related to giant red blood cell dyskinesia), aggravating anemia.

Symptoms of megaloblastic anemia common symptoms, mental disorders, orbital edema, hepatosplenomegaly, short-term bleeding, depression, depression, asthma, effusion, jaundice, tongue pain

Gastrointestinal symptoms such as loss of appetite, abdominal distension, diarrhea and glossitis, etc., the most prominent tongue inflammation, red tongue, atrophy of the tongue and smooth surface, commonly known as "beef tongue", accompanied by pain. Vitamin B12 deficiency often accompanied by nervous system manifestations, such as fatigue, hand and foot numbness, sensory disturbance, walking difficulties and other peripheral neuritis, subacute or chronic spinal cord lateral dorsal cord combined degeneration, the latter more common in pernicious anemia, pediatric and elderly patients often appear spirit Symptoms such as no desire, lethargy or confusion. Lack of folic acid can cause emotional changes, and folic acid supplementation can disappear. Vitamin B12 deficiency can affect neutrophil function.

(a) Symptoms

Anemia is a common symptom, and the onset is slow, but the rate of anemia development is significantly accelerated when hemoglobin falls to a certain critical value. Most of the cases are moderate, severe anemia, dizziness, lack of sleep, weakness, and shortness of breath after activity.

(ii) Signs

Red tongue, atrophy of the tongue, mild manifestation of the nervous system, peripheral neuritis is common, a few cases may also have pyramidal tract signs, ataxia, etc., due to malnutrition, eyelid edema, lower extremity is invasive edema, severe Abdominal effusion or multi-serial effusion, jaundice, easy infection and bleeding tendency, a few cases of hepatosplenomegaly due to extramedullary hematopoiesis.

Examination of megaloblastic anemia

(1) Blood image

Anemia is a large cell positive color type, the red blood cells in the blood film are not uniform in size, and the abnormal shape is obvious. The oval red blood cells are more, the cabot is bad and the well-jolly body is visible in the red blood cells, and the white blood cell and platelet counts are mostly mild. Reduction, excessive neutrophil lobulation, >5% above 5 leaves, the most may have 16 leaves, this phenomenon does not mean cell senescence, but abnormal nuclear division or chromatin abnormalities, occasionally giant Erythrocytes and myelocytes suggest that there may be extramedullary hematopoiesis in the liver and spleen.

(2) Bone marrow

Bone marrow cells, especially erythroid hyperplasia, are significantly reduced, and the ratio of granules: red is decreased. The erythroid cells are characterized by obvious megaloblastic cells: the cell volume is enlarged, the nuclear chromatin is fine-grained, loosely dispersed, forming a special gap. The development of the pulp is more mature than the nucleus, forming a phenomenon of "nuclear young pulp", which can completely disappear within 24-96 hours after the treatment of specific drugs, and similar changes occur in the granulocyte system and the megakaryocyte system. Giant late-young and giant rod-shaped nucleated cells, giant and lobulated megakaryocytes, increased bone marrow iron, but can be reduced after appropriate treatment.

(three) analysis of gastric juice

The secretion of gastric juice is reduced, and most of the free hydrochloric acid is lacking or significantly reduced. A small amount of free hydrochloric acid may appear in a few patients with folate deficiency after injection of histamine, and the gastric free hydrochloric acid of patients with pernicious anemia often disappears forever.

(4) Biochemical examination

Serum indirect bilirubin is often high or mild beyond the normal range, urinary bile increases, serum lactate dehydrogenase, serum iron and serum ferritin increase, serum haptoglobin, uric acid and alkaline phosphatase are reduced, serum folate is low At 6.81 nmol/l (3 ng/ml), serum vitamin b12 was below 74 pmol/l (100 pg/ml).

(5) Iminomethylglutamic acid (formiminoglutamic acid figlu)

Excretion test, when folic acid is deficient, figlu excretion is increased by giving patients 15-20 g of histidine orally, and then measuring figlu in urine. Normal people are 9 mg/24 hours of urine, such as an increase in urine figlu, indicating folate deficiency in the body. Because tetrahydrofolate is needed in the metabolism of histidine, when the folic acid is deficient, a large amount of intermediate metabolite figlu is excreted in the urine.

(6) Radioactive vitamin b12 absorption test (schilling test)

In the first part, the subjects took oral radioactive cobalt (57co or co) labeled vitamin b 122 micrograms, while intramuscular injection of vitamin b121000 micrograms, and then measured the radiation of urine within 48 hours, vitamin b12 absorbed normal within 48 hours of the intake of radioactivity 5-40% of cobalt, vitamin b12 absorption defects, such as pernicious anemia, gastric or ileal resection, tropical nutritional megaloblastic anemia, urine radiation is less than 5%, the second part, if poor absorption The test should be repeated. The internal factor and vitamin b12 should be taken orally at the same time. If the discharge is normal, the pernicious anemia can be differentiated from the tropical nutritional megaloblastic anemia.

Diagnosis and diagnosis of megaloblastic anemia

Diagnostic criteria

(1) Detailed medical history of pregnancy, diet, improper baby feeding, partial eating habits, alcoholism, gastrointestinal diseases, common drugs, etc. can cause malnutrition.

(two) clinical manifestations

1. Anemia symptoms.

2. Digestive symptoms and tongue pain, reddish color, nipple disappeared, smooth surface.

3. Neurological symptoms, such as posterior bundle degeneration of the spinal cord, manifested as deep symmetry of the lower limbs and loss of vibration, severe imbalance and walking disorders, and peripheral neuropathy and mental depression. Expressed as mental disorders and mental retardation.

(3) Blood image

1. Moderate to severe anemia, red blood cell morphology is mainly large cells (MCW>100fl), lack of central light-stained area, visible polychromatic, alkalophilic spot color, Haojiao body, Kappa ring.

2. The number of white blood cells decreased, and the nucleus with excessive neutrophil lobulation shifted to the left (5-leaf >5% or 6-leaf >1%).

3. Platelets are slightly reduced, showing giant platelets.

(4) The bone marrow is compensatory hyperplasia, the three lines are giant young, the most obvious is the red line, the giant red blood cells appear, the giant red blood cells are >10%, mainly in the middle and young, the nucleoplasm development is unbalanced, the granules, The megakarytes have changed dramatically.

Differential diagnosis

1. According to the medical history, clinical manifestations and various experimental examinations, it is not difficult to diagnose the disease. VitB12 deficiency and folic acid deficiency have many similarities in clinical practice, but the therapeutic drugs are different. The determination of serum folic acid and VitB12 contributes to both. Identification.

2. This disease is often the first symptom of digestive tract symptoms, so it is easy to be misdiagnosed as stomach disease, chronic gastroenteritis, intestinal obstruction, intestinal tuberculosis, etc., must be identified with these diseases, as long as blood and bone marrow examination, identification is not difficult, There is bleeding, accompanied by complete blood cell reduction, and some contain a small number of immature cells, need to be identified with aplastic anemia, thrombocytopenic purpura, leukemia, myelodysplastic syndrome.

3. In the cell morphology, attention should be paid to the identification of normal young red blood cells and giant red blood cells, and the identification of giant red blood cells and normal young red blood cells.

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