Nutritional megaloblastic anemia

Introduction to nutritional giant erythrocyte anemia Nutritional megaloblastic anemia (Nutritional Megaloblastic Anemia), also known as vegetative large cell anemia, is more common in infants and young children, especially within 2 years of age. It is more common in rural areas of North China, Northeast China and Northwest China, and has been significantly reduced in recent years. Mainly due to lack of vitamin B12 or folic acid. Its characteristics are: red blood cells are more normal than normal, red blood cells are more obvious than hemoglobin reduction, granulocytes and thrombocytopenia, granulocyte nuclei shift right, bone marrow appears giant red blood cells and other hematopoietic characteristics, and it is effective by vitamin B12 and folic acid treatment. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: diarrhea

The cause of nutritional megaloblastic anemia

Insufficient intake (30%):

Vitamin B12 is mainly found in animal foods, with more liver, kidney and meat, and less milk. Folic acid is rich in fresh green leafy vegetables, liver and kidney. The main requirement for vitamin B12 is ~3g per day for adults and ~1g per day for infants. The physiological requirement of folic acid is 75g per day for adults. Infants are ~20g daily. If you do not add food supplements in time, or long-term partial eclipse in older children, it is prone to vitamin B12 or folic acid deficiency.

Absorption and utilization barriers (25%):

In the small bowel resection of chronic diarrhea, localized ileitis, intestinal tuberculosis, etc. can affect the absorption of vitamin B12 and folic acid, liver disease, acute infection, gastric acid reduction or vitamin C deficiency, can affect the metabolism or utilization of vitamin B12 and folic acid.

Increase in demand (25%):

Immature children, rapid growth during neonatal and infancy. The amount of hematopoietic material needs to increase relatively, such as insufficient intake, it is easy to lack. When the infection is repeated, the consumption of vitamin B12 folate is increased, so that the amount of demand is increased and it is easy to cause deficiency.

Insufficient storage (10%):

The fetus can pass through the placenta and obtain vitamin B12 folic acid stored in the liver. If the pregnant woman suffers from vitamin B12 or folic acid deficiency, the newborn is stored less and is prone to deficiency.

Pathogenesis

Folic acid and vitamin B12 are essential for DNA synthesis in the nucleus. The key to the proliferation and division of cells is the replication and doubling of DNA. The DNA is composed of two polynucleotide chains, and the basic unit is composed of four different bases. A polymer composed of nucleotides, four bases being adenine, guanine, thymine, and cytosine.

Folic acid becomes active TFA in the liver through the action of dihydrofolate reductase. TFA is a coenzyme that transfers a carbon group in the body. These groups are derived from the catabolism of some amino acids and compounds such as formic acid, which can be attached to the molecule of THFA. It can be transferred to other intermediate metabolites and participate in the synthesis of important compounds such as nucleic acids, such as the synthesis of purines, the biosynthesis of pyrimidines, the conversion of amino acids, and the formation and utilization of formate.

Vitamin B12 is mainly involved in four important metabolic reactions in the human body:

1 Inactive methylated THFA is converted to active THFA, increasing folic acid utilization.

2 promote folic acid into the cell.

3 involved in the production of deoxythymidine nucleotides, it can be seen from the above, vitamin B12 deficiency is caused by folic acid metabolism disorders, causing DNA synthesis disorders, so it causes clinical manifestations and morphological changes of anemia, difficult to distinguish from anemia caused by folic acid deficiency, This explains why vitamin B12 can improve the anemia of folate deficiency, and a large amount of folic acid can change the hematological changes of vitamin B12 deficiency.

4 Vitamin B12 can promote the metabolism of fat metabolites involved in the tricarboxylic acid cycle, which is related to the formation of lipoproteins in the myelin sheath, thus maintaining the complete function of the central and peripheral myelinated nerve fibers. When vitamin B12 is deficient, Nerve fiber lesions, and thus neuropsychiatric symptoms, because folic acid does not participate in this metabolism, can not change the nervous system damage caused by vitamin B12 deficiency, folic acid increases the utilization of vitamin B12 by hematopoietic cells, it can aggravate the symptoms of the nervous system.

Nutritional megaloblastic anemia prevention

Prevention of this disease should start from improving the dietary structure of the population and changing living habits. For susceptible individuals, the awareness of drug prevention should be improved. The recommended daily folic acid requirement by WHO is: 40-50 g for infants in the month of June, 120 g for 7-12 months, 1~ 12g 200g, 13+400g, pregnant women 800g, lactation 600g, for the intake of vegetables, processing methods should be publicized and guided, vegetarian diet should have vitamin content provisions, for the higher incidence of rural areas should be changed Propaganda and education of their living habits.

Nutritional megaloblastic anemia complications Complications, diarrhea

Iron deficiency is a common complication of this disease, especially in the effective treatment process, due to increased hematopoietic levels, increased iron consumption and "mixed anemia."

Nutritional megaloblastic anemia symptoms common symptoms malnutrition fatigue diarrhea reflex hyperreactivity dull convulsion lymph node swelling tremor

The onset is slow, more common in infants and young children, especially children under 2 years old, folic acid deficiency occurs 4 to 7 months, while vitamin B12 deficiency occurs after 6 months, of which breastfeeding alone does not add food supplement The vast majority.

The main clinical manifestations are as follows:

(A) general performance: more chubby body shape or mild edema, hair thinning, yellowing, occasionally skin bleeding points.

(B) anemia performance: mild or moderate anemia accounted for the majority, facial yellow, fatigue, weakness, due to anemia caused by extramedullary hematopoietic reaction, and a three-line reduction phenomenon, it is often accompanied by liver, spleen, lymph nodes.

(3) Symptoms of mental and neurological symptoms: sluggish expression, lethargy, slow response to the outside world, less crying or crying, mental development and backward development of movement, or even backwards. If you have already recognized people, you will climb, etc. In addition, there are still uncoordinated and involuntary movements, limbs, head, tongue and even whole body tremors, increased muscle tone, hyperreflexia, positive sputum, shallow reflexes disappeared, and even convulsions.

(D) digestive system symptoms: loss of appetite, glossitis, sublingual ulcers, diarrhea and so on.

Examination of nutritional giant erythrocyte anemia

(1) Blood image

Anemia is more serious, red blood cell reduction is lower than hemoglobin, MCV and MCH> normal, MCHC is normal; red blood cells are mildly uneven in size, larger in larger, darker in color, less visible in central pale area, common oval red blood cells; The number of reticulocytes is often lower than normal. The total number of white blood cells is slightly lower or normal, the lymphocytes are relatively increased, the granulocytes are decreased, the cell bodies are large, the nuclear chromatin is loose, and the nucleus is shifted to the right. Macronuclear neutrophils are seen. The number of platelets can be reduced in severe cases.

(2) bone marrow elephant

The number of nucleated cells can be slightly increased, normalized or reduced. The young red blood cells in each stage are giant and young, such as the original red and early red blood cells, it is more diagnostic. The white blood cell classification is mostly close to normal, and lymphocytes can sometimes increase relatively. Giant neutrophils, giant late-young or giant rod-shaped neutrophils may appear in neutrophils. In severe cases, the number of megakaryocytes can be reduced and the morphology is also changed.

(3) Special test

1 serum vitamin B12 determination. It can be reduced in vitamin B12, folic acid and iron deficiency.

2 Vitamin B12 absorption test, such as poor absorption, the excretion of the isotope-labeled vitamin B12 in the urine is reduced.

3 histidine tolerance test (formiminoglutamic acid test), after the conversion of histidine into N-iminomethylglutamate (FIGLU) in vivo, tetrahydrofolic acid is required to further degrade into glutamic acid. If the patient is given a histidine load, due to folic acid deficiency, FIGLU is accumulated and the amount of urine is increased. However, in addition to false positives and false negatives, this test is positive in the absence of folic acid and vitamin B12.

4 serum folate determination, methodology is still unstable.

5 erythrocyte internal folate determination, currently considered more reliable.

Serum vitamin B12 content decreased, red blood cell or serum folate content is normal or increased, suggesting vitamin B12 deficiency; serum vitamin B12 content is normal, red blood cell or serum folate content is decreased, suggesting folate deficiency; the above reduction can be seen in vitamin B12 And / or folic acid deficiency.

Diagnosis and diagnosis of nutritional megaloblastic anemia

diagnosis

After diagnosis of this disease, it is best to be clear that vitamin B12 deficiency or folic acid deficiency, if the above special test can not be carried out, can be a therapeutic diagnosis, patients must have no obvious infection, no malignant disease in the kidney, no folate High foods such as meat, viscera, fresh green leaves or yellow leaf vegetables and juice, daily vitamin B121 ~ 5g intramuscular injection or folic acid 50 ~ 100g orally, such as the application of one of the above vitamins, reticulocytes rapidly rise, that is to prove For the lack of this substance.

Children with nutritional megaloblastic anemia are most likely to be confused with nutritional mixed anemia with obvious neurological symptoms. In nutritional mixed anemia, the red blood cell size is very different, and the central red area of red blood cells is enlarged. At the same time, there are macroscopic changes of young red blood cells and granulocytes and insufficient hemoglobin formation due to iron deficiency in young red blood cells.

Differential diagnosis

(1) Brain hypoplasia: More development than post-natal development, in addition to neurological symptoms, there is still mental retardation, no anemia, no improvement in neurological symptoms after treatment with vitamin B12.

(B) chronic liver disease megaloblastic anemia, due to chronic liver disease, may have vitamin B12 and folic acid metabolism and storage disorders, such anemia, often accompanied by chronic liver damage, liver, spleen enlargement and portal hypertension , ascites, etc.

(3) Red blood stage of erythroleukemia: There are nucleated red blood cells in the blood image, and the treatment and post-treatment are different from the nutritional giant erythrocyte anemia.

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