Folic acid deficiency in children

Introduction to folic acid deficiency in children Folic acid is a water-soluble B vitamin. Due to the deepening of research on the relationship between folic acid and birth defects and cardiovascular diseases, it has become an extremely important micronutrient. It is clinically caused by folic acid deficiency and neural tube defects. Giant erythrocyte anemia is not uncommon in rural areas of northwestern China, north China and southwest China, and it is necessary to strengthen prevention and treatment. basic knowledge The proportion of illness: 10% (10% of children with anemia) Susceptible people: children Mode of infection: non-infectious Complications: nutritional megaloblastic anemia, neural tube defects in children

The cause of folic acid deficiency in children

(1) Causes of the disease

1. Insufficient intake: Mothers consume less folic acid-rich foods such as liver, kidney, eggs, beans, green leafy vegetables, etc. during breastfeeding; breastfeeding alone does not add artificial feeding and serious picky eaters in a timely manner, and children with partial eclipse are susceptible In this case, folic acid is not heat-resistant and is destroyed by about 50% to 90% after heating.

2. Increase in demand: The disease is more common in infants of 6 to 18 months. The growth and development is rapid, and the amount of nutrients required is relatively increased. If the food is not added in time or the quality and quantity are insufficient, the disease is easy to occur.

3. Disease factors: The amount of folic acid required during infection increases, especially in the case of diarrhea, affecting the absorption of folic acid, liver disease affecting the metabolism of folic acid, and malnutrition ingesting folic acid deficiency, which can cause folate deficiency.

4. Increase in demand: When vitamin C is deficient, folic acid cannot be converted into active tetrahydrofolate. Folic acid can replace tyrosine metabolism instead of vitamin C. When vitamin C is deficient, it can cause the body to increase the requirement of folic acid, causing folic acid. insufficient.

5. Reduced activity of binding enzyme: Zinc acts as a cofactor for folate-binding enzyme and plays an important role in the absorption of folic acid. Zinc deficiency can reduce the activity of binding enzyme and reduce the amount of bound enzyme to reduce the absorption of folic acid.

6. Drug effects: Some anticonvulsants can inhibit the absorption of folic acid. Aspirin can reduce the ability of folic acid to bind to plasma proteins, thereby reducing the storage of folic acid and increasing the amount of folic acid. Broad-spectrum antibiotics inhibit intestinal bacteria and reduce folate synthesis. It can also trigger the disease.

(two) pathogenesis

Folic acid is a group of compounds called pteroylglutamic acid, which is a combination of pteroic acid and glutamic acid. The food is mostly in the form of polyglutamic acid folate, in the intestine. It is absorbed by the intestinal mucosa by hydrolysis of folic acid-binding enzyme into monoglutamic acid folic acid, and forms various physiological forms such as methyltetrahydrofolate by methylation and reduction. The liver is the main storage site of folic acid, which accounts for the body. About 50% of the total amount of folic acid, the liver releases about 0.1mg of folic acid to the blood every day to maintain serum folic acid levels. The folic acid in blood and tissue fluid is mainly 5-methyltetrahydrofolate, and folic acid is excreted through the urine and bile, and then passed through the kidney. And the small intestine absorbs, the amount of discharge is very small, and the amount of fecal discharge is difficult to determine due to the synthesis of folic acid by intestinal bacteria.

Folic acid is a coenzyme, a carbon-based transfersome involved in the methyl transfer reaction, including the internal conversion of amino acids, the formation of anthracyclines, etc., so folic acid plays an important role in cellular DNA and RNA synthesis. Folic acid is involved in hemoglobin and The synthesis of methyl compounds such as adrenaline, choline, etc., therefore, folic acid plays a very important role in cell division, proliferation and tissue growth.

Prevention of folic acid deficiency in children

1. Prevent the deficiency of folic acid in pregnant women and lactating mothers: Pay attention to the supply of folic acid before pregnancy, early pregnancy and lactating mothers. The average dietary folic acid intake of women of childbearing age in China is 266g/d. If the cooking loss is subtracted, the estimated intake is less than 200g/d. Studies have confirmed that women can supplement 400g of folic acid every day from 1 month before pregnancy to 3 months before pregnancy to prevent the initial onset of neural tube defects in high-risk populations with birth defects in China, reducing the effect to 85%; Oral administration of 4 mg/d folic acid can prevent recurrent neural tube defects.

2. Reasonable feeding: Feed the baby reasonably and add food rich in folic acid on time.

3. Timely treatment of induced diseases: Early diagnosis and treatment induced causes, such as infant diarrhea, acute infection, malnutrition, etc., can be added with appropriate amount of folic acid during the treatment process, pay attention to reasonable nutrition during the recovery period.

4. Appropriate supplementation of folic acid.

Pediatric folate deficiency complications Complications , megaloblastic anemia, pediatric neural tube defects

Folic acid deficiency can be complicated by megaloblastic anemia and neural tube defects. Pediatric neural tube defects are one of the main causes of death and disability in perinatal infants in China.

Symptoms of folic acid deficiency in children Common symptoms Loss of appetite, iron deficiency, anemia, bloating, constipation, tongue inflammation, redness, weight loss, vitamin B1 deficiency, hepatosplenomegaly, tongue pain

The incidence is mostly slow, mainly due to anemia, followed by gastrointestinal symptoms such as glossitis and gastritis.

1. Digestive system symptoms: Tonggu pain, tongue mastoid atrophy, smooth tongue, tongue blush and angular cheilitis, small mucosal ulcers, etc., a small number of jaundice can occur, common appetite loss, abdominal distension after eating, common diarrhea, also Constipation, the child gradually lose weight, hair yellow, thin, dry, sparse, hepatosplenomegaly.

2. Anemia: Folic acid deficiency can cause nuclear giant red blood cell anemia in infants. The onset of this disease is often not noticed by parents. The severity of systemic symptoms and the degree of anemia are not necessarily proportional. The skin color of the child is pale, lips, conjunctiva, and nails. The bed is pale, and sometimes it is accompanied by symptoms of iron deficiency anemia, which is easy to cause misdiagnosis.

3. Neural tube malformation: Pregnant women in the early pregnancy such as lack of folic acid, the possibility of birth of deformed children is greater, spina bifida, meningocele, no brain malformation, etc., sometimes accompanied by vitamin B1 deficiency and symptoms of peripheral nerves.

4. Others: The lack of folic acid in the diet will increase the level of homocysteine in the blood, easily cause arteriosclerosis, and induce colon cancer and breast cancer.

Examination of folic acid deficiency in children

1. Serum folic acid content: In order to reflect the recent dietary folic acid intake, the normal serum folic acid value is 11.3-36.3 nmol/L (5-16 ng/ml), and serum folic acid <6.8 nmol/L (3 ng/ml) indicates lack. .

2. Erythrocyte folate content: an indicator reflecting the reserve of folic acid in the body, which is indicated when the erythrocyte folate is <318 nmol/L (140 ng/ml).

3. Plasma homocysteine content: When the subject's vitamin B6 and vitamin B12 nutritional status is appropriate, plasma homocysteine can be used as a sensitive indicator to reflect folic acid status, folate deficiency in the blood folic acid levels decreased, while plasma The homocysteine content is increased, generally higher than normal with a homocysteine content of >16mol/L, and its normal value is 5-15mol/L. When the plasma homocysteine concentration is increased, the intracellular folate is reacted. The lack of function or the function of folate-dependent response is impaired, but lacks specificity, which can be verified by a rapid decrease in plasma homocysteine concentration after taking folic acid.

4. Bone marrow examination: Large cell anemia, characterized by giant erythrocytes in the bone marrow.

5. Radiological examination: spina bifida can be found.

6. B-ultrasound: Meningocele can be found, no brain malformation.

Diagnosis and differential diagnosis of folic acid deficiency in children

diagnosis

1. There is no obvious abnormality in the clinical manifestations of subclinical folate deficiency, but the biochemical examination has changed.

(1) Phase I: Early negative balance, showing serum folic acid below 6.8 nmol/L (3 ng/ml), but the erythrocyte folate reserve in vivo is still greater than 454 nmol/L (200 ng/ml).

(2) Phase II: Erythrocyte folic acid is lower than 363 nmol/L (160 ng/ml).

(3) Phase III: DNA synthesis defects, positive in vitro deoxyuracil inhibition test, excessive granulocyte division.

2. Clinical folic acid deficiency, the fourth stage, is diagnosed according to feeding history, clinical manifestations and laboratory examinations, and manifests as megaloblastic anemia.

Differential diagnosis

1. Blood disease: It must be differentiated from hemolytic anemia with jaundice, red blood disease, erythroleukemia, other secondary large cell anemia, and iron deficiency anemia.

2. Vitamin B1 deficiency: Attention to the lack of vitamin B1 and the symptoms of peripheral nerves, atypical cases are easily misdiagnosed.

3. Liver disease: When jaundice occurs, loss of appetite, abdominal distension after eating, etc., pay attention to the identification of liver disease.

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