folic acid deficiency
Introduction
Introduction to folic acid deficiency Folic acid deficiency refers to a clinical syndrome characterized by megaloblastic anemia caused by insufficient folate intake or malabsorption. Lack of folic acid can cause emotional changes, and folic acid supplementation can disappear. The lack of folic acid in pregnant women can increase the incidence of pre-eclampsia and placental stripping. Pregnant women with megaloblastic anemia are prone to intrauterine growth retardation, preterm birth and low birth weight. Lack of folic acid in early pregnancy, but also easy to cause fetal neural tube defects (such as spina bifida, no brain deformity, etc.). Folate deficiency can cause hyperhomocysteinemia, which increases the risk of cardiovascular disease. basic knowledge The proportion of the disease: the probability of the population is 0.35% Susceptible people: no special people Mode of infection: non-infectious Complications: megaloblastic anemia, hypertension, malnutrition
Cause
Causes of folic acid deficiency
Therapeutic drugs interfere with folate metabolism (20%):
Such as anticonvulsants, sulfadiazine can cause folic acid absorption disorder in some people, methotrexate and other inhibition of dihydrofolate reductase, so that dihydrofolic acid can not be converted into biologically active tetrahydrofolate, oral contraceptive, fluorouracil, Drugs such as cytarabine, isoniazid, pyrimethamine, and cycloserine can affect the absorption and metabolism of folic acid, and ethanol also affects folate metabolism.
The increase in demand caused a relative lack (15%):
During pregnancy, especially in the first 3 months, folic acid requirements can be increased by 5 to 10 times. In addition, lactating mothers, infants, infections, fever, hyperthyroidism, leukemia, hemolytic anemia, malignant tumors, and folic acid requirements during hemodialysis are also Increase, if not increase the intake of folic acid caused a lack.
Insufficient intake (25%):
Commonly found in malnourished, partial eclipse, picky eaters or improperly fed infants, folic acid derivatives are not heat-resistant, food cooking time is too long or repeated heating can cause damage caused by insufficient intake.
Absorption barrier (20%):
Various diseases that affect the absorption of jejunal mucosa, such as short bowel syndrome, tropical inflammatory diarrhea and enzyme deficiency in certain congenital diseases, affect the absorption of folic acid in the small intestine.
Pathogenesis
Folic acid in natural foods is present in the form of polyglutamate, which is catalyzed by rL-glutamyl carboxypeptidase from jejunal microvilli epithelial cells, which is hydrolyzed to diglutamate and monoglutamate by passive (high concentration) When taken and active (at low concentrations), monoglutamate is reduced and methylated into N5-methyltetrahydrofolate into the plasma after entering the intestinal cells, loosely binding to albumin in the plasma, and transported to the liver and other tissues. And combined with folic acid receptors with high affinity for folic acid, in these tissue cells, N5-methyltetrahydrofolate is demethylated under the action of vitamin B12 to recombine into polyglutamate, stored in cells or Coenzyme, monoglutamate in bile can be reabsorbed by the small intestine, and folic acid is degraded and excreted in the urine.
In the food, folic acid is reduced to a physiologically active form of tetr- ahydrofolic acid (THFA), which is a carrier of a carbon group in the biochemical reaction in vivo. Folic acid carries a carbon group to form N5- Methyl THFA, methylene THFA, etc. participate in the synthesis of purine and thymine, further synthesize DNA and RNA, participate in the interaction between glycine and serine, between histidine and glutamic acid, and between cysteine and methionine. Transformation, etc., involved in the synthesis of many important substances, such as hemoglobin, adrenaline, choline, creatine and so on.
Prevention
Folic acid deficiency prevention
Reasonable diet, avoid alcohol abuse, natural folic acid is widely found in animal and plant foods, such as meat, liver, kidney, yeast, mushrooms, fresh vegetables (spinach, lettuce, asparagus), beans and fruits, should be more Eat this type of food.
Complication
Folic acid deficiency complications Complications, megaloblastic anemia, hypertension, malnutrition
Nutritional megaloblastic anemia caused by folate deficiency occurs in pregnancy and infancy, and one-third of pregnant women have folic acid deficiency. Gestational megaloblastic anemia in pregnancy often occurs in the end of pregnancy and Postpartum, infection, drinking, pregnancy-induced hypertension syndrome and combined hemolysis, iron deficiency and excessive bleeding during childbirth can induce the disease.
Symptom
Symptoms of folic acid deficiency common symptoms fatigue, hand, foot, numbness, sensory disturbance, loss of appetite, thrombocytopenia, abdominal distension, abortion, pernicious anemia
1, causing megaloblastic anemia:
The clinical manifestations of vitamin B12 and folic acid deficiency are basically similar, which can cause megaloblastic anemia, leukopenia and thrombocytopenia, as well as digestive symptoms such as loss of appetite, bloating, diarrhea and glossitis. The most prominent tongue inflammation is red tongue. Tongue nipple atrophy, smooth surface, commonly known as "beef tongue", with pain, vitamin B12 deficiency often accompanied by nervous system manifestations, such as fatigue, numbness of hands and feet, sensory disturbances, difficulty walking, peripheral neuritis, subacute or chronic spinal cord Combined degeneration, the latter is more common in pernicious anemia. Pediatric and elderly patients often have psychiatric symptoms such as no desire, lethargy or mental disorder. Folic acid deficiency can cause emotional changes, folic acid supplementation can disappear, vitamin B12 deficiency can affect neutrality. The main clinical types of granulocyte function are:
(1) Nutritional megaloblastic anemia: mainly folate deficiency, China is more common in the northwestern region, mainly found in Shanxi, Shaanxi, Henan provinces, often with a history of nutritional deficiencies, low intake of fresh vegetables and very few Food, coupled with poor diet and cooking habits, is often accompanied by complex dystrophic manifestations, such as iron deficiency, lack of vitamin B1, B2, C and protein, dystrophic megaloblastic anemia in infants occurs in 6 months 2 years old infants, especially those who use goat milk and boiled milk, mothers are malnourished, children with infection and vitamin C deficiency are prone to this disease, vitamin C has the effect of protecting folic acid from damage.
(2) Pernicious anemia: the destruction of autoimmune (toxic T lymphocytes) in the gastric parietal cells, the lack of internal factors in the gastric mucosa atrophy, and the absorption of vitamin B12, which occurs in Scandinavians in northern Europe. Most cases occur in 40 cases. Above the age, the incidence rate increases with age, but there are also a few juvenile type of pernicious anemia, which may be related to congenital deficiency or abnormality of endogenous factors and ileal mucosal receptor defects. About 90% of patients have parietal cell antibodies in serum, 60 % of patients found in the serum and gastric juice found in the internal factor antibodies, and some can find thyroid antibodies, malignant anemia can be seen in hyperthyroidism, chronic lymphocytic thyroiditis, rheumatoid arthritis, etc., gastroscopy showed significant atrophy of the gastric mucosa, there are A large number of lymphatic, inflammatory infiltration of plasma cells, the disease and heredity also have a certain relationship, the prevalence of patients in the family is 20 times higher than the general population, spinal cord lateral cord combined degeneration and peripheral neuropathy occurred in 70% to 95% of cases It can also appear before anemia, the gastric acid deficiency is significant, and there is no free acid after the injection of histamine.
(3) drug-induced megaloblastic anemia: this group of drugs includes the aforementioned drugs that interfere with the absorption and utilization of folic acid or vitamin B12, as well as anti-metabolites, etc. Drug-induced megaloblastic anemia can be divided into two groups: one group is used Folic acid or vitamin B12 is effective, and the other group is ineffective.
2, causing fetal neural tube defects:
In a randomized controlled clinical trial, intervention with a folic acid-containing nutritional supplement prior to conception can effectively and significantly reduce the occurrence of neural tube defects in children (spinal fissure and no brain), another random and The control trial also showed that if a woman who had had a child with a neural tube defect had given a large dose of folic acid (4 mg/d) before she was pregnant again, it could effectively prevent neural tube defects in the next child and increase folic acid intake. The mechanism of preventing neural tube defects is still unclear, but it is certain that neural tube defects are the result of interactions between complex genetic and nutritional factors.
3. Relationship between folic acid and intrauterine growth retardation:
There is a significant correlation between folate levels in pregnant women and birth weight in infants. It has been reported that serum and erythrocyte folate levels (especially erythrocyte folate levels) can be used as predictors of neonatal birth weight at 3 months of pregnancy, while pregnant women Folic acid levels are associated with abortion, the incidence of preterm birth, high levels of folate, and low incidence.
4. Folic acid and cardiovascular disease:
After folic acid forms N5-methylTHFA, the methyl group is transferred to homocysteine to synthesize methionine. When folic acid is deficient, methionine synthesis is blocked, blood homocysteine is increased, and high concentration of homocysteine is on vascular endothelial cells. It produces damage and activates platelet adhesion and aggregation, which is a risk factor for cardiovascular disease. Adequate folic acid intake has a certain preventive effect on cardiovascular disease.
Examine
Examination of folic acid deficiency
1, serum folic acid content:
Reflecting the recent dietary folate intake, less than 6.8nmoL / L (3ng / ml) is a lack.
2, red blood cell folic acid content:
Reflecting the storage of folic acid in the body, less than 318nmoL / L (140ng / ml) is a lack.
3. Histidine load test:
After oral administration of histidine at a dose of 8h or 24h, the release of urinary imine methyl glutamate increased, but the specificity of this index was poor and the application was not common.
4. Determination of plasma homocysteine:
Homocysteine levels were elevated when subjects had vitamin B6 and B12 nutrient and folate deficiency.
Diagnosis
Diagnosis and identification of folic acid deficiency
diagnosis
According to clinical manifestations and laboratory tests, the diagnosis can be confirmed.
Differential diagnosis
Identification of megaloblastic anemia caused by vitamin B12 deficiency. According to the results of peripheral blood and bone marrow examination, it is difficult to distinguish folic acid or vitamin B deficiency, but no neuropathy when folic acid is lacking.
