Folate deficiency neuropathy

Introduction

Introduction to folate deficiency neuropathy Folic acid deficiency refers to a clinical syndrome characterized by megaloblastic anemia caused by insufficient folate intake or malabsorption. Folic acid is a fat-soluble vitamin rich in vegetables, yeast, liver, kidney, milk and other foods, but it is easily destroyed after cooking. Folic acid is an anti-anemia factor. Human deficiency can cause similar symptoms of malignant anemia. When folic acid is deficient, DNA synthesis is impeded, which causes the rapidly dividing hematopoietic system and gastric mucosa to develop lesions, which can be complicated by nervous system damage. basic knowledge Sickness ratio: 0.1% Susceptible people: no special people Mode of infection: non-infectious Complications: dementia spina bifida

Cause

Folate deficiency neuropathy

Therapeutic drugs interfere with folate metabolism (10%):

Such as anticonvulsants, sulfadiazine can cause folic acid absorption disorders in some people, methotrexate and other inhibition of dihydrofolate reductase, so that dihydrofolic acid can not be converted into biologically active tetrahydrofolate, oral contraceptives, 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 (5%):

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 deficiency and the pathogenesis of neurological damage, it is currently believed that folic acid plays a large role in the metabolism of neurons, because folic acid is a coenzyme necessary for nuclear protein DNA and RNA synthesis, in the central nervous system, folic acid deficiency or Metabolic disorders can make RNA synthesis disorder, and RNA plays an important role in protein synthesis. The protein synthesis in the central nervous system is fast. Because neurons require abundant energy and transmitters, they lack energy and neurotransmitter synthesis. Symptoms of neurological damage appear in the clinic, and there is no more detailed information on folic acid deficiency.

Prevention

Folic acid deficiency neuropathy prevention

In nature, 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. Reasonable diet and health care during pregnancy, perinatal period and infant feeding period.

Complication

Folic acid deficiency neuropathy Complications dementia spina bifida

Folic acid deficiency has a variety of clinical manifestations, depending on the degree of folic acid deficiency, the performance is different, that is, complications other than nervous system damage.

Symptom

Folic acid deficiency neuropathy symptoms common symptoms inflammatory dynamism disorder cerebellar ataxia nystagmus reflexes hyperactivity dementia

1. The performance of nervous system damage is more severe in patients with severe folate deficiency

(1) Cerebellar and spinal cord damage: folic acid deficiency can cause obvious nystagmus, ataxia and other symptoms of cerebellar damage, limb weakness and deep sensory loss in spinal cord injury, closed eyes difficult to stand, physical examination, hyperreflexia and Babin The performance of subacute spinal cord combined degeneration such as sigma positive.

(2) Peripheral neuropathy: The symptoms of peripheral neuropathy in the absence of folic acid are characterized by a decrease in the "glove" and "socks" of the distal extremities of the limbs, and the sputum reflexes are dull, and the distal end of the limbs may have numbness, tingling and burning sensation. Electromyography showed signs of neuronal damage, and electrophysiological examination showed that both sensory conduction velocity and motor conduction velocity were slow.

(3) Psychiatric symptoms: Folic acid deficiency is characterized by irritability, forgetfulness and insomnia. When folic acid deficiency causes megaloblastic anemia, mental confusion, dementia, and disorientation disorder occur. When patients with epilepsy take anti-epileptic drugs for a long time, the folic acid content is reduced. It is characterized by mental retardation, indifference, lack of energy, and lack of initiative in language.

2. Other clinical manifestations of folate deficiency

(1) causing megaloblastic anemia.

(2) Causes fetal neural tube defects: In a randomized controlled clinical trial, intervention with folic acid-containing nutritional supplements prior to conception can effectively and significantly reduce infant neural tube defects (spine spine and brainless) The occurrence of another randomized and controlled trial also showed that if a woman who had previously had a child with a neural tube defect had given a large dose of folic acid (4 mg/d) before she became pregnant again, it could effectively prevent the next child from happening. Neural tube defects, but the mechanism by which folic acid intake can prevent 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 of infants. It is reported that serum and erythrocyte folate levels (especially erythrocyte folate levels) can be observed in pregnant women at 3 months. As a predictor of neonatal birth weight, folic acid levels in pregnant mothers are associated with abortion, the incidence of preterm birth, high levels of folate, and low incidence.

(4) Folic acid and cardiovascular disease: After folate forms 5-methylTHF, 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 Homocysteine damages vascular endothelial cells and activates platelet adhesion and aggregation, which is a risk factor for cardiovascular disease. Adequate folate intake has a certain preventive effect on cardiovascular disease.

A reliable evidence for folate deficiency is the determination of serum folic acid, which has a normal serum folate level of 13.4 to 47.67 nmoL/L. If it is lower than 6.8 nmoL/L, folate deficiency can be diagnosed.

Examine

Folic acid deficiency neurological examination

1. The serum folic acid content reflects the recent dietary folate intake, which is less than 6.8 nmol/L (3 ng/ml).

2. The folate content of red blood cells reflects the storage of folic acid in the body, which is less than 318 nmol/L (140 ng/ml).

3. Histidine load test After oral administration of histidine load for 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. Plasma homocysteine determination When the subjects' vitamin B6 and B12 are properly nutritious and folic acid is deficient, the level of homocysteine is increased.

5. The nervous system CT and MRI have differential diagnosis significance for central nervous system damage.

Diagnosis

Diagnosis and identification of folic acid deficiency neuropathy

diagnosis

The auxiliary diagnostic indicator has a histidine load test, and a positive responder is helpful for diagnosis.

Differential diagnosis

Clinically, multiple peripheral neuropathy with unknown etiology, cerebellar and myelopathy, mental retardation and dementia, organic mental disorder and long-term use of anti-epileptic drugs, infants with unexplained mental and neurological symptoms, determination Serum folic acid is helpful in differential diagnosis.

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