Vitamin E deficiency

Introduction Vitamin E (tocopherol) is a generic term for a class of compounds with one color full ring, one isoprenoid side chain, and alpha-tocopherol bioactivity. Vitamin E family includes -, -, - and -tocopherol, which varies to some extent with the methylation of the color-filled ring. D-alpha-tocopherol is the only naturally occurring stereoisomer, and the biological assay has the highest potency (1.49 IU/mg); The fully synthesized racemic-alpha tocopherol is completely racemic and its biological activity is smaller than that of dextro--tocopherol (1.1 IU/mg). The international standard is racemic--tocopherol acetate ( 1.0 IU/mg). In summary, tocopherol acts like an antioxidant to prevent lipid peroxidation of polyunsaturated fatty acids on cell membranes. Antioxidant activity of alpha-tocopherol and glutathione containing selenium Peroxidase is similar (see Section 4 Selenium). Human plasma tocopherol levels vary with total plasma lipid levels, which affects the division of plasma and adipose tissue, which is the main reservoir of tocopherol. Normal Plasma alpha-tocopherol levels ranged from 5 to 10 g/ml (11.6 to 23.2 mol/L).

Cause

Reasons for vitamin E deficiency:

The baby is born in a state of relative vitamin E deficiency, and the plasma alpha-tocopherol level is lower than 5 g/ml (11.6 mol/L). The smaller and the earlier the baby is, the greater the deficiency. The vitamin deficiency of premature infants lasts after birth. In the first few weeks, this is due to limited transfer of vitamin E placenta, low tissue concentration at birth, lack of relative diet in the baby, malabsorption of the small intestine, and rapid growth. The digestive system is mature, vitamin E absorption is improved, and blood vitamin levels are improved. It has also improved. Malabsorption in children and adults generally causes vitamin E deficiency. Genetic abnormalities in vitamin E transport can also play a role.

an examination

Related inspection

Vitamin E Vitamin E (VitE, VE)

Premature infant hemolytic anemia can be a manifestation of vitamin E deficiency. Such infant hemoglobin levels range from 7 to 9 g/dl, plasma vitamin E levels are low, reticulocytes increase and blood bilirubin is excessive. No beta lipids Proteinemia (Bassen-Kornzweig syndrome), due to loss of apo-lipoprotein B gene, causes severe fat malabsorption and fatty spasm, with progressive neuropathy and retinopathy in the first 20 days after birth (see section 16) Children with chronic cholestatic hepatobiliary disease or cystic fibrosis present with vitamin E deficiency syndrome. Its signs are spinal cord cerebellar ataxia with deep sputum reflexes, torso and limbs ataxia, vibration and location. Feelings disappear, eye muscle paralysis, muscle weakness, ptosis and dysarthria. In adults with malabsorption, spinal cord cerebellar ataxia due to vitamin E deficiency is extremely rare. There is no doubt that there are a large number of adult fat tissue Vitamin E stocks. The clinical characteristics of vitamin E deficiency are listed in Table 3-3. Rare fat-free malabsorption of vitamin E genotype patients, the liver seems to lack normal when dextran--tocopherol from the liver VLDL transported to a protein and thus can not maintain normal plasma - tocopherol levels.

Laboratory examination and diagnosis

Premature infants lacking vitamin E have muscle weakness, creatineuria, and necrotic waxy pigmentation in muscle biopsy. Increased peroxide hemolysis is also observed. Plasma tocopherol levels <4g/ml (<9.28mol/L) Adults with plasma tocopherol levels <5g/ml (<11.6mol/L) and red blood cells sensitive to hydrogen peroxide can be considered as vitamin E deficiency. If there is hyperlipidemia, -tocopherol level rises High, when the tocopherol level is <0.7mg / g (<1.6mol / g) plasma fat, that is equivalent to <5g / ml (<11.6mol / L) of normal blood lipids, can be diagnosed as lack. Vitamin E deficiency Excess creatineuria and elevated levels of plasma creatine phosphokinase may occur in a creatinine-free diet. Patients with myeloid encephalopathy may have a large axon-medullary axon that may disappear and the posterior horn of the spinal cord may be degenerated.

Differential diagnosis

Differential diagnosis of vitamin E deficiency:

Lack of vitamin A:

There are concave lines in the nails, itchy skin, peeling, rough hair, tears in the eyes, blurred vision, night blindness, dry eye inflammation, hair loss, memory loss, confusion, low sexual desire. Therefore, you should eat more salmon, halibut, shark, cod liver oil, chicken, sheep, liver, egg yolk, butter, margarine, cheese, citrus, jujube, sweet potato, carrot, parsley, leeks, leeks, spinach, day lily, lettuce leaves, Tomatoes, beans and other foods rich in vitamin A, of which chicken liver contains the highest vitamin A.

Lack of vitamin B1:

Beriberi, indigestion, poor color, allergic to sound, occasional pain in the calf, constipation, anorexia, vomiting in severe cases, edema of limbs, etc. Therefore, we must pay attention to eat more pork, animal liver and kidney, whole milk powder, millet, corn, beans, peanuts, nuts, pumpkin, loofah, bayberry, seaweed and other foods containing more vitamin B1, of which peanuts contain vitamin Bl .

Lack of vitamin B2:

The mouth is ulcerated, the nose is red and swollen, insomnia, headache, mental fatigue, eyesight, light on the cornea, oily skin, increased dandruff, and burning heart and heart. Therefore, it is necessary to eat more animal liver and heart, chicken, eggs, milk, soybeans, black fungus, green vegetables and other foods containing high vitamin B2. The liver of the animal liver contains vitamin B2 in the food.

Lack of vitamin B3:

Tongue swelling, bad breath. Therefore, you should eat more lean meat, beef liver and other foods.

Lack of vitamin B6:

The lips and tongue are swollen, the mucous membranes are dry, the muscles are paralyzed, and the pregnant woman is overly nausea and vomiting. Eat more potatoes, pumpkins, beer and other foods.

Lack of vitamin B12:

Rough skin, thin hair, loss of appetite, vomiting, diarrhea, tingling in fingers and toes. It is advisable to eat fish, shrimp, poultry, eggs and various animal livers.

Lack of vitamin C:

Osteoporosis and dentin are loose, the wound is difficult to heal, the gums are bleeding, the tongue has deep marks, can not adapt to environmental changes, is prone to colds, microvascular rupture, severe sepsis. Pay attention to eat more fresh dates, hawthorn, citrus, kiwi, persimmon, mango, cucumber, white radish, loofah, tomato, spinach, coriander, leeks, bean sprouts and other foods rich in vitamin C, including fresh dates in the fruit Contains the highest vitamin C.

Lack of vitamin D:

Rickets, softening the disease, often sweating on the head. The foods that should be eaten more are fish and shrimp, egg yolk, dairy products, mushrooms, and eggplant.

Lack of vitamin E:

Muscle atrophy, dry scalp, split ends, easy to sweat, low sexual function, dysmenorrhea in women. Eat more meat, eggs, milk and their products, peanut oil, corn oil, sesame oil and other foods.

Lack of vitamin P:

Capillaries become brittle and break bleeding, atherosclerosis. Eat more buckwheat, cowpea, lentils, apricots, grapes, eggplant, celery and other foods. Premature infant hemolytic anemia can be a manifestation of vitamin E deficiency. Such infant hemoglobin levels range from 7 to 9 g/dl, plasma vitamin E levels are low, reticular cells increase, and blood bilirubin is excessive.

No beta lipoproteinemia (Bassen-Kornzweig syndrome), due to loss of the apolipoprotein B gene, causes severe fat malabsorption and fatty spasm, and is associated with progressive neuropathy and retinopathy in the first 20 days after birth.

Children with chronic cholestatic hepatobiliary disease or cystic fibrosis present with vitamin E deficiency syndrome. Its signs are spinal cord cerebellar ataxia with deep sputum reflexes, torso and limbs ataxia, loss of vibration and positional sensation, ocular paralysis, muscle weakness, ptosis and dysarthria. In adults with malabsorption, spinal cord cerebellar ataxia due to vitamin E deficiency is extremely rare. There is no doubt that there is a large amount of vitamin E stock in adult fat tissue.

A rare form of vitamin E genotype with no fat malabsorption, the liver appears to lack a protein that normally transports dextro--tocopherol from hepatocytes to very low-density lipoprotein, thus failing to maintain normal plasma alpha-tocopherol Level.

The disease caused by vitamin E deficiency varies greatly according to species. Lack can cause reproductive disorders; muscle, liver, bone marrow and brain dysfunction; red blood cell hemolysis; embryogenesis defects; and exudative quality, which is a capillary permeability Obstruction can produce skeletal muscle atrophy, in some species, with myocardial lesions. The main manifestations of human vitamin E deficiency are: (1) mild hemolytic anemia caused by red blood cell hemolysis. (2) spinal cerebellar disease (see section 179) Cerebellum and spinal cord encephalopathy), which is mainly found in children, is due to no beta lipoproteinemia, chronic cholestatic hepatobiliary disease, celiac disease or a genetic abnormality of vitamin E metabolism and fat malabsorption. Premature retinopathy Also known as post-lens fibrous tissue formation (see Section 260 Premature Retinopathy) can be improved with vitamin E. Similarly, some cases of neonatal intraventricular and subependymal hemorrhage can be improved.

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