Fat-soluble vitamin deficiency
Introduction
Introduction Fat-soluble vitamins include vitamins A, D, E, and K, which are insoluble in water and soluble in lipids and fatty solvents. Fat-soluble vitamins coexist in the food with lipids and are absorbed along with the lipids. The absorbed fat-soluble vitamin is transported in the blood by specifically binding to lipoproteins and certain specific binding proteins. The fat-soluble vitamins A, D, E, and K have certain biological functions, and once they are lacking, the corresponding symptoms will appear.
Cause
Cause
There are many reasons for the occurrence of vitamin deficiency, but with the progress of society and the development of science, the typical vitamin deficiency such as night blindness, scurvy, beriberi and so on are rare. In addition to the effects of the disease, in the current social situation, the cause of vitamin deficiency is not due to poverty in life, but mostly due to insufficient scientific knowledge of nutrition and health, as follows:
(1) Insufficient intake of vitamins
Unreasonable food composition and dietary allocation or severe partial eclipse may result in insufficient supply of certain vitamins; or improper storage, processing and cooking of food may result in substantial destruction and loss of vitamins. Excessive rice scouring, cooking porridge with alkali, flour processing too fine, can make a lot of vitamin B loss and destruction; vitamins in fried pasta are also destroyed; fresh food storage for too long, vitamin C can be destroyed; vegetables cut first, then wash , stir fry or add alkali, and almost all of the vitamin C is lost.
(two) vitamin absorption disorder
More common in patients with digestive tract diseases. Obstacles such as lipid digestion and absorption can seriously reduce the absorption of fat-soluble vitamins.
(3) Increase in demand
The body's need for vitamins is particularly increased under certain physiological or pathological conditions. If not added in time, it will cause relatively insufficient vitamins. Such as children in growth and development, pregnant women, nursing mothers, heavy manual workers or infectious diseases.
(4) Insufficient supply of vitamins other than food
If long-term use of antibiotics can inhibit the growth of normal intestinal flora, which affects the synthesis of certain vitamins, such as vitamin K, B6, folic acid, PP, etc.; insufficient sun exposure can often cause insufficient production of vitamin D in the skin. This causes rickets in children or rickets in adults.
Examine
an examination
Related inspection
Fat Soluble Vitamins Vitamin A Vitamin A (VitA) Vitamin K (VitK, VK) Vitamin E
Vitamin A
1. Vitamin A is a substance that senses weak light in visual cells - the constituents of rhodopsin:
The visual pigment is composed of 11-cis retinal and different opsin in the visual cells. In the cone-shaped cells that feel strong light, there are red, opal, and blue, and the rod-shaped cells have rhodopsin that feel weak light or dark light. When rhodopsin is sensitive, 11-cis retinoic acid in the visual pigment is converted into all-trans retinal under the photoisomerism that occurs, and is separated from opsin and eclipsed. All-trans retinal can be slowly re-isomerized into 11-cis-retinal via isomerase, but most of it is reduced to all-trans retinol, which flows through the bloodstream to the liver to become 11-cis retinol, and then Then, the blood is returned to the retina and oxidized to 11-cis retinal to synthesize the visual pigment. In this visual cycle, some of the all-trans retinal is decomposed into useless substances, so vitamin A should be added frequently. The photoreceptor process of other visual pigments is the same as rhodopsin.
In the absence of vitamin A, it will inevitably cause insufficient supplementation of 11-cis retinoic acid, decrease in rhodopsin synthesis, decrease sensitivity to low light, and weaken sunlight adaptability. In severe cases, "night blindness" will occur.
2. Vitamin A is also essential for maintaining the structure and function of epithelial tissue:
When vitamin A is deficient, it can cause dryness, hyperplasia and keratinization of epithelial tissue, resulting in dry eye disease, dry skin, hair loss and the like.
3. Other effects: Vitamin A can promote the synthesis of mucopolysaccharides, glycoproteins and nucleic acids, thus promoting the growth of the body.
Vitamin D
The target cells of the biologically active 1,25-(OH)2-D3 are the small intestinal mucosa, the kidney and the renal tubules. The main role is to promote the absorption of calcium and phosphorus, which is conducive to bone formation and calcification. In the absence of vitamin D, children can develop rickets, and adults cause rickets.
Vitamin E
1. Vitamin E is the most important antioxidant in the body, can avoid the production of lipid peroxide, and protect the structure and function of biofilm. The free radicals in the body have strong oxidizing properties, such as superoxide anion radicals (O2-), peroxide radicals (ROO?), and hydroxyl radicals (OH?). The role of vitamin E is to capture free radicals to form tocopherol free radicals, which can be further reacted with another free radical to form a non-free radical product - fertility.
Selenium is an essential factor in glutathione peroxidase and is generally considered to be the second line of defense against peroxidation. Vitamin E and selenium work synergistically in this antioxidant process.
2. Vitamin E is commonly known as tocopherol. When animals lack vitamin E, their reproductive organs are impaired or even infertile, but humans have not found infertility caused by vitamin E deficiency. Vitamin E is commonly used clinically to treat threatened abortion and habitual abortion.
3. Promote heme metabolism. Neonatal deficiency of vitamin E can cause anemia, which may be related to decreased hemoglobin synthesis and shortened red blood cell life. Therefore, pregnant women, lactating women and newborns should pay attention to vitamin E supplementation. Vitamin E is generally not easy to be deficient, and can cause deficiency in certain diseases such as fat malabsorption. It is manifested by a decrease in the number of red blood cells, a shortened life span, an increase in erythrocyte fragility such as anemia in vitro, and occasionally a neurological disorder.
Vitamin K
The main biochemical role of vitamin K is to maintain the normal levels of Factor II, IX, and X in the body. The conversion of these coagulation factors from inactive to active requires that the 10 glutamic acid residues (Glu) of the precursor be carboxylated to become gamma-carboxyglutamic acid (Gla). Gla has a strong ability to bind Ca2+, thus transforming it into an active form. The catalyzed reaction is gamma-carboxylase, and vitamin K is a cofactor for the enzyme.
The daily vitamin K requirement for adults is 60-80 g, because vitamin K is widely distributed in animals and plants, and bacteria in the intestinal tract can also be synthesized, which is generally not easy to lack. However, because vitamin K can't pass through the placenta, there is no bacteria in the intestine after birth, so newborns may cause vitamin K deficiency. Vitamin K in normal children's blood may also be slightly lower, but eating can restore it to normal. The main symptom of vitamin K deficiency is prolonged clotting time. Long-term use of antibiotics and enteric sterilization can also cause vitamin K deficiency.
Diagnosis
Differential diagnosis
Differential diagnosis of fat-soluble vitamin deficiency:
1. Vitamin D deficiency: symptoms of vitamin D deficiency in the body due to dietary structure and sunshine.
2, vitamin C deficiency: scurvy (scurvy) is due to long-term lack of vitamin C (ascorbic acid, ascorbic acid) caused by the body disease, is currently rare, but in the northern pastoral areas lacking vegetables, fruits, or city, township Artificial feeding children neglect complementary food supplements, especially in remote areas of rural areas, which are still caused by improper feeding.
3, vitamin B1 deficiency: vitamin B1, thiamine (Thiamine), in vivo active type of thiamine pyrophosphate (TPP), in the absence of it, can cause a series of nervous system symptoms of the circulatory system, called beriberi .
4, vitamin K deficiency: vitamin K deficiency is due to the lack of vitamin K caused by coagulopathy.
5, vitamin B1 deficiency: vitamin B1, thiamine (Thiamine), in vivo active type of thiamine pyrophosphate (TPP), in the absence of it, can cause a series of nervous system symptoms of the circulatory system, called beriberi .
6. Vitamin E deficiency: Vitamin E (tocopherol) is a generic term for a class of compounds with one color full ring, one isoprenoid side chain, and alpha-tocopherol biological activity. 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 is most effective ( 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 and containment of alpha-tocopherol Selenium is similar to glutathione peroxidase. The level of human plasma tocopherol varies with total plasma lipid levels, which affects the division of plasma and adipose tissue. Adipose tissue is the main reservoir of tocopherol. Normal plasma The level of -tocopherol is 5~10g/ml (11.6~23.2mol/L). The disease caused by vitamin E deficiency varies greatly according to species. Lack can cause reproductive disorders; muscle , liver, bone marrow and brain dysfunction; erythrocyte hemolysis; embryogenesis defects; and exudative quality, which is a capillary osmotic disorder that can produce skeletal muscle atrophy, in some species, with myocardial lesions. The main manifestations of vitamin E deficiency are:
(1) Mild hemolytic anemia caused by hemolysis of red blood cells.
(2) Spinal encephalopathy. The disease is mainly seen in children 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 can be improved with vitamin E treatment. Similarly, some cases of neonatal intraventricular and subependymal hemorrhage can also be improved. Etiology, the baby is born in a state of relative vitamin E deficiency, plasma The level of -tocopherol is lower than 5g/ml (11.6mol/L). The smaller and more premature the baby, the greater the deficiency. The vitamin deficiency in premature infants lasts for the first few weeks after birth, which is attributed to vitamin E placental transport. Limited, low tissue concentration at birth, lack of relative diet for 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 also improved.
Malabsorption in children and adults generally causes vitamin E deficiency. Genetic abnormalities in vitamin E transport can also play a role.
Premature infant hemolytic anemia can be a manifestation of vitamin E deficiency. Such infants have hemoglobin levels in the range of 7 to 9 g/dl, low plasma vitamin E levels, increased reticular cells, and excessive blood bilirubin. No beta lipoproteinemia (Bassen-Kornzweig syndrome) due to apoxia Loss of lipoprotein B gene, causing severe fat malabsorption and fatty spasm, with progressive neuropathy and retinopathy in the first 20 days after birth, vitamin E in children with chronic cholestatic hepatic biliary tract disease or cystic fibrosis Lack of syndrome. Its signs are spinal cord cerebellar ataxia with deep sacral reflexes disappeared, torso and limbs ataxia, vibration and positional sensation disappeared, ophthalmoplegia, muscle weakness, ptosis and dysarthria. Adults, due to vitamin E deficiency, the spinal cerebellar ataxia is extremely rare. There is no doubt that there is a large amount of vitamin E stock in adult adipose tissue. Rare fat-free malabsorption of vitamin E genotype patients, the liver seems to be missing Normally, dextro--tocopherol is transported from hepatocytes to a protein of very low-density lipoprotein, and thus normal plasma alpha-tocopherol levels cannot be maintained.
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-myelinated axon that may disappear and the posterior horn of the spinal cord may be degenerated.
The preventive dose of -tocopherol is 0.5mg/kg for infants born in full-term, and 5-10mg/kg for premature infants. The obvious deficiency caused by malabsorption should be given 15~25mg/kg -tocopherol every day, orally mixed with water. D-A-tocopheryl acetate (1 mg = 1.4 IU). Larger dose (up to 100 mg/kg daily, oral mean) for the treatment of early neuropathy without beta lipoproteinemia or overcoming absorption and transport defects It is needed. These treatments can alleviate the symptoms of young patients and control the neuropathy of older patients. For genetic patients with vitamin E deficiency without fat malabsorption, high doses of alpha-tocopherol (100 to 200 IU per day) can improve the deficiency. And can prevent the sequelae of neuropathy.
Vitamin A
1. Vitamin A is a substance that senses weak light in visual cells - a component of rhodopsin
The visual pigment is composed of 11-cis retinal and different opsin in the visual cells. In the cone-shaped cells that feel strong light, there are red, opal, and blue, and the rod-shaped cells have rhodopsin that feel weak light or dark light. When rhodopsin is sensitive, 11-cis retinoic acid in the visual pigment is converted into all-trans retinal under the photoisomerism that occurs, and is separated from opsin and eclipsed. All-trans retinal can be slowly re-isomerized into 11-cis-retinal via isomerase, but most of it is reduced to all-trans retinol, which flows through the bloodstream to the liver to become 11-cis retinol, and then Then, the blood is returned to the retina and oxidized to 11-cis retinal to synthesize the visual pigment. In this visual cycle, some of the all-trans retinal is decomposed into useless substances, so vitamin A should be added frequently. The photoreceptor process of other visual pigments is the same as rhodopsin.
In the absence of vitamin A, it will inevitably cause insufficient supplementation of 11-cis retinoic acid, decrease in rhodopsin synthesis, decrease sensitivity to low light, and weaken sunlight adaptability. In severe cases, "night blindness" will occur.
2. Vitamin A is also a substance necessary to maintain the structure and function of epithelial tissues.
When vitamin A is deficient, it can cause dryness, hyperplasia and keratinization of epithelial tissue, resulting in dry eye disease, dry skin, hair loss and the like.
3. Other effects Vitamin A can promote the synthesis of mucopolysaccharides, glycoproteins and nucleic acids, thus promoting the growth of the body.
Vitamin D
The target cells of the biologically active 1,25-(OH)2-D3 are the small intestinal mucosa, the kidney and the renal tubules. The main role is to promote the absorption of calcium and phosphorus, which is conducive to bone formation and calcification. In the absence of vitamin D, children can develop rickets, and adults cause rickets.
Vitamin E
1. Vitamin E is the most important antioxidant in the body, can avoid the production of lipid peroxide, and protect the structure and function of biofilm. The free radicals in the body have strong oxidizing properties, such as superoxide anion radicals (O2-), peroxide radicals (ROO?), and hydroxyl radicals (OH?). The role of vitamin E is to capture free radicals to form tocopherol free radicals, which can be further reacted with another free radical to form a non-free radical product - fertility.
Selenium is an essential factor in glutathione peroxidase and is generally considered to be the second line of defense against peroxidation. Vitamin E and selenium work synergistically in this antioxidant process.
2. Vitamin E is commonly known as tocopherol. When animals lack vitamin E, their reproductive organs are impaired or even infertile, but humans have not found infertility caused by vitamin E deficiency. Vitamin E is commonly used clinically to treat threatened abortion and habitual abortion. 3. Promote heme metabolism. Neonatal deficiency of vitamin E can cause anemia, which may be related to decreased hemoglobin synthesis and shortened red blood cell life. Therefore, pregnant women, lactating women and newborns should pay attention to vitamin E supplementation. Vitamin E is generally not easy to be deficient, and can cause deficiency in certain diseases such as fat malabsorption. It is manifested by a decrease in the number of red blood cells, a shortened life span, an increase in erythrocyte fragility such as anemia in vitro, and occasionally a neurological disorder.
Vitamin K
The main biochemical role of vitamin K is to maintain the normal levels of Factor II, IX, and X in the body. The conversion of these coagulation factors from inactive to active requires that the 10 glutamic acid residues (Glu) of the precursor be carboxylated to become gamma-carboxyglutamic acid (Gla). Gla has a strong ability to bind Ca2+, thus transforming it into an active form. The catalyzed reaction is gamma-carboxylase, and vitamin K is a cofactor for the enzyme. The daily vitamin K requirement for adults is 60-80 g, because vitamin K is widely distributed in animals and plants, and bacteria in the intestinal tract can also be synthesized, which is generally not easy to lack.
However, because vitamin K can't pass through the placenta, there is no bacteria in the intestine after birth, so newborns may cause vitamin K deficiency. Vitamin K in normal children's blood may also be slightly lower, but eating can restore it to normal. The main symptom of vitamin K deficiency is prolonged clotting time. Long-term use of antibiotics and enteric sterilization can also cause vitamin K deficiency.
