Vitamin A deficiency in children
Introduction
Introduction to vitamin A deficiency in children Vitamin A deficiency (vitamin Adeficiency) is a systemic disease mainly caused by the lack of vitamin A in the body, which is mainly caused by infants and young children. It often coexists with malnutrition, accompanied by protein-energy malnutrition. Vitamin A has many important functions in the body. It plays an important role in the function of the retina. It is obviously necessary for the growth and differentiation of epithelial tissues, and is also required for bone growth, reproduction and embryonic development. It also has a stable effect on various cell membranes. Thereby adjusting the permeability of the membrane. The function of vitamin A is achieved by different molecular forms, and visual effects are retinal. Retinol acts on the reproductive process, while retinoic acid or a metabolite is important for other functions. basic knowledge Sickness ratio: 0.1% Susceptible people: children Mode of infection: non-infectious Complications: corneal ulcer conjunctivitis hydrocephalus
Cause
The cause of vitamin A deficiency in children
(1) Causes of the disease
1. Vitamin A and Vitamin A deficiency Vitamin A is fat-soluble and exists in food in two forms: mainly retinol or vitamin A, present in liver, fat, milk and egg yolk of animals; Carotene, also known as vitamin A, is found in plants. It is most important for beta carotene. Yellow-red vegetables such as carrots, sweet potatoes, pumpkins, tomatoes, and persimmons are the most abundant. Carotene can be converted into vitamin A in small intestinal mucosa and liver cells. For human application, vitamin A is absorbed in the intestines depending on the presence of fat and bile, stored in the liver, and converted to vitamin A in the liver.
Vitamin A and carotene are insoluble in water, stable in oil, heat, acid, alkali; vitamin E, C and other antioxidants can enhance its stability, human vitamin A is mainly derived from food, animal food in the liver The content is the most, followed by milk and egg yolk. In plant foods, carrots, tomatoes, sweet potatoes, pumpkins, beans, green leafy vegetables and bananas, persimmons, peaches and other carotenoids (precursors of vitamin A) are abundant.
Primary vitamin A deficiency, usually caused by long-term lack of diet, mainly due to inadequate diet, so vitamin A deficiency is often associated with protein-thermal malnutrition (marasmus or kwashiorkor), vitamin A deficiency is the lack of carotene Endemic epidemics in South Asia and East Asia, where rice is the staple food.
The cause of secondary vitamin A deficiency may be insufficient conversion of carotene, or the absorption, storage or transport of vitamin A is disturbed, because the storage and transport of vitamin A is defective, and absorption or storage disorders may occur in abdominal diseases. Such as diarrhea, hepatobiliary disease, gallbladder fibrosis, pancreatic disease, duodenal shunt, congenital jejunal obstruction, bile duct obstruction, giardiasis and cirrhosis; increased demand such as high fever, severe infection, etc. It also causes a deficiency of secondary vitamin A.
2. The main function of vitamin A
(1) Photosensitive substances in the visual cells: rhodopsin in the retinal stem cells, lack of vitamin A can affect the synthesis of rhodopsin, resulting in visual impairment under dark or weak light, and night blindness.
(2) Maintain the integrity of epithelial cells: When vitamin A is deficient, epithelial cells proliferate in the surface of keratinized desquamation, sebaceous glands and sweat glands are atrophied, the ability to defend against pathogens is reduced, hair is dry, and nails become brittle.
(3) Promote growth and development: Vitamin A promotes the synthesis of mucopolysaccharides such as chondroitin sulfate. When it is lacking, it will affect the growth and development of bone tissue.
(4) Effects on immune function: Vitamin A is an immunostimulant. When it is lacking, both cellular immunity and humoral immunity are reduced, and it is highly susceptible to respiratory and digestive tract infections.
(5) Others: For example, vitamin A has a certain effect on maintaining the normal function of the reproductive system; beta carotene can alleviate the sensitivity of children with porphyria to light, thereby alleviating symptoms.
3. The cause of vitamin A deficiency
(1) Insufficient intake: Vitamin A is rarely stored in the liver at birth. The main source of vitamin A after birth is food. Vitamin A is abundant in breast milk. Vitamin A deficiency does not occur in breast-feeding children. Therefore, during the baby period, breastfeeding should be promoted. When artificial feeding, fat-containing milk should be given. If the baby is fed by condensed milk, skim milk, soy milk, rice flour and other foods, it is prone to vitamin A deficiency. Vitamin A in the liver of premature infants. Less storage, limited fat absorption capacity, faster growth and development, it is more prone to vitamin A deficiency, such as long-term intravenous rehydration without vitamin A in the disease state, or because of dietary restrictions, Will lead to vitamin A deficiency.
(2) Reduced absorption: Vitamin A deficiency can be seen in a variety of clinical conditions, such as malabsorption syndrome, chronic diarrhea, chronic dysentery, chronic hepatitis, biliary obstruction, gallbladder fibrosis, hookworm disease, intestinal infection, etc. can affect vitamins Absorption of A.
(3) Increased consumption: When zinc deficiency is insufficient, vitamin A can not be used and excreted, resulting in vitamin A deficiency. When children suffer from tuberculosis, measles, chickenpox, pneumonia and high fever, the consumption of vitamin A increases. Failure to replenish in time resulted in a decrease in the plasma concentration of vitamin A.
(4) use of obstacles: such as children with liver, kidney, thyroid disease, pancreatic cystic fibrosis and protein-energy malnutrition will lead to abnormal metabolism of plasma retinol binding protein (RBP), leading to vitamin A deficiency.
(5) premature infants: due to insufficient storage of vitamin A in the liver, the absorption capacity of fat at the time of birth is poor, coupled with rapid growth and development, prone to vitamin A deficiency.
(two) pathogenesis
Vitamin A is a light yellow oil solution, which is unscented and oily. It is unstable to light and air, but it is not easily oxidized and degraded by air in oil solution. It should be stored between 15 and 30 °C, and should not exceed 40 °C. Vitamin A The original compound is all-trans retinol. Natural vitamin A is only found in animals and is divided into two types: vitamin A1 (retinol) and vitamin A2 (3-dehydroretinol). Insufficient, rapid growth and development, in the disease state, increased consumption of vitamin A and vitamin A absorption, utilization disorders, as well as zinc deficiency, iron deficiency, protein-energy malnutrition lead to plasma retinol binding protein (RBP) Metabolic abnormalities, vitamin A binding protein, prealbumin, vitamin A reductase are reduced, so that vitamin A can not be used to excrete, while limiting the bioavailability of vitamin A, leading to vitamin A deficiency.
Insufficient vitamin A in the blood will affect the regeneration of rhodopsin and its photochemical reaction, and cause night blindness. In addition, vitamin A can maintain the normal structure of epithelial cells, and can cause epithelial hyperplasia, surface keratinization and desquamation. , often involving the eye, trachea, digestive tract, urinary tract and other mucous membranes and whole body skin, prone to diarrhea, respiratory infections, etc., the possible role of vitamin A also includes maintaining the stability of lysosomes and participating in the synthesis of mucopolysaccharides and proteins Wait.
Prevention
Prevention of vitamin A deficiency in children
Vitamin A can be stored in the body and does not need to be replenished daily. The recommended daily intake of vitamin A is 1000RE (or 5000U) to prevent deficiencies in adults, and 800RE (4000U) for women during pregnancy. The latest recommended intake is not recommended to increase, but if during lactation, an additional 500RE (or 2500U) can be added in the first 6 months, and an additional 400 RE (or 2000U) in the next 6 months. During pregnancy and lactation, mothers should pay attention to vitamin A supplementation during pregnancy and lactation to prevent vitamin A deficiency. For example, if taking vitamin A preparation, the preventive or therapeutic dose should not exceed 2 times RDA, so as to avoid damage to the fetus.
Complication
Pediatric vitamin A deficiency complications Complications corneal ulcer conjunctivitis hydrocephalus
1. Eye complications due to dry eye syndrome with conjunctivitis, corneal ulcers, corneal leukoplakia; such as perforation, iris lens prolapse, infection, can be blind, in most developing countries, vitamin A deficiency is still blind for young children main reason.
2. The body's resistance to infection is reduced, and it is easy to re-infect, especially in the respiratory tract, and pus can also occur.
3. The nervous system can cause mental, mental disorders, and even hydrocephalus.
4. Skeletal system enamel dysplasia and affect bone development.
Symptom
Symptoms of vitamin A deficiency in children Common symptoms Horny conjunctival dry skin Rough eye dry photophobia night blind vision deformation secondary infection visual impairment fat-soluble vitamin deficiency conjunctival dry spots
In the absence of vitamin A, growth retardation in children is a common sign, and the performance of various organs of the body is as follows:
1. Eye symptoms and signs
Due to the lack of vitamin A and vitamin A deficiency, specific changes are limited to the eye, corneal softening characterized by dryness, ulceration, cornea and membrane dryness, as acute symptoms are seen in severely lacking food. Young children, usually with ophthalmia and bitot spots, are the leading signs of severe visual impairment and even blindness.
(1) Early stage: Firstly, the dark adaptation ability decreases firstly. The initial dark adaptation time is prolonged. Afterwards, the visual acuity declines under dark light. At dusk, the visually unclear vision develops into night blindness. In small infants, this symptom is not obvious. If you do not observe it carefully, it is easy to be ignored. First, it is discovered by the mother that the child is quiet in the dark environment, unclear, walking, and difficult to orient.
(2) Drying of the conjunctiva: dry eye discomfort, frequent blinking, conjunctival dryness caused by the occlusion of the epithelial cells of the lacrimal duct, which causes the tears to decrease, and then the conjunctiva loses luster and elasticity, mainly due to the proliferation of the conjunctiva and nearby glandular tissues. The secretion is reduced and then dried. When the eyeball rotates to both sides, the conjunctiva folds to form a wrinkle circle concentric with the cornea. At the exposed part of the bulbar conjunctiva, outside the corneal sclera near the limbus, the exfoliated corneal epithelium, epithelial debris and secretions The superficial triangular white foam-like plaque formed is not easy to wipe off. It is called Bitot spot. When it occurs in young children and has other manifestations of vitamin A deficiency, it is likely to be caused by vitamin A deficiency. Caused by it.
(3) corneal dryness: if vitamin A continues to be deficient, conjunctival xerosis occurs after several weeks and months, and corneal dryness will occur, the cornea will dry, infiltrate and begin to blur, photophobia, and subsequent visual distortion, accompanied by The meibomian glands are swollen, and a series of characteristic blisters appear along the rim, and the continuity of the surface epithelium is destroyed, accompanied by non-inflammatory ulcer formation and matrix infiltration, and corneal softening occurs rapidly, with some or all Corneal liquefaction, degeneration, the result of corneal ulcers occurs in the late stage of vitamin A deficiency, easy to secondary infection, can leave white spots after healing, affecting vision; severe perforation, even rupture and other damage, the contents of the eyeballs are squeezed out, The lens, the iris is prolapsed, and then the eyeball atrophy (eyeball palpebral) or anterior bulging of the eyeball (corneal displacement and anterior grape edema), eventually causing damage to the entire eye, leading to blindness, usually bilateral, unilateral morbidity is rare.
2. Skin changes
Skin symptoms are more common in older children. When vitamin A is deficient, sweat glands may appear atrophic and keratinized squamous cell metaplasia. At the beginning, the skin is more dry than normal, desquamation, and later due to hair follicle epithelial keratinization, involving hair follicles and sebaceous glands. The keratin is stuffed in the hair follicle and protrudes from the leather surface to form a papule, which looks like a "chicken skin". It has a rough feeling, especially in the limbs. The skin lesions are first seen on the upper side, the lower limbs are stretched out, and later on other parts, mainly distributed in the thighs. The anterior lateral side, the posterior side of the upper arm, and then gradually extended to the extension of the upper and lower limbs, the shoulder and the lower abdomen, rarely involving the chest, back and buttocks, the papules are firm and dry, the color is dark brown, mostly follicular, and the needle is large to large grain. Conical, the center of the papule has a thorny horny plug, hard to touch, leaving a pit-like depression after removal, no inflammation, no subjective symptoms, dense papules like molting, called phrynoderma, rash occurs in the face There are many blackheads.
The patient's hair is dry, lacks luster, easy to fall off, is diffuse and sparse, and the nail is thin and thin. The surface has vertical and horizontal grooves or dot-like depressions, which are easy to break.
3. Skeletal changes
Vitamin A deficiency also has a significant effect on the elongation of bones, especially long bones, making the bones shorter and thicker. The concentration of vitamin A is determined by chromatography, which proves that vitamin A concentration and body weight and BMI have statistical significance. Vitamin A has a significant impact on the growth and development of children. The child's physical and intellectual development is mildly backward, often accompanied by malnutrition, anemia and other vitamin deficiency, and enamel dysplasia.
4. Respiratory system
When vitamin A is deficient, it also affects the respiratory system to varying degrees, causing the cells in the middle layer of the epithelial cells of the trachea and bronchi to proliferate, becoming scaly, keratinized, and causing the cilia of the epithelial cells to fall off, and the mucous secretion of the bronchial respiratory epithelium becomes For keratinization, the normal protective function of epithelial tissue is lost, respiratory infection is prone to occur, and the elasticity of lungs and other tissues is also reduced, which often causes respiratory infections in children. A large amount of literature at home and abroad confirms that children lack vitamins. A is one of the most important causes of repeated respiratory infections in children. Clinical practice has also confirmed that vitamin A is effective in preventing and treating repeated respiratory infections in children.
5. The gastrointestinal tract
People with vitamin A deficiency often have taste and olfactory disorders, which is undoubtedly caused by keratinization. The intestinal mucosa shows that the goblet cells are greatly reduced, but not keratinized, intestinal epithelial deformation and pancreatic duct epithelial metaplasia are common. It is associated with diarrhea that is occasionally seen during vitamin A deficiency.
6. Other
Vitamin A deficiency can make children's immunity low, easy to recurrent infection, often accompanied by respiratory, digestive and urinary tract infections; easy to have mental disorders, and even hydrocephalus, hearing can also be reduced.
Genitourinary disorders, often associated with urinary calculi in vitamin A deficiency, reproductive abnormalities include spermatogenesis disorders, testicular degeneration, miscarriage and fetal malformations.
Examine
Pediatric vitamin A deficiency check
Laboratory inspection
1. Determination of serum vitamin A level is a common indicator for evaluating the nutritional status of vitamin A. It is also the most reliable indicator. Except for the history of insufficient intake of vitamin A, there is no indication of vitamin A depletion in the preclinical stage, and liver storage has been At the time of depletion, plasma retinol levels decreased.
The normal range of plasma vitamin A in normal fasting is 20 ~ 80g / dl (0.70 ~ 2.8mol / L); 10 ~ 19g / dl (0.35 ~ 0.66mol / L) is lower, and <10g / dl (<0.35mol / L) is a deficiency, the diagnosis of the disease can be confirmed, the average plasma retinol binding protein (RBP) of adult men is 47g / ml, women are 42g / ml, before the age of 10, this range is 20 ~ 30g / ml, lack Plasma vitamin A is reduced in state and acute infection.
2. Plasma retinol binding protein assay (RBP) Recently, it has been suggested that RBP is positively correlated with human vitamin A levels. The RBP content can reflect the nutritional level of human vitamin A. The plasma RBP content of normal children is 23.1 mg/L.
3. Relative dose response test When the serum vitamin A concentration is within the normal range, the liver vitamin A may be depleted. Therefore, the relative dose reation (RDR) method of vitamin A is used to indirectly evaluate the vitamin A in the individual. The amount of storage.
METHODS: Oral 1000 mg of vitamin A palmitic acid was administered, and serum vitamin A concentration was measured before oral administration and 5 hours after oral administration. If 5 hours after administration, the RDR rate was 20%, indicating that the storage of vitamin A in the liver was at a critical state. Further determine the subclinical status of vitamin A deficiency.
4. Mid-stage urine examination in the middle of the urine for epithelial cell count, vitamin A deficiency is increased, the degree of epithelial keratinosis is more visible under high power microscope.
Film degree exam
1. Visual dark adaptation function The earliest change dysfunction can be detected by dark adaptation measurement, dark spot measurement or retinal current tracing. These detection methods require patient cooperation.
Patients with vitamin A deficiency have poorer dark adaptation ability than normal people, but other factors can also cause dark adaptation, such as optic atrophy, retinitis pigmentosa, and lack of sleep.
2. Conjunctival keratinocyte epithelial examination The children's eyelids were exposed for 4 to 5 minutes separately, and the cotton swabs were used to wash the saline, and the keratinocytes were visually observed under the microscope.
Diagnosis
Diagnosis and differential diagnosis of vitamin A deficiency in children
diagnosis
In combination with feeding history and eye or skin symptoms, the diagnosis is generally not difficult. In addition, when vitamin A is deficient, the urinary system epithelial cells also have lesions. In the urine sediment examination, more epithelial cells are often keratinized, or often A secondary infection is associated with the diagnosis of this disease.
1. History and symptoms Careful inquiry of medical history, such as patients with insufficient intake of vitamin A, or the presence of vitamin A absorption, utilization disorders, or diseases that cause excessive consumption of vitamin A, while dark adaptation disorders, night blindness, conjunctival dryness, cornea Soften, or have follicular keratotic papules on the extremities.
2. Corresponding examinations can be basically diagnosed by dark-adapted examination and determination of plasma vitamin A concentration. If serum vitamin A levels are at normal low values, the storage of vitamin A in the liver may also be exhausted, in this suspicious case. Sensitive and reliable relative dose response tests can be used to further determine the lack of subclinical vitamin A, try to diagnose as early as possible, treat as early as possible, and prevent serious consequences.
Differential diagnosis
Other causes of night blindness, such as retinitis pigmentation, must be ruled out, secondary infection can worsen corneal changes, and the therapeutic dose of vitamin A can help diagnose.
(l) Temporary night blindness. Due to the lack of vitamin A in the diet or the absorption of vitamin A due to certain digestive diseases, the retinal rod cells do not synthesize rhodopsin, which causes night blindness. This night blindness is temporary. As long as you eat more pig liver, carrots, cod liver oil, etc., you can supplement the deficiency of vitamin A and will soon heal.
(2) Acquired night blindness. Often caused by malnutrition of the retinal rod cells or its own pathology. Common in diffuse choroiditis, extensive choroidal ischemia and atrophy, such night blindness gradually improved with effective treatment and disease healing.
(3) Congenital night blindness. It is a congenital hereditary eye disease, such as retinitis pigmentosa, rod cell dysplasia, loss of the function of synthesizing rhodopsin, so night blindness occurs.
