Vitamin A deficiency is a pathological condition caused by insufficient intake or impaired absorption of retinol. It is manifested by hemeralopia, hyperkeratosis, thinning of nails, hair loss, a tendency to pustular skin lesions, frequent respiratory infections. It is diagnosed by determining the concentration of retinol in blood plasma, ophthalmological examination, radiography, endoscopy of the gastrointestinal tract. The treatment regimen includes diet therapy, taking monopreparations of vitamin A, vitamin and mineral complexes, etiopathogenetic therapy of the disease that caused retinol deficiency.
ICD 10
E50 Vitamin A deficiency
Meaning
In developed countries, vitamin A deficiency (hypovitaminosis a) is a relatively rare disease, which is associated with the nutritional value of most residents. Being a fat-soluble vitamin, retinol, with its sufficient intake into the body, accumulates by the liver. The created reserve, even with the complete exclusion of vitamin A products from the diet, is enough to meet the needs of the body for 2-3 years. In developing countries with low incomes of citizens, retinol deficiency caused by alimentary factors is a common severe pathology that develops mainly in children and becomes one of the key causes of acquired blindness.
Vitamin A deficiency causes
The occurrence of the disease may be associated with a violation of any stage of vitamin A metabolism: intake into the body with food, biological transformation, transportation, assimilation in sensitive tissues. In most patients, retinol insufficiency is acquired in nature. According to the observations of gastroenterologists, the main causes of vitamin A deficiency are:
- Unbalanced nutrition. The biosynthesis of retinol and its precursors does not occur in the human body. Therefore, hypovitaminosis most often occurs in patients whose diet contains few foods containing vitamin A and its vitamers (carotene, retinoic acid, etc.). For the absorption of the compound, a sufficient amount of fats in the chyme is also necessary.
- Enteropathy. In patients suffering from intestinal enzymopathies, chronic pancreatitis, adductor loop syndrome, there is a deficiency of enzymes necessary for the breakdown of retinol esters, carotenoids. Vitamin B transport in epithelial cells is disrupted in irritable bowel syndrome, intestinal lymphangiectasia, and other diseases of the small intestine.
- Hepatobiliary pathology. The development of hypovitaminosis is caused by diseases that cause biliary stasis and mechanical jaundice, in which the intake of bile necessary for the absorption of vitamin decreases. With hepatitis, fibrosis, cirrhosis of the liver, the depositing function of the organ suffers and the production of proteins necessary for retinol transport decreases.
- Increased consumption of vitamin A. An increased need for retinoids is observed with significant physical exertion, prolonged exposure to very low or high ambient temperatures, and chronic stress. Pregnant women, patients suffering from cancer and other serious diseases need to increase the daily dose of retinol.
Hereditary forms of Vitamin A deficiency are associated with an insufficient reaction of the patient’s tissues to the vitamin present in the body in normal amounts. Due to a decrease in the number, changes in the structure of the receptors, the flow of the compound into the cells is usually disrupted. The failure of the enzyme systems necessary for the use of vitamin is also possible.
Pathogenesis
The mechanism of development of Vitamin A deficiency is associated with a violation of the physiological processes in which this compound participates. Due to the insufficient amount of retinal, the process of transformation of the visual pigment is disrupted, which causes the destruction of rods, deterioration of twilight and night vision. With a further increase in vitamin deficiency, there is a functional failure of the cones responsible for color perception.
Prolonged vitamin deficiency leads to severe organic changes on the part of the organ of vision, including irreversible damage to the retina and optic nerves. With a low level of retinoic acid, the expression of genes that regulate the differentiation of epithelial cells and prevent metaplasia of glandular cells into the flat keratinizing epithelium is disrupted. Against the background of retinol hypovitaminosis, keratinization of the epithelial membranes of various organs occurs, accompanied by drying of the mucous membranes, deterioration of their barrier and other functions.
In patients with vitamin deficiency, the proliferation of lymphocytes slows down, especially T-killers, phagocytosis is inhibited, which potentiates a decrease in immunity. With insufficient biosynthesis of chondroitin sulfates, osteogenesis is disrupted. A decrease in the antioxidant effect of vitamin A is accompanied by an increase in lipid peroxidation, increased thrombosis.
Classification
The systematization of clinical forms of the disease is carried out taking into account its causes and the degree of retinol insufficiency. Depending on the origin, the deficiency is more often acquired and less often hereditary. Taking into account the leading etiological factor, there is a primary retinol deficiency caused by malnutrition, and a secondary one that arose against the background of another pathology. According to the severity of symptoms , specialists in the field of modern gastroenterology and dietetics distinguish 3 stages of vitamin deficiency:
- Stage I (prehypovitaminosis A). The decrease in the level of retinol is determined only in the laboratory. There are no clinical symptoms. To correct the condition, it is enough to enrich the diet with foods containing vitamin.
- Stage II (Vitamin A deficiency). It is characterized by an uncomplicated course, mainly with ophthalmological and dermatological symptoms, mild immunodeficiency. Oral administration of retinol is recommended.
- Stage III (beriberi A). Against the background of a significant retinol deficiency, multiple organ disorders occur. A complicated course is characteristic. To make up for the deficiency, vitamin A is administered parenterally.
Vitamin A deficiency symptoms
The first sign of pathology is the deterioration of vision in low light (at dusk), the lengthening of the period of adaptation of the eyes to darkness to 8 seconds or more, the flashing of “flies” in front of the eyes. With the progression of the disease, there is a feeling of dryness and “sand” in the eyes. Cutaneous manifestations of retinol deficiency are represented by fine-grained peeling of the skin, roughness of the knees, elbows, decreased secretion of sweat and sebaceous glands.
The clinical picture is aggravated by changes in the appendages of the skin — increased fragility of the nail plates, thinning and hair loss, the appearance of dandruff. Drying out of the nasal mucosa leads to a deterioration of the sense of smell. In childhood, with a lack of vitamin A, there may be a delay in physical and mental development, a decrease in appetite, muscle dystrophy.
Complications
Complicated course is usually observed in stage III hypovitaminosis. A decrease in local resistance factors and pathological changes in the skin become the causes of activation of opportunistic infection with the development of pustular rashes on the skin and mucous membranes. With dysfunction of the mucous membranes of the upper respiratory tract, rhinitis, sinusitis are observed. Insufficient ventilation of the lungs due to obstruction of the bronchial tree can provoke prolonged bronchitis and pneumonia. Excessive keratinization of the mucous membranes of the urinary system potentiates urination disorders, urethritis, cystitis, sand formation in the kidneys, urolithiasis.
Beriberi A is characterized by a decrease in libido, menstrual cycle disorders in women (hypomenorrhea, anovulatory bleeding, amenorrhea), spermatogenesis in men. With endometrial keratosis, egg implantation is disrupted, female infertility is formed. A dangerous complication of vitamin A deficiency is progressive dystrophy and opacity of the cornea of the eye caused by xerophthalmia. In the absence of treatment, such patients show erosions and ulcers up to corneal perforation, keratomalacia, and panophthalmitis. With prolonged vitamin deficiency, blindness occurs. Against the background of a decrease in immunity, the risk of oncogenesis increases.
Diagnostics
Diagnosis can be difficult, due to the variety and non-specificity of symptoms, which is similar to the manifestations of dermatological, ophthalmological diseases. The possible development of vitamin A deficiency is evidenced by anamnestic data on insufficient, unbalanced nutrition, gastrointestinal diseases. They are the most informative in diagnostic terms:
- Determination of the level of retinol in the blood. Hypovitaminosis is diagnosed with a decrease of less than 0.3 mmol/l. To verify the diagnosis, repeated analysis is recommended after trial treatment with vitamin A. Additionally, the concentration of prealbumin and retinol-binding protein of blood serum is measured.
- Ophthalmological examination. With hypovitaminosis, the time of dark adaptation in the test with a sheet of white paper is prolonged. To exclude other ophthalmological pathology, the functional activity of the retina is measured in all patients using electroretinography and visual field defects are detected during scotometry.
- Contrast X-ray examination of the gastrointestinal tract. To detect possible structural changes in the digestive tract, radiography of the passage of barium through the small intestine, retrograde cholangiopancreatography is performed. If necessary, the examination is supplemented with esophagogastroduodenoscopy, CT of the abdominal cavity.
A decrease in the level of hemoglobin and erythrocytes in the general blood test is more often observed with hypovitaminosis in children, leukocytosis and increased ESR are detected in the case of secondary infection. Hypoproteinemia may be noted in the biochemical analysis of blood. Chest x-ray and bronchoscopy are recommended to assess the state of the respiratory organs, which allows detecting areas of metaplasia of the epithelium of the respiratory tract.
Retinol deficiency is differentiated with skin diseases (congenital ichthyosis, seborrheic dermatitis, eczema), eye diseases (retinitis pigmentosa, cataracts, diabetic retinopathy), other forms of vitamin and mineral deficiency (zinc deficiency, hypovitaminosis E), bronchopulmonary pathology (chronic obstructive pulmonary disease, cystic fibrosis). In addition to the examination of a gastroenterologist, the patient may be shown an examination by a dermatologist, ophthalmologist and other specialists.
Vitamin A deficiency treatment
The choice of therapeutic tactics depends on the etiology and severity of vitamin deficiency. For patients with alimentary retinol deficiency of stage 1, it is enough to correct the diet with the introduction of products with a high vitamin content. It is recommended to increase the amount of consumed milk, eggs, butter. Pork, beef, chicken, fish liver are natural depots of retinol and contain it in an easily digestible form. Vegetables of orange and red color — carrots, tomatoes, red pepper, pumpkin are useful from vegetable products. Also rich in vitamin are black currants, gooseberries, parsley, spinach, lettuce leaves.
The use of pharmaceuticals is indicated with moderate alimentary hypovitaminosis. As monotherapy, simple vitamin A preparations can be used. However, vitamin and mineral complexes are more effective, which also include tocopherol, which prevents the oxidation of retinol in the intestine, and zinc, which is involved in the activation and transport of the substance. At stage 3 of hypovitaminosis, vitamin preparations are administered parenterally. In secondary forms of vitamin deficiency, treatment is supplemented with etiopathogenetic therapy of the underlying disease in accordance with recommended protocols.
Prognosis and prevention
The probability of complete regression of pathological symptoms depends on the degree and form of vitamin A deficiency, the timeliness of diagnosis of the disease. The prognosis is relatively favorable for the primary form of the disease, which is well adjusted by a special diet. In advanced cases, disability is possible due to irreversible changes in the eyeball. To prevent hypovitaminosis, a varied diet with the inclusion of appropriate products in the diet, the use of balanced mixtures for artificial feeding of children, early diagnosis and adequate treatment of diseases of the digestive system, preventive administration of retinol to children in developing countries is recommended.
Literature
- Wiseman EM, Bar-El Dadon S, Reifen R. The vicious cycle of vitamin a deficiency: A review. Crit Rev Food Sci Nutr. 2017 Nov 22;57(17):3703-3714. – link
- D’Ambrosio DN, Clugston RD, Blaner WS. Vitamin A metabolism: an update. Nutrients. 2011 Jan;3(1):63-103. link
- Hombali AS, Solon JA, Venkatesh BT, Nair NS, Peña-Rosas JP. Fortification of staple foods with vitamin A for vitamin A deficiency. Cochrane Database Syst Rev. 2019 May 10;5(5):CD010068. link
- Harrison EH. Mechanisms involved in the intestinal absorption of dietary vitamin A and provitamin A carotenoids. Biochim Biophys Acta. 2012 Jan;1821(1):70-7. link
- Senoo H, Mezaki Y, Fujiwara M. The stellate cell system (vitamin A-storing cell system). Anat Sci Int. 2017 Sep;92(4):387-455. – link