Hypovitaminosis in pregnancy is a pathological condition characterized by a deficiency during gestation of low–molecular organic compounds (vitamins) necessary for the implementation of metabolic functions in the body of the mother and fetus and the normal development of the latter. Hypovitaminosis can manifest signs of early toxicosis, weakness, fatigue, severe dryness of the skin, edema, neurological disorders, increased bleeding. The diagnosis is made based on the results of a physical examination, anamnestic data, laboratory tests. Conservative treatment – correction of the diet, taking vitamin-containing drugs.
E56.9 Vitamin deficiency, unspecified
Hypovitaminosis in pregnanсу is a deficiency of vitamins in the body of a pregnant woman, formed both before and during gestation. The lack of these substances adversely affects the health of the mother and the unborn child, in some cases leads to congenital anomalies of the fetus. Deficiency of carotenoids (precursors of vitamin A – retinol) is observed in 25-94% of women, B vitamins (B1 – thiamine, B2 – riboflavin, B3–PP, or nicotinic acid, B6 – pyridoxine, B9 – folic acid, B12 – cyanocobalamin) – in 20-100%, vitamin C (ascorbic acid) – at 13-50%. Often there is a lack of vitamin D (calciferol), less often – vitamin E (tocopherol). Regardless of the season, region of residence, age category and professional affiliation, 70-80% of pregnant women have polyhypovitaminosis (deficiency of three or more vitamins).
The main cause of hypovitaminosis at the stage of gestation is a physiologically justified increased need for vitamins. Thus, the daily need for ergocalciferol (one of the forms of calciferol) increases fivefold, folic acid – by two, and other vitamins – by 10-50%. However, hypovitaminosis can develop even before pregnancy, and at the stage of fetal gestation there may be additional causes of vitamin deficiency:
- Lack of intake of vitamins from food. A meager diet (intentional or forced reduction of nutrition, for example, in order to lose weight), mono-diets (rice, leading to thiamine deficiency, or corn, carrying nicotinic acid deficiency), an imbalance of optimal ratios between vitamins in the daily diet can lead to alimentary vitamin deficiency. Factors that reduce the concentration of vitamins in products include long-term storage, heat treatment, irrational use (for example, sufficient fat in the diet is necessary for the absorption of vitamins A, E, D, and some products are not recommended to be consumed together due to the high content of enzymes that destroy vitamins).
- Increasing the need. The rate of vitamin intake increases when it is too early (up to 18 years) or late (after 35 years) pregnancy, intense physical and psycho-emotional stress, living in southern (retinol deficiency) or northern (calciferol deficiency) regions. Tobacco smoking and alcohol consumption also increase the daily norms of vitamins.
- Violation of assimilation. Taking certain medications (antibiotics, calcium channel blockers, antidepressants, salicylates, neuroleptics, glucocorticosteroids), regular use of mineral oils and other laxatives can lead to violations of the cleavage, absorption of vitamins and their normal transformations in the body.
- Diseases. Various pathologies can contribute to impaired absorption of vitamins at any stage, increase the need for them, disrupt their synthesis in the body. Diseases that increase the risk of hypovitaminosis include diabetes mellitus, infections and intoxication, lesions of the hepatobiliary system, pancreas, stomach and intestines, thyroid pathology, genetic disorders of vitamin metabolism.
Vitamins, not being nutrients, are necessary to ensure the normal course of all life processes, their lack leads to various pathologies associated with functional disorders and organic damage to the nervous, immune, hematopoietic and other systems, both mother and fetus. Derivatives of water-soluble vitamins (C and group B) are involved in the catalysis of protein, carbohydrate and fat metabolism. The result of the lack of ascorbic acid is increased permeability and fragility of the vessel walls. Deficiency of B3 leads to disorders of cellular respiration, redox processes, lipid metabolism, protein synthesis.
Thiamine and pyridoxine deficiency leads to a violation of the transmission of nerve impulses. The lack of riboflavin adversely affects the functions of the central and autonomic nervous system, tissue respiration, regulation of erythropoiesis, reduces hemoglobin synthesis. The lack of folic acid and cyanocobalamin causes disorders of the processes of hematopoiesis, regeneration and growth, and the functioning of the nervous system. A decrease in protein and nucleic acid synthesis associated with hypovitaminosis B5 inhibits the growth of rapidly growing fetal cells and dramatically increases the risk of birth defects. Hypovitaminosis B6, B9 and B12 leads to an increase in the blood plasma of the amino acid homocysteine, which has cyto- and neurotoxic effects, which contributes to the development of gestosis and carries the threat of miscarriage.
Fat-soluble vitamins A and E have an antioxidant effect, in addition, retinol, like calciferol, have a hormone-like effect. Retinol deficiency leads to a slowdown in epithelial renewal and a decrease in the synthesis of the pigment rhodopsin, which provides night vision. The lack of calciferol leads to a violation of the absorption of calcium, a violation of the regulation of cell growth. The consequence of the lack of tocopherol is a decrease in the synthesis of collagen and elastane, the destruction of red blood cells.
By origin, hypovitaminosis is usually divided into exogenous, or alimentary (associated with a lack of vitamin intake), and endogenous (due to reduced assimilation or increased consumption). In pregnant women, the lack of most vitamins is endogenous in nature. Vitamin deficiency develops gradually. According to the degree of its severity , there are three consecutive stages:
- Stage I – prehypovitaminosis (subnormal vitamin supply). Externally, it is characterized by general signs and the absence of specific ones. It is possible to detect the disease at this stage only with the help of laboratory tests.
- Stage II – hypovitaminosis. At this stage, specific signs of a lack of a specific vitamin (vitamins) begin to appear, which is confirmed by a laboratory blood test.
- Stage III – beriberi. The extreme form of vitamin deficiency is characterized by an almost complete absence of vitamin in body fluids and tissues and bright specific symptoms. In obstetrics in developed countries, pregnant women with beriberi are very rare. These are women, mostly from the poorest strata of society or with a serious illness that prevents the normal absorption of vitamins. Some previously widespread extreme forms of vitamin deficiency have received their own names: scurvy (vitamin deficiency C), beriberi (pronounced B1 deficiency), pellagra (significant shortage of nicotinic acid).
At the first stage, vitamin deficiency is manifested by an indefinite general symptoms: lack of appetite, weakness, apathy, drowsiness, decreased performance and the ability to concentrate attention. There is a decrease in the body’s resistance, expressed by a tendency to colds, slowing down wound healing. Later, with the transition to the stage of hypovitaminosis in pregnancy, characteristic signs of vitamin deficiency begin to appear, at first wearing a worn character and gaining clearer and brighter expression as vitamin deficiency increases.
Hypovitaminosis B1 has neurological symptoms: weakness in the lower extremities, unsteadiness of gait, a feeling of “goosebumps” tightening the “stocking” or “sock” on the legs, pronounced pain with light touches. Lack of B2 is accompanied by pericorneal injection (red-purple wide rim around the iris), cheilosis, angular stomatitis, glossitis. The tongue is swollen, with hypertrophied papillae, sometimes with a sloughed mucous membrane. Lack of vitamin B6 leads to irritability or lethargy, seizures, edema, early toxicosis. The severity of manifestations increases with combined hypovitaminosis B12 and B9.
Vitamin B3 deficiency is expressed by skin manifestations (dryness and peeling of the skin of the abdomen, sides, extensor surfaces of the arms and legs, the appearance of foci of redness and hyperpigmentation on exposed parts of the body, thickening and roughness of the tongue), diarrhea. In some cases, neurological and mental disorders may develop – from the peripheral nervous system (similar to hypovitaminosis B1), headaches, dizziness, dementia. Hypovitaminosis B9 is not accompanied by pronounced symptoms (weakness, anxiety, insomnia, dry mouth, redness of the tongue may occur), but it has the most detrimental effect on fetal development. The combined lack of vitamin B12 exacerbates the severity of external signs and the teratogenic effect.
The lack of ascorbic acid is accompanied by bleeding gums, frequent nosebleeds. Gray- or purple-cyanotic nodules may appear on the skin of the buttocks, thighs, shins and the inner surface of the hands in the area of hair follicles. As a result of minor physical impact, subcutaneous hemorrhages and intramuscular hematomas (bluish-colored swellings hot to the touch) are formed, accompanied by severe pain and localized most often in the lower extremities. Hemorrhages in the joints may develop with a local increase in temperature, limited mobility, swelling, pain in the area of the affected joint.
The result of vitamin A deficiency is increased dryness of the skin with a tendency to keratinization, especially clearly manifested in the flexor area of the elbow joints, a tendency to acne. Xerophthalmia is also observed (manifested by lacrimation and pain with visual tension and in bright light conditions) and increased sensitivity of tooth enamel, at a late stage – hemeralopia. Vitamin D deficiency is manifested by sleep disorders, dryness and burning in the mouth, over time there is a tendency to spontaneous bone fractures. Vitamin E deficiency leads to muscle weakness, speech disorders, impaired coordination and vision.
Mothers with vitamin deficiency B1, even after treatment, may have residual symptoms of polyneuritis for many years. The most serious consequences of hypovitaminosis are the adverse effects on the course of pregnancy and the fetus. A significant shortage of vitamins E, A, and group B can lead to a slowdown in embryo growth, stillbirth, fetal abortion and premature birth. Studies confirm that at least a third of neural tube development defects (cerebral hernias, anencephaly) are associated with a lack of folic acid. Hypovitaminosis A can lead to abnormalities of the development of the genitourinary system and the organ of vision, lack of B2 – congenital heart defects, deformities of the limbs, cleavage of the hard palate, hydronephrosis and hydrocephalus, vitamin D deficiency – neonatal rickets, cataract, defects of tooth enamel.
Hypovitaminosis in pregnancy can affect various organs and tissues, its diagnosis is difficult due to the need to differentiate disorders caused by hypovitaminosis with disorders of other etiology: neurodermatitis, psoriasis, hepatitis and hepatosis, hemorrhagic vasculitis, infectious, diabetic and toxic polyneuropathy. Diagnostic measures are carried out with the participation of an obstetrician-gynecologist, therapist, gastroenterologist, dermatovenerologist, neurologist and include the following studies:
- Clinical examination. During the survey and examination, according to the anamnesis (assessment of the composition of the diet, information about existing diseases, surgical operations performed, the use of medicines and biologically active additives) and the results of the examination (the presence of characteristic skin lesions, changes in nerve reflexes), mono- or polyhypovitaminosis can be suspected.
- Laboratory blood tests. A general clinical analysis can detect megaloblastic anemia, indirectly indicating a long-term deficiency of cyanocobalamin and folic acid. Biochemical blood testing for vitamins allows you to verify the diagnosis – to obtain quantitative data on the content of vitamins.
Treatment of hypovitaminosis in pregnancy is carried out under the guidance of an obstetrician-gynecologist with the involvement of a nutritionist and a clinical pharmacologist. Hypovitaminosis in pregnancy is treated with conservative methods – medication and diet. Currently, results have been obtained concerning the effective correction of the level of hypovitaminosis D in pregnant women with the help of UVI, but this method has not yet found widespread use.
- Medical treatment. Vitamin therapy is prescribed (one or several, if necessary) in a therapeutic dose until the deficiency is fully compensated. In the future, maintenance doses are used in a continuous course throughout pregnancy (usually in the form of multivitamin complexes).
- Diet therapy. In order to reduce the therapeutic dose of the drug and maintain vitamin supply after drug correction, an optimal diet is selected – balanced and varied (including fresh vegetables and fruits, cereals, meat, fish, easily digestible fats). Since during pregnancy it is impossible to fully satisfy the need for vitamins only by receiving them from food, additional use of multivitamin complexes is mandatory.
Prognosis and prevention
For the mother, the prognosis is favorable in most cases – vitamin therapy most often contributes to the complete restoration of functions disrupted due to vitamin deficiency. For the fetus, the outcome is not so optimistic due to the fact that a number of severe anomalies develop already in the first month of pregnancy and are a consequence of hypovitaminosis in pregnancy that occurred much earlier than conception. Thus, prevention should ideally begin three months before the planned pregnancy (during this period, the protective concentration of folates in red blood cells is achieved). Preventive measures include the organization of a full-fledged, balanced diet in vitamins, macro- and microelements, as well as the intake of multivitamin complexes, daily sun exposure for half an hour, starting from the stage of pre-pregnancy preparation and before childbirth.