Classification of Vitamin Deficiency
Based on the severity of the deficiency, three consecutive stages are distinguished:
- Suboptimal Status — the preclinical stage. It is characterized by latent disturbances in physiological and metabolic processes that require the nutrient. Clinical symptoms are either absent or isolated.
- Hypovitaminosis — a pronounced decrease in vitamin levels with a full clinical picture.
- Avitaminosis — the extreme degree of deficiency with complete depletion of reserves.
By etiology, the pathology is divided into two main groups: exogenous and endogenous. Exogenous forms result from insufficient dietary intake of vitamins (below the physiological requirement). They are typically seasonal and present with a latent course.
Endogenous Hypovitaminosis: Primary and Secondary
Endogenous forms are associated with impaired release of nutrients from food, disruptions in their synthesis, or factors blocking their effects. They are subdivided into hereditary (congenital) and acquired.
Primary (hereditary) forms manifest in early childhood. Their etiology includes genetic defects in cellular structures, tissues, and organs, as well as inadequate nutrient supply to the fetus during the prenatal period. Genetic metabolic defects have been described for all fat-soluble vitamins, as well as for vitamins $B_1$, $B_2$, $B_6$, $B_{12}$, folic acid, niacin, and biotin.
Secondary (acquired) forms develop postnatally under the influence of external and internal factors. The main mechanisms of their pathogenesis include:
- Dietary deficiency in children: use of unadapted infant formulas or low nutrient content in breast milk.
- Impaired digestion and absorption (malabsorption): stomach and intestinal diseases that prevent the release and assimilation of vitamins, anorexia, and dysbiosis (suppression of the microflora that synthesizes a number of vitamins).
- Increased requirement: occurs during pregnancy, fever, heavy physical exertion, hyperthyroidism, hypoxia, infections, diatheses, and allergies.
- Transport disorders: deficiency of specific blood transport proteins, most commonly resulting from liver pathology, where the majority of these proteins are synthesized.
- Impaired dissociation: the inability to release the active substance from the transport protein–vitamin complex.
- Receptor and intracellular disorders: disruptions in interaction with cellular receptors, blocking of intracellular effects, or impaired transformation of the vitamin into its active form (coenzyme).
Dysvitaminosis and Vitamin A Deficiency
An imbalance of vitamins in the body is termed dysvitaminosis. It is caused by unbalanced nutrition, selective gastrointestinal malabsorption, metabolic shifts, and altered physiological requirements. An important role is played by iatrogenic (behavioral) factors—unjustified supplementation with specific vitamins that can disrupt the metabolism of other nutrients.
As an example of specific pathology, consider vitamin A deficiency (hypovitaminosis A). It can be acquired or hereditary. The hereditary form is rare and characterized by impaired cell division, maturation, and subsequent cell destruction. Clinically, this manifests as corneal lesions with severe inflammation (keratitis) and night blindness (nyctalopia).