Hypovitaminoses

Classification of vitamin deficiency

According to the severity of the deficiency, three consecutive stages are distinguished:

1. Subnormal vitamin status — the preclinical stage. It is characterized by latent disorders of physiological and metabolic processes involving the nutrient. Clinical symptoms are either absent or isolated.
2. Hypovitaminosis — a pronounced decrease in vitamin levels with a full-blown clinical picture.
3. Avitaminosis — the extreme degree of deficiency and complete depletion of reserves.

According to origin, the pathology is divided into two main groups: exogenous and endogenous. Exogenous forms arise due to insufficient dietary intake of vitamins with food (below physiological requirements). They are typically characterized by seasonality and a latent (hidden) course.

Endogenous hypovitaminoses: primary and secondary

Endogenous forms are associated with impaired release of nutrients from food, disruption of their synthesis, or the presence of factors blocking their effects. They are subdivided into hereditary (congenital) and acquired.

Primary (hereditary) forms manifest at an early age. Their etiology includes genetic defects in cellular structures, tissues, and organs, as well as insufficient nutrient supply to the fetus during the intrauterine 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 in the postnatal period under the influence of external and internal factors. The main mechanisms of their pathogenesis:

• Alimentary deficiency in children: the use of unadapted 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 demand: occurs during pregnancy, fever, heavy physical exertion, hyperthyroidism, hypoxia, infections, diathesis, and allergies.
• Transport disorders: deficiency of specific blood transport proteins. Most often, this is a consequence of liver pathology, where the majority of such proteins are synthesized.
• Impaired dissociation: the inability of the active substance to dissociate from the transport protein–vitamin complex.
• Receptor and intracellular disorders: disruptions in interaction with cellular receptors, blocking of effects inside the cell, or impaired transformation of the vitamin into its active form (coenzyme).

Dysvitaminosis and vitamin A deficiency

Disruption of the vitamin balance in the body is called dysvitaminosis. Its development is caused by an unbalanced diet, selective malabsorption in the gastrointestinal tract, metabolic shifts, and changes in physiological requirements. A separate role is played by the iatrogenic (behavioral) factor — the unjustified intake of certain vitamin supplements, which can disrupt the metabolism of other nutrients.

As an example of a specific pathology, we can consider vitamin A hypovitaminosis. It can be acquired or hereditary. The hereditary form is rare and is characterized by impaired cell division, maturation, and subsequent destruction. Clinically, this manifests as lesions of the corneal cells with the development of severe inflammation (keratitis) and the onset of night blindness.

Class and exam questions

What else to study on this topic

• Mechanisms of malabsorption syndrome development in gastrointestinal pathologies.
• The role of the intestinal microflora in vitamin synthesis and the consequences of dysbiosis.
• Congenital metabolic defects of fat-soluble and water-soluble vitamins.
• Pathogenesis of keratitis and night blindness in hereditary vitamin A deficiency.
• The impact of hypoxia, infections, and allergic diseases on vitamin requirements.

Other topics in "Chapter 14. Vitamin Metabolism Disorders"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.