Primärer und sekundärer Vitaminmangel – Symptome, Folgen und Ursachen von Nährstoffdefiziten

Vitamin deficiency, clinically referred to as hypovitaminosis, represents a pathological condition arising from inadequate intake of one or more essential vitamins in the body. This state manifests through a spectrum of specific dysfunctions and disease syndromes, the nature of which depends on the type of deficient vitamin. The primary etiologic factor behind this disorder is a prolonged, improperly balanced diet lacking in necessary nutrients, though other causes—such as malabsorption or increased physiological demand—cannot be ruled out.

Although the human body requires only relatively modest quantities of vitamins compared to macronutrients, insufficient intake of these micronutrients can disrupt homeostatic equilibrium and impair cellular and systemic function. **Primary hypovitaminosis** arises from a sustained yet moderate dietary deficiency of one or more vitamins, independent of confounding absorptive or metabolic disturbances. In contrast, **secondary hypovitaminosis** stems from malabsorption syndromes (e.g., celiac disease or inflammatory bowel disorders), pharmacologic interference (such as prolonged antibiotic use suppressing vitamin-B-synthesizing gut microbiota), or elevated physiological demand (as observed during pregnancy, rapid growth phases, or chronic oxidative stress conditions). Prolonged, severe deficiency—or the absolute absence—of a vitamin or vitamin complex culminates in **avitaminosis**, a clinically severe state associated with a heightened risk of permanent organ damage.

Whether dealing with hypervitaminosis or deficiency, the symptoms of vitamin imbalance are seldom pathognomonic or exclusive to a single nutrient. Nevertheless, their emergence should prompt immediate consideration of one’s overall health status alongside a thorough evaluation of dietary patterns and potential nutritional gaps. The most prevalent clinical manifestations of avitaminosis include: excessive xerosis and desquamation of the epidermis, hyperkeratinization (thickening of the stratum corneum), onychorrhexis (brittleness and lamellar splitting of the nail plates), trichorrhexis (loss of hair elasticity resulting in fragility and diffuse alopecia), xerostomia and angular cheilitis (dryness of oral mucosa with fissuring at the labial commissures), gritty sensation beneath the eyelids and conjunctival burning, persistent fatigue and reduced physical endurance, dyssomnia (sleep disturbances), impaired cognitive focus, emotional lability characterized by irritability or depressive mood swings, recurrent cephalalgia and vertigo, gastrointestinal dysfunction (including constipation and anorexia), heightened susceptibility to viral and bacterial pathogens, delayed tissue repair (e.g., protracted wound healing), menstrual cycle irregularities in women, and myalgic complaints such as muscle cramps, stiffness, and generalized myalgia.

Insufficient intake of vitamin A disrupts retinal function, manifesting as impaired vision—particularly under low-light conditions (a condition known as *nyctalopia* or "night blindness")—as well as corneal xerosis, ulceration, and potential irreversible vision loss in advanced stages. Additionally, the skin undergoes hyperkeratinization, becoming rough, dull, and thickened. Prolonged deficiency may compromise the mucosal integrity of the gastrointestinal tract, respiratory pathways, and urinary system; induce neurological impairments; weaken immune responses; and disrupt reproductive functions. Hypovitaminosis D triggers demineralization of bone tissue: in pediatric populations, this presents as rickets (including thoracic deformities and delayed dentition), whereas in adults, it progresses to osteomalacia or osteoporosis. Vitamin E deficiency promotes peroxidation of polyunsaturated fatty acids, resulting in cellular membrane damage, myopathic dystrophy, premature cutaneous aging, and neurological dysfunctions; in infants, it may precipitate anemia. A lack of vitamin K reduces prothrombin levels, prolongs coagulation time, impairs tissue regeneration, and provokes epistaxis, gastrointestinal hemorrhage, and urogenital bleeding; in women, it exacerbates menorrhagia, while in neonates, it can lead to hemorrhagic disease. Deficiencies in B-complex vitamins yield diverse clinical outcomes depending on the specific vitamin: these include peripheral neuropathy and muscle atrophy (thiamine), growth retardation and oral mucosal lesions (riboflavin), anemia (pyridoxine), *burning feet syndrome* and hair depigmentation (pantothenic acid), neural tube defects in fetuses and megaloblastic anemia (folic acid), psoriasiform dermatological changes on the extremities, hypercholesterolemia, and alopecia (biotin). Ascorbic acid deficiency culminates in scurvy—characterized by tooth loosening and loss, gingival hemorrhage, heightened susceptibility to infections, impaired collagen biosynthesis, and delayed wound healing.

The primary etiology of vitamin deficiencies stems from an inadequately balanced diet, particularly one deficient in plant-based foods—vegetables and fruits—which constitute the optimal source of these micronutrients. Irregular meal consumption, skipping meals, or ingesting insufficient portions further exacerbates the restricted availability of not only vitamins but also other essential nutrients. Additionally, hypovitaminosis frequently arises from improper food processing techniques that degrade heat-sensitive vitamins during preparation. Pharmacological interventions also contribute to deficiencies, as certain medications may disrupt vitamin metabolism or absorption. Gastrointestinal disorders impairing nutrient uptake, alongside specific physiological states, further compound the risk. Of particular concern is pregnancy, during which the demand for select vitamins (e.g., folic acid, vitamin D) increases substantially; inadequate intake may precipitate severe complications for both maternal and fetal health. Environmental factors also play a critical role: seasonal variations (e.g., reduced sunlight exposure in winter months) and geographic latitude—such as in temperate zones like Poland—commonly result in vitamin D deficiency due to insufficient cutaneous synthesis from limited solar radiation. Vitamins are indispensable for maintaining systemic homeostasis, governing metabolic pathways, cellular growth and differentiation, and immune function. Their deficiency can precipitate significant dysfunctions, underscoring the necessity of recognizing individual requirements, which fluctuate with age, sex, and health status.