Etiology of Pyridoxine Deficiency
The development of vitamin B6 deficiency in humans is often associated with external factors, particularly ongoing pharmacotherapy. Pathophysiology identifies two main mechanisms leading to decreased levels of this vitamin:
- Suppression of normal intestinal bacterial flora. Intestinal bacteria are known to synthesize pyridoxine independently, covering part of the body's requirement for this substance. However, antibacterial therapy suppresses these microorganisms. As a result, endogenous synthesis ceases, becoming a significant factor in deficiency development.
- Use of drugs that act as direct vitamin B6 antagonists. Certain drugs directly interfere with normal pyridoxine metabolism. These include antituberculosis drugs (isonicotinic acid hydrazide derivatives), glucocorticoid hormones, and oral contraceptives containing estrogens.
Clinical Presentation of Hypovitaminosis
The clinical picture of pyridoxine deficiency develops gradually. Depending on the severity of the vitamin shortage, the pathological process is divided into two sequential stages.
1. Stage of B6 Prehypovitaminosis At this initial stage, non-specific changes occur, primarily affecting the psychoemotional sphere and general well-being. Characteristic signs of prehypovitaminosis include:
- Marked generalized fatigue and rapid exhaustion under routine exertion.
- Increased irritability.
- General psychomotor slowing.
- Sleep disturbances manifesting as persistent insomnia.
2. Stage of B6 Hypovitaminosis and Avitaminosis With further depletion of vitamin stores, specific clinical signs develop, affecting the skin, mucous membranes, peripheral nervous system, and hematopoiesis:
- Dermatological disorders: development of seborrheic dermatosis. Typical localization of skin rashes includes the face, neck, and scalp.
- Mucous membrane lesions: inflammatory processes in the oral cavity and lips, clinically manifesting as stomatitis, glossitis, and cheilosis.
- Neurological disorders: peripheral polyneuropathies. The condition manifests as paresthesias (subjective sensory disturbances), which progress to complete loss of reflexes.
- Hematological changes: peripheral blood tests show a decreased lymphocyte count (lymphopenia) and anemia. In most cases, the anemia is normoblastic and hypochromic, though megaloblastic anemia may rarely develop.
Vitamin B6 Hypervitaminosis
Importantly, not only deficiency but also an excess of pyridoxine can cause severe pathological changes. Vitamin B6 hypervitaminosis develops exclusively from the intake of excessive doses of the vitamin.
High-dose pyridoxine toxicity has a pronounced neurological profile. Characteristic features of hypervitaminosis include:
- Progressive ataxia — a steadily worsening impairment in the coordination of voluntary movements.
- Dissociated sensory loss in the lower extremities. This specific neurological phenomenon involves the selective impairment of sensory modalities. The patient experiences a complete loss of deep proprioceptive sensitivity (muscle-joint sense) and vibratory sensation, while superficial sensory modalities — pain, temperature, and tactile sensitivity — remain completely intact.