Vitamin B1

Dry form (peripheral polyneuropathy)

The dry form of deficiency is characterized by pronounced damage to the peripheral nervous system. The pathological process in this form is a bilateral symmetric lesion of the nerve trunks, with the lower extremities being primarily and most severely affected.

Key clinical symptoms of the dry form include the following complex of manifestations:

• Sensory disturbances: patients regularly experience paresthesias and a distressing burning sensation in the feet. Notably, these symptoms show a marked tendency to significantly worsen at night.
• Pain syndrome and cramps: intense leg pain and painful cramps, localized predominantly in the calf muscles, are highly characteristic of the clinical picture.
• Motor disorders: there is a persistent feeling of muscle weakness and rapid fatigability, which manifest even during routine activities.
• Gait disturbance: due to the combination of pain syndrome, progressive weakness, and nerve fiber damage, patients develop a characteristic limp when walking.

Cardiovascular (wet) form

The wet form is distinguished by the predominance of cardiovascular pathology and hemodynamic disorders, although other organ systems are also involved in the pathological process.

This form is characterized by the development of the following pathological conditions:

• Myocardial dystrophy: profound impairment of trophism and contractile function of the myocardium.
• Vascular changes: a pathological decrease in peripheral vascular resistance occurs.
• Gastrointestinal tract involvement: dystrophic lesions of the mucous membrane and structures of the gastrointestinal tract develop.
• Neurological and sensory disorders: the wet form may be accompanied by marked visual impairment, as well as various psychiatric disorders.

Etiology of hypovitaminosis

The following mechanisms for the development of both primary and secondary hypovitaminosis are distinguished (including conditions associated with concomitant vitamin $B_2$ deficiency).

1. Primary hypovitaminosis Develops predominantly under the influence of alimentary factors, when nutrient intake does not cover the body's basic requirements:

• Direct lack of the vitamin in the daily diet.
• Excessive consumption of cow's milk, as well as products containing an excessive amount of animal proteins, leading to imbalance.

2. Secondary hypovitaminosis Caused by internal pathologies that disrupt metabolism and by iatrogenic factors:

• Impaired absorption processes (malabsorption syndrome) directly in the intestine.
• Increased physiological or pathological demand of the body for vitamin $B_2$.
• Nutrient assimilation disorders arising against the background of severe comorbid pathologies: chronic diarrhea, various liver diseases, and chronic alcoholism.
• Prolonged parenteral nutrition without the adequate inclusion of vitamin $B_2$ in infusion media.

Clinical picture and stages of development

The clinical manifestations of hypovitaminosis steadily progress depending on the degree of increasing deficiency and are traditionally divided into two main stages.

Stage of prehypovitaminosis At this initial stage, nonspecific functional disorders arise that require a thorough medical history taking:

• General malaise and systemic disorders of the patient's general condition.
• Night vision impairment, manifested by deteriorated visual adaptation under conditions of insufficient lighting.

Stage of pronounced hypo- and avitaminosis Characterized by a full-blown and severe clinical picture involving multiple systems:

• Angular cheilitis: the pathology begins with maceration and pronounced skin pallor at the corners of the mouth. Then, superficial cracks form in these areas, which subsequently undergo scarring. When a secondary fungal infection joins (specifically, Candida albicans), characteristic perleche is formed.
• Glossitis: the tongue becomes inflamed, acquires a characteristic bright red color, and its mucous membrane becomes pathologically dry.
• Dermatological manifestations: objectively observed redness of the skin, peeling, and development of seborrhea (pathological accumulation of sebaceous gland secretion directly in the hair follicles).
• Neurological disorders: join in the later stages and include the appearance of paresthesias, pathological hyperreflexia of tendon reflexes, and the development of ataxia.
• Hematological changes: formation of hypochromic anemia, as well as hemolytic anemia. The latter is pathogenetically closely related to the deficiency of the enzyme pyruvate kinase in erythrocytes.
• Effect on the fetus: with pronounced deficiency in the mother during pregnancy, there is an extremely high risk of developing severe skeletal anomalies in the fetus.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of myocardial dystrophy development in the wet form.
• Pathogenesis of decreased peripheral vascular resistance.
• The link between erythrocyte pyruvate kinase deficiency and hemolytic anemia.
• Role of Candida albicans in the complication of angular cheilitis.
• Impact of excessive animal protein and milk intake on the development of primary hypovitaminosis.

Other topics in "Chapter 14. Vitamin Metabolism Disorders"

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