Vitamin B1

*Vitaminum B1*

For medical students2 min readUpdated 2026-10-10

Vitamin B1 (thiamine) is an essential micronutrient whose deficiency leads to severe systemic disorders. The classic presentation manifests as a dry form (peripheral neuropathy) or a wet form (cardiovascular), each with a specific pathogenesis and set of clinical symptoms.

Dry formManifests as bilateral symmetrical involvement of the nerve trunks of the lower extremities.

Wet formCharacterized by myocardial dystrophy (cardiomyopathy) and decreased peripheral vascular resistance.

Risk factorsChronic alcoholism, liver disease, chronic diarrhea, and malabsorption syndromes.

AnemiaHypochromic and hemolytic anemia may develop (pyruvate kinase deficiency).

Dry Form (Peripheral Polyneuropathy)

The dry form of deficiency is characterized by pronounced damage to the peripheral nervous system. The pathological process presents as bilateral symmetrical involvement of nerve trunks, with the lower extremities being affected first and most severely.

Key clinical symptoms of the dry form include:

Sensory disturbances: Patients regularly experience paresthesias and a distressing burning sensation in the feet. Notably, these symptoms tend to worsen significantly at night.
Pain and cramps: Intense leg pain and painful cramps, predominantly localized in the calf muscles, are highly characteristic.
Motor disorders: A constant sensation of muscle weakness and rapid fatigability occur, manifesting even during routine activities.
Gait abnormalities: Due to the combination of pain, progressive weakness, and nerve fiber damage, patients develop a characteristic limping gait.

Cardiovascular (Wet) Form

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

This form is characterized by the following pathological conditions:

Myocardial dystrophy: Profound impairment of trophic support and contractility of the heart muscle.
Vascular changes: A pathological decrease in peripheral vascular resistance occurs.
Gastrointestinal involvement: Dystrophic lesions develop in the mucous membranes and structures of the gastrointestinal tract.
Neurological and sensory disorders: The wet form may be accompanied by marked visual impairment and various psychiatric disorders.

Etiology of Hypovitaminosis

Both primary and secondary hypovitaminosis mechanisms are distinguished (including states associated with concomitant vitamin $B_2$ deficiency).

1. Primary Hypovitaminosis Develops primarily due to dietary factors when nutrient intake fails to meet basic bodily requirements:

Direct dietary deficiency of the vitamin.
Excessive consumption of cow's milk and products containing excess animal proteins, leading to imbalance.

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

Impaired intestinal absorption processes (malabsorption syndrome).
Increased physiological or pathological requirement for the vitamin.
Impaired nutrient assimilation against the background of severe comorbidities: chronic diarrhea, various liver diseases, and chronic alcoholism.
Prolonged parenteral nutrition without adequate inclusion of vitamins in infusion fluids.

Clinical Presentation and Stages of Development

Clinical manifestations of hypovitaminosis progress steadily depending on the severity of the deficiency and are traditionally divided into two main stages.

Stage of Pre-hypovitaminosis At this initial stage, non-specific functional disorders arise, requiring a thorough history taking:

General malaise and systemic disorders of the patient's general condition.
Impairment of dark adaptation, manifesting as worsened visual adaptation in low-light conditions.

Stage of Manifest Hypo- and Avitaminosis Characterized by a fully developed and severe clinical picture involving multiple systems:

Angular cheilitis: Pathology begins with maceration and pronounced skin pallor at the corners of the mouth. Superficial fissures then form in these areas, which subsequently undergo scarring. When a secondary fungal infection joins (particularly Candida albicans), specific perleche (angular stomatitis) forms.
Glossitis: The tongue becomes inflamed, acquires a characteristic bright red color, and its mucous membrane becomes pathologically dry.
Dermatological manifestations: Objectively observed skin redness, scaling, and development of seborrhea (pathological accumulation of sebaceous gland secretions directly within hair follicles).
Neurological disorders: Join in later stages and include paresthesias, pathological hyperreflexia of deep tendon reflexes, and ataxia.
Hematologic changes: Development of hypochromic anemia and hemolytic anemia. The latter is pathogenetically closely related to erythrocyte pyruvate kinase deficiency.
Fetal impact: With severe maternal deficiency during pregnancy, there is an extremely high risk of severe skeletal anomalies in the fetus.

Mnemonic

Dry form = Nerves and Legs (symmetrical polyneuropathy, limp, cramps). Wet form = Heart and Vessels (myocardial dystrophy, dropped vascular resistance).

Frequently asked questions

What are the causes of primary vitamin B1 hypovitaminosis?

Primary vitamin B1 hypovitaminosis develops due to insufficient dietary vitamin intake. The source also notes excessive consumption of milk and foods containing animal proteins.

What factors lead to the development of secondary vitamin B1 hypovitaminosis?

The cited sources do not separately list the factors for secondary vitamin B1 hypovitaminosis alone. For secondary hypovitaminosis, the text lists: impaired intestinal absorption; increased bodily requirement for vitamin B2; assimilation disorders against the background of chronic diarrhea, liver disease, chronic alcoholism; parenteral nutrition without B2 inclusion.

What is the biochemical function of vitamin B1 in the body?

The biochemical function of vitamin B1 lies in the biological activity of its coenzyme forms. The most active coenzyme form is thiamine diphosphate. Vitamin B1 participates in metabolism as follows:

Maintenance of enzymatic activity — prevents drops in transketolase activity.
Oxidative reactions — ensures oxidative decarboxylation reactions of pyruvate and 2-oxoglutarate.

The vitamin is essential for the energy supply of carbohydrate-dependent tissues (especially nervous tissue) and prevents the inhibition of nucleic acid, steroid, and higher fatty acid synthesis reactions.

What is the daily requirement of vitamin B1 for an adult?

The daily requirement of vitamin B1 for an adult is 1–3 mg. Sources of vitamin B1 include whole grain bread, peas, beans, and meat products.

What is the nature of nerve damage in the dry form of deficiency?

The dry form is characterized by strictly bilateral symmetrical involvement of nerve trunks, which predominantly and most severely affects the lower extremities.

What hematologic changes are observed in severe avitaminosis?

In the fully developed stage, hypochromic anemia develops, as well as hemolytic anemia, the pathogenesis of which is directly related to erythrocyte pyruvate kinase deficiency.

How does vitamin deficiency affect intrauterine fetal development?

If severe deficiency is observed in the mother during pregnancy, it can lead to the formation of severe congenital skeletal malformations in the fetus.

What is angular cheilitis and how does it develop?

It is a lesion of the corners of the mouth: first, maceration and skin pallor occur, followed by superficial fissures and scarring. When infected with the fungus Candida albicans, angular stomatitis develops.

Go deeper

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.
The role of Candida albicans in complicating angular cheilitis.
The impact of excess animal protein and milk on the development of primary hypovitaminosis.