Vitamin B12 Deficiency and Addison-Biermer Disease
A classic manifestation of cyanocobalamin deficiency is Addison-Biermer disease. The pathogenesis of this disease is based on marked gastric mucosal atrophy. This structural alteration predictably leads to a severe deficit of Castle's intrinsic factor, without which intestinal absorption of the vitamin becomes impossible.
The key and most severe neurological complication of this condition is funicular myelosis — profound degenerative processes in the spinal cord structures. The symptom complex of funicular myelosis includes:
- Paresthesias (various sensory disturbances).
- Shaky, unsteady gait.
- Attenuation of normal reflex responses and the appearance of pathological reflexes.
- Mental disorders (develop in severe and prolonged courses of the pathology).
Hereditary forms of deficiency
Genetically determined (hereditary) deficiency of Vitaminum B12 occurs due to congenital defects at various stages of its complex metabolism. The etiology of such conditions includes impaired synthesis of Castle's intrinsic factor, failures in the mechanisms of intestinal absorption of cobalamins, as well as quantitative or structural anomalies of transport proteins — transcobalamins I and II (their complete absence, significant decrease in concentration, or functional efficiency).
The clinical presentation of hereditary deficiency is characterized by three main manifestations:
- Megaloblastic anemia.
- Metabolic acidosis, which is caused by a toxic excess of methylmalonate.
- Decreased efficiency of immunobiological surveillance, making the organism extremely vulnerable and promoting the frequent development of infectious diseases.
B12 Hypervitaminemia: Causes and Clinical Significance
In real clinical practice, true hypervitaminosis is extremely rare. Doctors much more often encounter the phenomenon of B12 hypervitaminemia — an abnormally high content of the vitamin directly in the blood serum.
The causes of such a pathological increase in cyanocobalamin levels are quite diverse:
- Excessive intake into the body (typically during unjustified medical use of Vitaminum B12 preparations).
- Massive release of the vitamin from internal tissue depots.
- Excessive production or impaired elimination of transcobalamins.
- Deficiency or complete absence of affinity of transcobalamins for the vitamin.
It is important to understand that a high level of the vitamin in the blood is a symptomatic sign. It signals the presence of severe, potentially life-threatening pathologies.
Diseases associated with B12 excess
Symptomatic hypervitaminemia accompanies a number of serious systemic disorders.
| Pathology group | Examples of associated diseases |
|---|---|
| Oncological | Solid neoplasms, hemoblastoses |
| Hepatobiliary | Hepatoses, including severe hepatic failure |
| Systemic | Kidney diseases, bronchopulmonary pathologies, multiple organ failure |
| Immune and toxic | Immune autoaggressive forms of pathology, alcoholism |
Hypervitaminemia in itself is not a benign condition and can cause a number of side effects. These include various allergic reactions, pronounced hepatotoxic effects, and, upon exposure to large doses of the vitamin, even a procarcinogenic effect. Elimination of hypervitaminemia is achieved exclusively by identifying and treating the underlying pathology that led to the excess of the vitamin in the blood.
Briefly: answers to topical questions
Where exactly in the gastrointestinal tract does the absorption of the vitamin B12-Castle's intrinsic factor complex occur?
The attachment of the vitamin B12-Castle's intrinsic factor complex occurs to the ileal epithelium, followed by its absorption into the blood.
Stages of transport and assimilation in the GI tract:
- Duodenum — here the vitamin forms a complex with the intrinsic factor.
- Ileum — attachment of the ready complex to the epithelium takes place.
Note: one of the sources also indicates that the absorption mechanism occurs in the stomach.
Which biochemical reactions are catalyzed by coenzyme forms of vitamin B12?
The coenzyme form of vitamin B12 participates in the biochemical reaction of methionine regeneration.
- Methionine restoration — the process of methionine regeneration from homocysteine, in which vitamin B12 in the form of methylcobalamin acts as a methionine synthase coenzyme.
To memorize the triad of hereditary B12 deficiency, use the mnemonic AAA: Anemia (megaloblastic), Acidosis (metabolic due to methylmalonate), Immunodeficiency (decreased surveillance).
Class and exam questions
What are the intrinsic and extrinsic Castle's factors?
The extrinsic factor is vitamin B12 (cyanocobalamin) itself, entering the body. The intrinsic factor is synthesized by the gastric mucosa and is absolutely essential for the absorption of the extrinsic factor in the intestine.
Why does metabolic acidosis develop in B12 deficiency?
Vitamin deficiency blocks normal metabolism, leading to the excessive accumulation of methylmalonate. It is this acid that shifts the acid-base balance of the blood toward acidosis.
Is specific treatment required for vitamin B12 hypervitaminosis?
No, there is no need to lower the vitamin level in isolation. Hypervitaminemia is a symptom, so it is necessary to diagnose and treat the underlying pathology (e.g., hepatosis or neoplasm).
What else to study on this topic
- Pathogenesis of megaloblastic hematopoiesis in cobalamin deficiency.
- Mechanisms of development of funicular myelosis and degeneration of spinal cord structures.
- The role of transcobalamins I and II in vitamin B12 transport.
- Biochemical basis of methylmalonate accumulation and acidosis development.
- Procarcinogenic effects of high doses of cyanocobalamin.
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